History of database changes

20 August, 2026 (Version: 20260820AU) (Latest version)

Changed Ceritinib in Non-small cell lung cancer with ALK EML4-ALK Fusion, Fusions: 1

Comments changed: PBS reimbursed. Requires fluorescence in situ hybridisation (FISH) testing for ALK gene rearrangement, defined as 15% (or greater) positive cells. ASCEND-5 – In post-crizotinib and chemotherapy setting, Ceritinib had superior median PFS than 5.4 v docetaxel 1.6 months. ASCEND-4 – In first-line setting, Ceritinib has superior PFS 16.6 vs platinum chemotherapy 8.1 months.PBS reimbursed. Requires fluorescence in situ hybridisation (FISH) testing for ALK gene rearrangement, defined as 15% (or greater) positive cells. ASCEND-5 – In post-crizotinib and chemotherapy setting, Ceritinib had superior median PFS than 5.4 v docetaxel 1.6 months. ASCEND-4 – In first-line setting, Ceritinib has superior PFS 16.6 vs platinum chemotherapy 8.1 months.. (First curated: 2020-04-16)

Changed Crizotinib in Non-small cell lung cancer with ALK EML4-ALK Fusion, Fusions: 1

Comments changed: PBS reimbursed. Requires fluorescence in situ hybridisation (FISH) testing for ALK gene rearrangement, defined as 15% (or greater) positive cells. PROFILE1014 trial – in the first-line setting, Crizotinib had a superior PFS 10.9 vs chemotherapy 7.0 months. In the second-line setting, Crizotinib had longer PFS 7.7 vs docetaxel 3.0 months. No OS difference shown in either trials due to crossover of subgroups.PBS reimbursed. Requires fluorescence in situ hybridisation (FISH) testing for ALK gene rearrangement, defined as 15% (or greater) positive cells. PROFILE1014 trial – in the first-line setting, Crizotinib had a superior PFS 10.9 vs chemotherapy 7.0 months. In the second-line setting, Crizotinib had longer PFS 7.7 vs docetaxel 3.0 months. No OS difference shown in either trials due to crossover of subgroups.. (First curated: 2020-04-16)

Changed Vemurafenib in Melanoma with BRAF V600E: 1

Comments changed: PBS reimbursed. However, single-agent not recommended. BRIM-3 – higher response rate 48% v dacarbazine 5% with superior OS (HR 0.37). Cutaneous SCC 12%.PBS reimbursed. However, single-agent not recommended. BRIM-3 – higher response rate 48% v dacarbazine 5% with superior OS (HR 0.37). Cutaneous SCC 12%.. (First curated: 2020-04-16)

Changed Dabrafenib + Trametinib in Melanoma with BRAF V600E, V600K: 1

Comments changed: PBS reimbursed. COMBI-D – Addition of trametinib to dabrafenib prolonged median PFS at 3 years (44 vs 32%).PBS reimbursed. COMBI-D – Addition of trametinib to dabrafenib prolonged median PFS at 3 years (44 vs 32%).. (First curated: 2020-04-16)

Changed Vemurafenib + Cobimetinib in Melanoma with BRAF V600E, V600K: 1

Comments changed: PBS reimbursed. CoBRIM – Addition of cobimetinib to vemurafenib prolonged median PFS 9.9 vs 6.2 months.PBS reimbursed. CoBRIM – Addition of cobimetinib to vemurafenib prolonged median PFS 9.9 vs 6.2 months.. (First curated: 2020-04-16)

Changed Rituximab with CD20 Protein expression: 1

Cancer type(s) changed: Non-Hodgkin’s lymphoma, Chronic lymphocytic leukaemia, Acute lymphoblastic leukaemia, Hodgkin’s lymphomaNon-Hodgkin’s lymphoma, Chronic lymphocytic leukaemia, Acute lymphoblastic leukaemia, Hodgkin’s lymphoma (First curated: 2020-04-16)

Changed Pembrolizumab + Cisplatin + Paclitaxel + Bevacizumab, Pembrolizumab + Carboplatin + Paclitaxel + Bevacizumab, Pembrolizumab + Cisplatin + Paclitaxel, Pembrolizumab + Carboplatin + Paclitaxel in Cervical cancer with CD274 Protein expression: 1

Comments changed: TGA approved. FDA approval for PD-L1-positive (CPS >=1) first-line treatment of cervical cancer (2021-10-13). KEYNOTE-826. N=548 patients with a PD-L1 CPS >= 1. Median PFS was 10.4 months (pembrolizumab) vs 8.2 months (placebo). OS at 24 months: 53% (pembrolizumab) vs 42% (placebo). No difference in PFS or OS was seen vs chemotherapy in the PD-L1 CPS <1 subgroup. Final analysis showed that the HR of OS results was significantly different in subgroups with or without bevacizumab: 77.1 months (pembrolizumab) versus 61.4 months (control) with bevacizumab, and 53.1 months (pembrolizumab) versus 33.7 months (control) without bevacizumab.TGA approved. FDA approval for PD-L1-positive (CPS >=1) first-line treatment of cervical cancer (2021-10-13). KEYNOTE-826. N=548 patients with a PD-L1 CPS >= 1. Median PFS was 10.4 months (pembrolizumab) vs 8.2 months (placebo). OS at 24 months: 53% (pembrolizumab) vs 42% (placebo). No difference in PFS or OS was seen vs chemotherapy in the PD-L1 CPS <1 subgroup. Final analysis showed that the HR of OS results was significantly different in subgroups with or without bevacizumab: 77.1 months (pembrolizumab) versus 61.4 months (control) with bevacizumab, and 53.1 months (pembrolizumab) versus 33.7 months (control) without bevacizumab.. (First curated: 2021-09-19)

Changed Nivolumab + FOLFOX, Nivolumab + CAPOX in Gastric cancer, Gastroesophageal junction adenocarcinoma with CD274 Protein expression: 1

Comments changed: TGA approved. FDA approved. Checkmate-649: Phase 3. First-line, HER2-negative gastric/GOJ carcinoma. Nivolumab plus chemotherapy improved PFS (7.7 vs 6.1 months) and OS (14.4 vs 11.1) over chemotherapy alone in PD-L1 CPS ≥ 5, as well as in CPS>= 1 (PFS: 7.5 vs 6.9 months) and (OS: 14.0 vs 11.3 months). No PFS or OS difference in PD-L1 CPS <5 or CPS <1 subgroups.TGA approved. FDA approved. Checkmate-649: Phase 3. First-line, HER2-negative gastric/GOJ carcinoma. Nivolumab plus chemotherapy improved PFS (7.7 vs 6.1 months) and OS (14.4 vs 11.1) over chemotherapy alone in PD-L1 CPS ≥ 5, as well as in CPS>= 1 (PFS: 7.5 vs 6.9 months) and (OS: 14.0 vs 11.3 months). No PFS or OS difference in PD-L1 CPS <5 or CPS <1 subgroups.. (First curated: 2020-09-29)

Changed Atezolizumab in Non-small cell lung cancer with CD274+EGFR+ALK CD274:Protein expression and NOT EGFR:Oncogenic mutations and NOT ALK:fusion: 1

Comments changed: PBS reimbused. Phase 3 IMpower110 trial (NCT02409342, N=572) evaluated first-line atezolizumab in EGFR and ALK negative NSCLC patients with PD-L1 expression ≥1% on tumor cells or tumor-infiltrating immune cells covering ≥1% of tumor area. Atezolizumab significantly improved median OS compared to chemotherapy (20.2 vs 13.1 months, improvement of 7.1 months).PBS reimbused. Phase 3 IMpower110 trial (NCT02409342, N=572) evaluated first-line atezolizumab in EGFR and ALK negative NSCLC patients with PD-L1 expression ≥1% on tumor cells or tumor-infiltrating immune cells covering ≥1% of tumor area. Atezolizumab significantly improved median OS compared to chemotherapy (20.2 vs 13.1 months, improvement of 7.1 months).. (First curated: 2020-12-11)

Changed Trastuzumab Emtansine in Breast cancer with ERBB2 Amplification, Overexpression: 1

Comments changed: PBS reimbursed if ISH positive. EMILIA (T-DM1 versus lapatinib + capecitabine) and TH3RESA trials (T-DM1 versus physicians choice). HER2-positivity was defined as IHC 3+ or FISH with amplification ratio ≥2.0.PBS reimbursed if ISH positive. EMILIA (T-DM1 versus lapatinib + capecitabine) and TH3RESA trials (T-DM1 versus physicians choice). HER2-positivity was defined as IHC 3+ or FISH with amplification ratio ≥2.0.. (First curated: 2020-04-16)

Changed Trastuzumab + Cisplatin + Fluorouracil, Trastuzumab + Cisplatin + Capecitabine in Gastric cancer, Gastroesophageal junction adenocarcinoma, Oesophageal adenocarcinoma with ERBB2 Amplification, Overexpression: 1

Comments changed: PBS reimbursed if ISH positive. ToGA trial: First-line treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer. OS: 13.8 vs 11.1 months. (HER2 positivity: IHC 3+ or FISH: HER2:CEP17 ratio ≥2 in the tral)PBS reimbursed if ISH positive. ToGA trial: First-line treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer. OS: 13.8 vs 11.1 months. (HER2 positivity: IHC 3+ or FISH: HER2:CEP17 ratio ≥2 in the tral). (First curated: 2020-05-15)

Changed Trastuzumab deruxtecan in Breast cancer with ERBB2 Protein expression and NOT Amplification, Low protein expression and NOT Amplification: 1

Comments changed: TGA approved. Phase 3. DESTINY-Breast04. NCT03734029. Compared with physician’s choice, T-DXD prolonged both PFS (10.1 v 5.4 months) and OS (23.9 v 17.5 months) in Hormone receptor-positive, HER2-low metastatic breast cancer. Similarly T-DXD also prolonged PFS (9.9 v 5.1 months) and OS (23.4 vs 16.8 months) compared to physician’s choice in the overall population. HER2-Low was defined as IHC a score of 1+ or 2+ with negative results on in situ hybridization. FDA approved 5/8/2022.TGA approved. Phase 3. DESTINY-Breast04. NCT03734029. Compared with physician’s choice, T-DXD prolonged both PFS (10.1 v 5.4 months) and OS (23.9 v 17.5 months) in Hormone receptor-positive, HER2-low metastatic breast cancer. Similarly T-DXD also prolonged PFS (9.9 v 5.1 months) and OS (23.4 vs 16.8 months) compared to physician’s choice in the overall population. HER2-Low was defined as IHC a score of 1+ or 2+ with negative results on in situ hybridization. FDA approved 5/8/2022.. (First curated: 2021-06-05)

Changed Ivosidenib in Cholangiocarcinoma with IDH1 R132: 1

Comments changed: TGA approved. PBS listed. FDA approved (2021-08-25). Phase 3 ClarIDHy trial: PFS improvement was shown in the ivosidenib group (2·7 months) vs placebo (1·4 months). Update 2025-07-07.TGA approved. PBS listed. FDA approved (2021-08-25). Phase 3 ClarIDHy trial: PFS improvement was shown in the ivosidenib group (2·7 months) vs placebo (1·4 months). Update 2025-07-07.. (First curated: 2020-05-27)

Changed Brentuximab Vedotin with TNFRSF8 Protein expression: 1

Cancer type(s) changed: Hodgkin’s lymphomaHodgkin’s lymphoma (First curated: 2020-06-15)

Changed Mogamulizumab with CCR4 Protein expression: 1B

Cancer type(s) changed: Cutaneous T-cell lymphoma, Sézary syndrome, Mycosis fungoidesCutaneous T-cell lymphoma, Sézary syndrome, Mycosis fungoides (First curated: 2021-07-03)

Changed Pembrolizumab in Cervical cancer with CD274 Protein expression: 1B

Comments changed: TGA approved. In the Phase 1b KEYNOTE-028 trial (NCT02054806; n=24) in PD-L1-positive advanced cervical cancer, pembrolizumab achieved an ORR of 17% (4 confirmed partial responses; 3 stable disease). In the Phase 2 KEYNOTE-158 study (NCT02628067; n=98) in previously treated advanced cervical cancer, pembrolizumab produced an ORR of 12.2% (3 complete responses; 9 partial responses), with all responses occurring in tumors with CPS ≥ 1% by 22C3 pharmDx assay (ORR 15% in PD-L1-positive cohort).TGA approved. In the Phase 1b KEYNOTE-028 trial (NCT02054806; n=24) in PD-L1-positive advanced cervical cancer, pembrolizumab achieved an ORR of 17% (4 confirmed partial responses; 3 stable disease). In the Phase 2 KEYNOTE-158 study (NCT02628067; n=98) in previously treated advanced cervical cancer, pembrolizumab produced an ORR of 12.2% (3 complete responses; 9 partial responses), with all responses occurring in tumors with CPS ≥ 1% by 22C3 pharmDx assay (ORR 15% in PD-L1-positive cohort).. (First curated: 2020-04-16)

Changed Pembrolizumab + Cisplatin + Fluorouracil in Oesophageal cancer, Oesophageal Adenocarcinoma, Oesophageal squamous cell carcinoma with CD274 Protein expression: 1B

Comments changed: TGA approved. Phase 3 KEYNOTE-590. FDA approved 2021-03-22. In the first-line setting, adding pembrolizumab to chemotherapy resulted in superior OS in PD-L1 positive subgroups (defined as CPS ≥ 10%, median 13.5 versus 9.4 mo), but also in ESCC and overall populations. Overall ORR in pembrolizumab arm was 45% (vs control 23%).TGA approved. Phase 3 KEYNOTE-590. FDA approved 2021-03-22. In the first-line setting, adding pembrolizumab to chemotherapy resulted in superior OS in PD-L1 positive subgroups (defined as CPS ≥ 10%, median 13.5 versus 9.4 mo), but also in ESCC and overall populations. Overall ORR in pembrolizumab arm was 45% (vs control 23%).. (First curated: 2020-09-29)

Changed Amivantamab + Lazertinib in Non-small cell lung cancer with EGFR Exon 19 deletion, L858R: 1B

Comments changed: Phase 3. MARIPOSA. NCT04487080. N=1074. In previously untreated EGFR-mutated NSCLC, a 2:2:1 randomized trial compared amivantamab-lazertinib vs osimertinib vs lazertinib. Amivantamab-lazertinib demonstrated superior PFS compared to osimertinib (23.7 vs 16.6 months; HR 0.70, 95% CI 0.58–0.85). ORR was similar between groups (86% vs 85%), but median response duration favored amivantamab-lazertinib (25.8 vs 16.8 months). OS HR was 0.80 (95% CI 0.61–1.05).Phase 3. MARIPOSA. NCT04487080. N=1074. In previously untreated EGFR-mutated NSCLC, a 2:2:1 randomized trial compared amivantamab-lazertinib vs osimertinib vs lazertinib. Amivantamab-lazertinib demonstrated superior PFS compared to osimertinib (23.7 vs 16.6 months; HR 0.70, 95% CI 0.58–0.85). ORR was similar between groups (86% vs 85%), but median response duration favored amivantamab-lazertinib (25.8 vs 16.8 months). OS HR was 0.80 (95% CI 0.61–1.05).. (First curated: 2025-07-30)

Changed Trastuzumab deruxtecan in Non-small cell lung cancer with ERBB2 Oncogenic mutation: 1B

Comments changed: TGA approved. Not PBS listed. Phase 2 trial. DESTINY-Lung02. NCT04961073. N=152. Dose optimization study. Confirmed ORR was 49% (Median DOR 16.8 months) and 56% (NE) in T-DXd 5.4mg/kg and 6.4 mg/kg respectively. Grade ≥3 treatment related adverse events occurred in 38.6% and 58% of patients receiving 5.4 and 6.4 mg/kg, respectively.TGA approved. Not PBS listed. Phase 2 trial. DESTINY-Lung02. NCT04961073. N=152. Dose optimization study. Confirmed ORR was 49% (Median DOR 16.8 months) and 56% (NE) in T-DXd 5.4mg/kg and 6.4 mg/kg respectively. Grade ≥3 treatment related adverse events occurred in 38.6% and 58% of patients receiving 5.4 and 6.4 mg/kg, respectively.. (First curated: 2023-11-05)

Changed Nivolumab + Ipilimumab in Non-small cell lung cancer with Tumour Mutational Burden High: 1B

Comments changed: TGA provisionally approved. Phase 3 CHECKMATE227 trial. Nivolumab + Ipilimumab significantly improved PFS (7.2 vs 5.5 months) and ORR (45.3% vs 26.9%) compared to chemotherapy in NSCLC patients with high TMB (≥10 mut/MB). Prespecified, prospective TMB cutoff of 10mut/MB in 57% of cohort but outcomes not correlated with TMB.TGA provisionally approved. Phase 3 CHECKMATE227 trial. Nivolumab + Ipilimumab significantly improved PFS (7.2 vs 5.5 months) and ORR (45.3% vs 26.9%) compared to chemotherapy in NSCLC patients with high TMB (≥10 mut/MB). Prespecified, prospective TMB cutoff of 10mut/MB in 57% of cohort but outcomes not correlated with TMB.. (First curated: 2020-11-26)

Changed Encorafenib + Binimetinib in Non-small cell lung cancer with BRAF V600E: 2

Comments changed: Not TGA approved. FDA approved. Phase 2, Open-Label Study of Encorafenib Plus Binimetinib in Patients With BRAFV600-Mutant Metastatic Non–Small-Cell Lung Cancer. NCT03148795. PHAROS. N=98. ORR was 75% (treatment naive) and 46% (previously treated). DCR after 24 weeks was 64% in treatment-naïve and 41% in previously treated patients. Median PFS was NE in treatment-naïve and 9.3 months in previously treated patients. Median OS 47.6 months in treatment-naive patients; 4-year OS probability 49%. Median OS 22.7 months in previously treated patients; 4-year OS probability 31%. Median duration of treatment 16.3 months (naive) and 5.5 months (treated).Not TGA approved. FDA approved. Phase 2, Open-Label Study of Encorafenib Plus Binimetinib in Patients With BRAFV600-Mutant Metastatic Non–Small-Cell Lung Cancer. NCT03148795. PHAROS. N=98. ORR was 75% (treatment naive) and 46% (previously treated). DCR after 24 weeks was 64% in treatment-naïve and 41% in previously treated patients. Median PFS was NE in treatment-naïve and 9.3 months in previously treated patients. Median OS 47.6 months in treatment-naive patients; 4-year OS probability 49%. Median OS 22.7 months in previously treated patients; 4-year OS probability 31%. Median duration of treatment 16.3 months (naive) and 5.5 months (treated).. (First curated: 2023-10-17)

Changed Rucaparib in Ovarian cancer, Peritoneal serous carcinoma, Fallopian tube carcinoma with BRCA1 Oncogenic mutations, Oncogenic mutations (germline): 2

Comments changed: Not TGA approved. NCT02855944. ARIEL4. Median PFS was significantly longer in rucaparib group than chemotherapy group (7.4 versus 5·7 months), including both platinum sensitive and resistant populations. Note, Rucaparib did not improve OS over chemotherapy (19.4 versus 25.4 months) in BRCA1/2-mutated relapsed ovarian cancer. 69% of patients in chemotherapy group crossed over to receive rucaparib.Not TGA approved. NCT02855944. ARIEL4. Median PFS was significantly longer in rucaparib group than chemotherapy group (7.4 versus 5·7 months), including both platinum sensitive and resistant populations. Note, Rucaparib did not improve OS over chemotherapy (19.4 versus 25.4 months) in BRCA1/2-mutated relapsed ovarian cancer. 69% of patients in chemotherapy group crossed over to receive rucaparib.. (First curated: 2022-04-09)

Changed Rucaparib in Ovarian cancer, Peritoneal serous carcinoma, Fallopian tube carcinoma with BRCA2 Oncogenic mutations, Oncogenic mutations (germline): 2

Comments changed: Not TGA approved. NCT02855944. ARIEL4. Median PFS was significantly longer in rucaparib group than chemotherapy group (7.4 versus 5·7 months), including both platinum sensitive and resistant populations. Note, Rucaparib did not improve OS over chemotherapy (19.4 versus 25.4 months) in BRCA1/2-mutated relapsed ovarian cancer. 69% of patients in chemotherapy group crossed over to receive rucaparib.Not TGA approved. NCT02855944. ARIEL4. Median PFS was significantly longer in rucaparib group than chemotherapy group (7.4 versus 5·7 months), including both platinum sensitive and resistant populations. Note, Rucaparib did not improve OS over chemotherapy (19.4 versus 25.4 months) in BRCA1/2-mutated relapsed ovarian cancer. 69% of patients in chemotherapy group crossed over to receive rucaparib.. (First curated: 2022-04-09)

Changed Benmelstobart + Anlotinib in Non-small cell lung cancer with CD274 Protein expression: 2

Comments changed: Phase 3. NCT04964479. In PD-L1 positive NSCLC patients, benmelstobart + anlotinib significantly improved PFS (11.0 vs 7.1 months) and ORR (57.3% vs 39.6%) compared to pembrolizumab, particularly in subgroups with squamous cell carcinoma and PD-L1 expression ≥50%.Phase 3. NCT04964479. In PD-L1 positive NSCLC patients, benmelstobart + anlotinib significantly improved PFS (11.0 vs 7.1 months) and ORR (57.3% vs 39.6%) compared to pembrolizumab, particularly in subgroups with squamous cell carcinoma and PD-L1 expression ≥50%.. (First curated: 2025-06-01)

Changed Sacituzumab Tirumotecan + Pembrolizumab in Non-small cell lung cancer with CD274 Protein expression: 2

Comments changed: Phase 3 OptiTROP-Lung05. NCT06448312. N=413. Sac-TMT plus pembrolizumab significantly improved PFS over pembrolizumab (median not reached vs 5.7 months; HR 0.35). ORR was 70.2% vs 42.0%. In PD-L1 TPS 1-49% subgroup, PFS HR 0.28; in TPS ≥50% subgroup, PFS HR 0.47. In non-squamous histology, PFS HR 0.28; in squamous, PFS HR 0.44. OS trend favored sac-TMT plus pembrolizumab (HR 0.55).Phase 3 OptiTROP-Lung05. NCT06448312. N=413. Sac-TMT plus pembrolizumab significantly improved PFS over pembrolizumab (median not reached vs 5.7 months; HR 0.35). ORR was 70.2% vs 42.0%. In PD-L1 TPS 1-49% subgroup, PFS HR 0.28; in TPS ≥50% subgroup, PFS HR 0.47. In non-squamous histology, PFS HR 0.28; in squamous, PFS HR 0.44. OS trend favored sac-TMT plus pembrolizumab (HR 0.55).. (First curated: 2021-06-16)

Changed Pembrolizumab in Oesophageal squamous cell carcinoma with CD274 Protein expression: 2

Comments changed: Not TGA approved. Not PBS reimbursed. KEYNOTE-181: superior OS in Pembrolizumab arm. PD-L1 positive (defined as CPS ≥ 10%), and overall groups.Not TGA approved. Not PBS reimbursed. KEYNOTE-181: superior OS in Pembrolizumab arm. PD-L1 positive (defined as CPS ≥ 10%), and overall groups.. (First curated: 2020-04-16)

Changed Sacituzumab Govitecan + Pembrolizumab in Triple-negative breast cancer with CD274+ESR1+ERBB2 NOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression and CD274:protein expression: 2

Comments changed: Phase 3 ASCENT-04/KEYNOTE-D19. NCT05382286. N=443. Sacituzumab Govitecan + Pembrolizumab significantly prolonged PFS over chemotherapy + Pembrolizumab (11.2 vs 7.8 months) in previously untreated PD-L1–positive advanced TNBC. Objective response rate was 60% vs 53%; median DOR 16.5 vs 9.2 months.Phase 3 ASCENT-04/KEYNOTE-D19. NCT05382286. N=443. Sacituzumab Govitecan + Pembrolizumab significantly prolonged PFS over chemotherapy + Pembrolizumab (11.2 vs 7.8 months) in previously untreated PD-L1–positive advanced TNBC. Objective response rate was 60% vs 53%; median DOR 16.5 vs 9.2 months.. (First curated: 2026-03-03)

Changed Savolitinib + Osimertinib in Non-small cell lung cancer with EGFR+MET EGFR:Oncogenic mutations and MET:amplification: 2

Comments changed: Phase 3 SACHI study. In EGFR-mutant, MET-amplified advanced NSCLC patients progressing on EGFR-TKI, savolitinib + osimertinib significantly improved PFS versus chemotherapy (8.2 vs 4.5 months, HR=0.34). MET amplification was defined as copy number ≥5 or MET/CEP7 ratio ≥2.0.Phase 3 SACHI study. In EGFR-mutant, MET-amplified advanced NSCLC patients progressing on EGFR-TKI, savolitinib + osimertinib significantly improved PFS versus chemotherapy (8.2 vs 4.5 months, HR=0.34). MET amplification was defined as copy number ≥5 or MET/CEP7 ratio ≥2.0.. (First curated: 2025-06-01)

Changed Telisotuzumab Vedotin in Non-small cell lung cancer with MET Overexpression: 2

Comments changed: Not TGA approved. FDA approved (accelerated). Phase 2 LUMINOSITY trial. NCT03539536. N=172. Telisotuzumab vedotin showed an ORR of 28.6% in patients with c-Met protein-overexpressing nonsquamous EGFR-wildtype NSCLC, with a median DoR of 8.3 months and median OS of 14.5 months. ORR in c-Met high subgroup (≥50% of tumor cells with 3+ by SP44) was 35% (n=78) vs 23% Intermediate (25-50% of tumor cells with 3+, n=83).Not TGA approved. FDA approved (accelerated). Phase 2 LUMINOSITY trial. NCT03539536. N=172. Telisotuzumab vedotin showed an ORR of 28.6% in patients with c-Met protein-overexpressing nonsquamous EGFR-wildtype NSCLC, with a median DoR of 8.3 months and median OS of 14.5 months. ORR in c-Met high subgroup (≥50% of tumor cells with 3+ by SP44) was 35% (n=78) vs 23% Intermediate (25-50% of tumor cells with 3+, n=83).. (First curated: 2025-05-26)

Changed Capivasertib + Abiraterone in Prostate cancer with PTEN Loss of protein expression: 2

Comments changed: Phase 3 CAPItello-281 trial. NCT04493853. N=1012. In PTEN-deficient metastatic hormone-sensitive prostate cancer, capivasertib plus abiraterone improved rPFS versus placebo plus abiraterone (median 33.2 versus 25.7 months; HR 0.81, 95% CI 0.66-0.98, P = 0.034). OS HR was 0.90 (95% CI 0.71-1.15, P = 0.401) at 26.4% maturity. Post hoc rPFS analyses for PTEN loss cut-offs ≥95%, ≥99%, and 100% showed consistent treatment arm performance with numerically improved treatment effect as cut-off increased.Phase 3 CAPItello-281 trial. NCT04493853. N=1012. In PTEN-deficient metastatic hormone-sensitive prostate cancer, capivasertib plus abiraterone improved rPFS versus placebo plus abiraterone (median 33.2 versus 25.7 months; HR 0.81, 95% CI 0.66-0.98, P = 0.034). OS HR was 0.90 (95% CI 0.71-1.15, P = 0.401) at 26.4% maturity. Post hoc rPFS analyses for PTEN loss cut-offs ≥95%, ≥99%, and 100% showed consistent treatment arm performance with numerically improved treatment effect as cut-off increased.. (First curated: 2026-04-02)

Changed Repotrectinib in Non-small cell lung cancer with ROS1 Fusion: 2

Comments changed: Not TGA approved. FDA approved. Phase 2 NCT03093116. TRIDENT-1 trial. N=296. Repotrectinib showed durable clinical activity in ROS1 TKI-naïve (ORR=88%) and -pretreated pts with or without BL CNS mets, including intracranial responses.Not TGA approved. FDA approved. Phase 2 NCT03093116. TRIDENT-1 trial. N=296. Repotrectinib showed durable clinical activity in ROS1 TKI-naïve (ORR=88%) and -pretreated pts with or without BL CNS mets, including intracranial responses.. (First curated: 2023-11-17)

Changed Asciminib in Chronic myelogenous leukaemia with ABL1 BCR-ABL1 Fusion, T315I, E255K, E255V, Y253H, F359V, Q252H, G250H, E459K: 3

Comments changed: Phase 1 NCT02081378. Asciminib in chronic-phase CML after TKI failure. N=150 heavily pretreated (70% ≥3 TKIs). Among those with hematologic relapse, 92% achieved complete hematologic response; 54% without CCyR at baseline achieved CCyR. Major molecular response (MMR) achieved or maintained by 12 months in 48% of evaluable patients, including 57% with ponatinib resistance/intolerance and 28% with T315I mutation at baseline. MMR maintained in 40 of 44 patients.Phase 1 NCT02081378. Asciminib in chronic-phase CML after TKI failure. N=150 heavily pretreated (70% ≥3 TKIs). Among those with hematologic relapse, 92% achieved complete hematologic response; 54% without CCyR at baseline achieved CCyR. Major molecular response (MMR) achieved or maintained by 12 months in 48% of evaluable patients, including 57% with ponatinib resistance/intolerance and 28% with T315I mutation at baseline. MMR maintained in 40 of 44 patients.. (First curated: 2020-05-21)

Changed Vemurafenib in Hairy cell leukaemia, Erdheim-Chester disease with BRAF V600: 3

Comments changed: Phase 2. AcSé vemurafenib basket study. NCT01895643. N=98. Vemurafenib showed clinical activity in BRAF mutated cancers including HCL (ORR 89.7%), ECD (80%), ovarian cancer (50%) and cholangiocarcinoma (18%). Median PFS was 8.8 months. Response were also seen in glioblastoma, ovarian, xanthoastrocytoma, ganglioglioma, sarcoma, GI adenocarcinoma, and prostate cancer.Phase 2. AcSé vemurafenib basket study. NCT01895643. N=98. Vemurafenib showed clinical activity in BRAF mutated cancers including HCL (ORR 89.7%), ECD (80%), ovarian cancer (50%) and cholangiocarcinoma (18%). Median PFS was 8.8 months. Response were also seen in glioblastoma, ovarian, xanthoastrocytoma, ganglioglioma, sarcoma, GI adenocarcinoma, and prostate cancer.. (First curated: 2023-12-22)

Changed Vemurafenib in Solid tumour with BRAF V600: 3

Comments changed: Phase 2. AcSé vemurafenib basket study. NCT01895643. N=98. Vemurafenib showed clinical activity in BRAF mutated cancers including HCL (ORR 89.7%), ECD (80%), ovarian cancer (50%) and cholangiocarcinoma (18%). Median PFS was 8.8 months. Response were also seen in glioblastoma, ovarian, xanthoastrocytoma, ganglioglioma, sarcoma, GI adenocarcinoma, and prostate cancer.Phase 2. AcSé vemurafenib basket study. NCT01895643. N=98. Vemurafenib showed clinical activity in BRAF mutated cancers including HCL (ORR 89.7%), ECD (80%), ovarian cancer (50%) and cholangiocarcinoma (18%). Median PFS was 8.8 months. Response were also seen in glioblastoma, ovarian, xanthoastrocytoma, ganglioglioma, sarcoma, GI adenocarcinoma, and prostate cancer.. (First curated: 2023-12-22)

Changed Vemurafenib in Non-small cell lung cancer with BRAF V600E, V600K, V600M: 3

Comments changed: Phase 2. AcSé. NCT02304809. ORR: 43 of 96 (45%) patients. Median PFS 5.2 months. Median OS 10 months.Phase 2. AcSé. NCT02304809. ORR: 43 of 96 (45%) patients. Median PFS 5.2 months. Median OS 10 months.. (First curated: 2021-11-10)

Changed Olaparib in Solid Tumours with BRCA1 Oncogenic mutations: 3

Comments changed: Phase 2. Belgian Precision trial. BRCA1/2-mutated advanced cancers. N=27 (BRCA1) and 27 (BRCA2). ORR 11% (27 BRCA1: 3 PRs including pancreatic, gallbladder) and 21% (27 BRCA2: 5 PRs in pancreatic, parathyroid, and 1 CR in colon). Median PFS ≥14 months (5-34+ months in responders). CBR 63% (BRCA1) and 46% (BRCA2).Phase 2. Belgian Precision trial. BRCA1/2-mutated advanced cancers. N=27 (BRCA1) and 27 (BRCA2). ORR 11% (27 BRCA1: 3 PRs including pancreatic, gallbladder) and 21% (27 BRCA2: 5 PRs in pancreatic, parathyroid, and 1 CR in colon). Median PFS ≥14 months (5-34+ months in responders). CBR 63% (BRCA1) and 46% (BRCA2).. (First curated: 2026-02-02)

Changed ZEN-3694 + Talazoparib in Triple-negative breast cancer with BRCA1+BRCA2 NOT BRCA1:Oncogenic mutations (germline) and NOT BRCA2:Oncogenic mutations (germline): 3

Comments changed: In germline BRCA-wildtype TNBCs, BET inhibitor ZEN-3694 creates “BRCAness” and renders sensitive to Talazoparib. Activity was demonstrated in the phase 2 portion of the trial met primary endpoint with CBR 30% (11/37). ORR was 22% (11/50) in the combined phase 1b and 2 cohort.In germline BRCA-wildtype TNBCs, BET inhibitor ZEN-3694 creates “BRCAness” and renders sensitive to Talazoparib. Activity was demonstrated in the phase 2 portion of the trial met primary endpoint with CBR 30% (11/37). ORR was 22% (11/50) in the combined phase 1b and 2 cohort.. (First curated: 2022-06-19)

Changed Olaparib in Solid Tumours with BRCA2 Oncogenic mutations: 3

Comments changed: Phase 2. Belgian Precision trial. BRCA1/2-mutated advanced cancers. N=27 (BRCA1) and 27 (BRCA2). ORR 11% (27 BRCA1: 3 PRs including pancreatic, gallbladder) and 21% (27 BRCA2: 5 PRs in pancreatic, parathyroid, and 1 CR in colon). Median PFS ≥14 months (5-34+ months in responders). CBR 63% (BRCA1) and 46% (BRCA2).Phase 2. Belgian Precision trial. BRCA1/2-mutated advanced cancers. N=27 (BRCA1) and 27 (BRCA2). ORR 11% (27 BRCA1: 3 PRs including pancreatic, gallbladder) and 21% (27 BRCA2: 5 PRs in pancreatic, parathyroid, and 1 CR in colon). Median PFS ≥14 months (5-34+ months in responders). CBR 63% (BRCA1) and 46% (BRCA2).. (First curated: 2026-02-02)

Changed Cadonilimab + Anlotinib in Non-small cell lung cancer with CD274 Protein expression: 3

Comments changed: Phase Ib/II trial. NCT04646330. N=69. Cadonilimab and anlotinib demonstrated manageable safety and activity with an ORR of 51% (25/49) at 15mg/kg Q3W and 60% (12/20) at 10mg/kg Q3W as first-line treatment in advanced NSCLC. ORRs differed between PD-L1-positive (60.5%) and PD-L1-negative (42.3%) patients. PD-L1 expression was assessed by immunohistochemistry using PD-L1 IHC 22C3 pharmDx (Dako Omnis), with PD-L1 positivity defined as a tumor proportion score (TPS) ≥1%. High PD-L1 expression was not required for entry into the trial.Phase Ib/II trial. NCT04646330. N=69. Cadonilimab and anlotinib demonstrated manageable safety and activity with an ORR of 51% (25/49) at 15mg/kg Q3W and 60% (12/20) at 10mg/kg Q3W as first-line treatment in advanced NSCLC. ORRs differed between PD-L1-positive (60.5%) and PD-L1-negative (42.3%) patients. PD-L1 expression was assessed by immunohistochemistry using PD-L1 IHC 22C3 pharmDx (Dako Omnis), with PD-L1 positivity defined as a tumor proportion score (TPS) ≥1%. High PD-L1 expression was not required for entry into the trial.. (First curated: 2025-04-23)

Changed SSGJ-707 in Non-small cell lung cancer with CD274 Protein expression: 3

Comments changed: Phase 2. NCT06361927. N=83. SSGJ-707 monotherapy in first-line advanced NSCLC with PD-L1 TPS>=1%. FDA-aligned dose 10 mg/kg Q3W (n=34): ORR 67.6%, median DOR NR, median PFS 12.4 months, median OS NR. Subgroup analysis: SQ histology ORR 75.0%, median PFS 8.9 months; NSQ histology ORR 63.6%, median PFS 12.4 months; TPS≥50% ORR 76.9%, median PFS 12.4 months. In patients with detectable ctDNA at baseline: median PFS NR for those with nondetectable ctDNA at C3D1 versus 7.6 months for those with detectable ctDNA at C3D1.Phase 2. NCT06361927. N=83. SSGJ-707 monotherapy in first-line advanced NSCLC with PD-L1 TPS>=1%. FDA-aligned dose 10 mg/kg Q3W (n=34): ORR 67.6%, median DOR NR, median PFS 12.4 months, median OS NR. Subgroup analysis: SQ histology ORR 75.0%, median PFS 8.9 months; NSQ histology ORR 63.6%, median PFS 12.4 months; TPS≥50% ORR 76.9%, median PFS 12.4 months. In patients with detectable ctDNA at baseline: median PFS NR for those with nondetectable ctDNA at C3D1 versus 7.6 months for those with detectable ctDNA at C3D1.. (First curated: 2026-06-03)

Changed SHR-A1904 in Gastric cancer, Gastroesophageal junction adenocarcinoma with CLDN18 Protein expression: 3

Comments changed: Phase 1. NCT04877717. SHR-A1904 showed anti-tumor activity in 73 patients with GC/GEJC, with ORR of 56% at 6.0 mg/kg (DCR 89%). Claudin 18.2 positivity in ≥ 1% of cellsPhase 1. NCT04877717. SHR-A1904 showed anti-tumor activity in 73 patients with GC/GEJC, with ORR of 56% at 6.0 mg/kg (DCR 89%). Claudin 18.2 positivity in ≥ 1% of cells. (First curated: 2024-09-15)

Changed XNW27011 in Gastric cancer, Gastroesophageal junction adenocarcinoma with CLDN18 Protein expression: 3

Comments changed: Phase 2. NCT06792435. N=26 evaluable at 3.0 mg/kg. cORR 65.4%, cDCR 84.6%. mPFS 5.7 months (6.8 months in ≥2 prior lines). mOS 11.7 months (11.9 months in ≥2 prior lines). Noted durable PFS of 11.3 months in one patient with prior CLDN18.2-targeted therapy. Phase 3 study ongoing.Phase 2. NCT06792435. N=26 evaluable at 3.0 mg/kg. cORR 65.4%, cDCR 84.6%. mPFS 5.7 months (6.8 months in ≥2 prior lines). mOS 11.7 months (11.9 months in ≥2 prior lines). Noted durable PFS of 11.3 months in one patient with prior CLDN18.2-targeted therapy. Phase 3 study ongoing.. (First curated: 2026-07-19)

Changed Obrixtamig in Small-cell lung cancer, Extrapulmonary neuroendocrine carcinoma, Large cell neuroendocrine carcinoma of the lung with DLL3 Protein expression: 3

Comments changed: Phase I dose-escalation. NCT04429087. Obrixtamig (BI 764532). N=168. DLL3-positive SCLC, epNECs, or LCNEC-L. 72% received ≥2 lines prior therapy. Overall ORR 23% (95% CI, 17.4% to 30.2%). Median DoR 8.5 months (95% CI, 6.2 to not reached). 6-month DoR rate 70%. Regimens B2/B3 ORR 28%. Subgroup ORRs for SCLC 21%, epNECs 27%, and LCNEC-L 70%. Supports further exploration in heavily pretreated DLL3-positive tumors.Phase I dose-escalation. NCT04429087. Obrixtamig (BI 764532). N=168. DLL3-positive SCLC, epNECs, or LCNEC-L. 72% received ≥2 lines prior therapy. Overall ORR 23% (95% CI, 17.4% to 30.2%). Median DoR 8.5 months (95% CI, 6.2 to not reached). 6-month DoR rate 70%. Regimens B2/B3 ORR 28%. Subgroup ORRs for SCLC 21%, epNECs 27%, and LCNEC-L 70%. Supports further exploration in heavily pretreated DLL3-positive tumors.. (First curated: 2026-03-04)

Changed Amivantamab in Non-small cell lung cancer with EGFR C797S, Exon 20 insertion: 3

Comments changed: Phase 1. JNJ-61186372 demonstrated a manageable safety profile with preliminary responses in advanced NSCLC patients with EGFR-driven third-generation TKI-relapsed and Exon20ins disease, achieving 28% ORR (25/88) at ≥ 700 mg dose.Phase 1. JNJ-61186372 demonstrated a manageable safety profile with preliminary responses in advanced NSCLC patients with EGFR-driven third-generation TKI-relapsed and Exon20ins disease, achieving 28% ORR (25/88) at ≥ 700 mg dose.. (First curated: 2020-06-28)

Changed Neratinib in Breast cancer with ERBB2 ERBB2:Oncogenic mutations and NOT ERBB2:amplification: 3

Comments changed: Phase 1/2 SUMMIT trial. NCT01953926. Neratinib showed activity in breast cancer (n=​25), ORR at week 8 was 32%.Phase 1/2 SUMMIT trial. NCT01953926. Neratinib showed activity in breast cancer (n=​25), ORR at week 8 was 32%.. (First curated: 2020-05-15)

Changed Zongertinib in Non-small cell lung cancer with ERBB2 Exon 20 insertions, A775_G776insYVMA, Tyrosine kinase domain mutations: 3

Comments changed: Phase Ib. Beamion LUNG 1. NCT04886804. N=74. First-line zongertinib in treatment-naïve advanced HER2-mutant NSCLC showed ORR 77%, DOR 80%, PFS at 6 months 79%.Phase Ib. Beamion LUNG 1. NCT04886804. N=74. First-line zongertinib in treatment-naïve advanced HER2-mutant NSCLC showed ORR 77%, DOR 80%, PFS at 6 months 79%.. (First curated: 2025-10-18)

Changed Lucitanib in Breast cancer with FGFR1 Amplification: 3

Comments changed: Phase 2. FINESSE. NCT02053636. In HR+/HER2− metastatic breast cancer, ORR was 19% in the FGFR1-amplified cohort (defined as gene/centromere ratio ≥2 or average copy number ≥6).Phase 2. FINESSE. NCT02053636. In HR+/HER2− metastatic breast cancer, ORR was 19% in the FGFR1-amplified cohort (defined as gene/centromere ratio ≥2 or average copy number ≥6).. (First curated: 2021-12-17)

Changed Bemarituzumab + mFOLFOX6 in Gastric cancer, Gastroesophageal junction adenocarcinoma with FGFR2 FGFR2b Overexpression, FGFR2-IIIb Overexpression: 3

Comments changed: Phase 3. FORTITUDE-101. NCT05052801. N=547. In FGFR2b ≥10% advanced Gastric and gastroesophageal cancer (Bemarituzumab n=159, Placebo n=165), bemarituzumab + mFOLFOX6 improved median OS vs placebo + mFOLFOX6 (17.9 vs 12.5 months; HR 0.61, P=0.005) at primary analysis. Median PFS 8.6 vs 6.7 months (HR 0.71, P=0.019). Follow-up analysis median OS 14.5 vs 13.2 months (HR 0.82).Phase 3. FORTITUDE-101. NCT05052801. N=547. In FGFR2b ≥10% advanced Gastric and gastroesophageal cancer (Bemarituzumab n=159, Placebo n=165), bemarituzumab + mFOLFOX6 improved median OS vs placebo + mFOLFOX6 (17.9 vs 12.5 months; HR 0.61, P=0.005) at primary analysis. Median PFS 8.6 vs 6.7 months (HR 0.71, P=0.019). Follow-up analysis median OS 14.5 vs 13.2 months (HR 0.82).. (First curated: 2026-04-02)

Changed ALK201 in Solid tumours with FGFR2 FGFR2b Overexpression, FGFR2-IIIb Overexpression: 3

Comments changed: Phase 1/2 NCT06656390. N=38. ALK201 showed ORR of 24% and DCR of 68% in evaluable patients (n=25); at ≥7.2 mg/kg, ORR was 35.7% and DCR was 100%.Phase 1/2 NCT06656390. N=38. ALK201 showed ORR of 24% and DCR of 68% in evaluable patients (n=25); at ≥7.2 mg/kg, ORR was 35.7% and DCR was 100%.. (First curated: 2021-06-16)

Changed Luveltamab tazevibulin in Ovarian cancer with FOLR1 Protein expression: 3

Comments changed: Phase 1. Dose expansion cohort of STRO-002-GM1. NCT03748186. N=44. Luveltamab tazevibulin showed activity (ORR 12 of 32, 38%) in recurrent epithelial ovarian cancer with FolRα expression as low as TPS>25%.Phase 1. Dose expansion cohort of STRO-002-GM1. NCT03748186. N=44. Luveltamab tazevibulin showed activity (ORR 12 of 32, 38%) in recurrent epithelial ovarian cancer with FolRα expression as low as TPS>25%.. (First curated: 2024-09-07)

Changed Mirvetuximab soravtansine in Ovarian cancer with FOLR1 Protein expression, Overexpression: 3

Comments changed: Phase 2. PICCOLO trial. NCT05041257. N=79. Mirvetuximab soravtansine showed ORR of 51.9% and median DOR of 8.25 months in FRalpha-positive, third-line or later, recurrent platinum-sensitive ovarian cancer. Positive FRα expression was defined as 75% of cells with 2+ staining intensity, assessed using the VENTANA FOLR1 RxDx Assay on either a fresh/recent biopsy or archival tumour tissue.Phase 2. PICCOLO trial. NCT05041257. N=79. Mirvetuximab soravtansine showed ORR of 51.9% and median DOR of 8.25 months in FRalpha-positive, third-line or later, recurrent platinum-sensitive ovarian cancer. Positive FRα expression was defined as 75% of cells with 2+ staining intensity, assessed using the VENTANA FOLR1 RxDx Assay on either a fresh/recent biopsy or archival tumour tissue.. (First curated: 2025-01-09)

Changed Elisrasib, Elisrasib + Pembrolizumab in Non-small cell lung cancer with KRAS G12C: 3

Comments changed: Phase 1/2 trial. NCT05410145. N=43 mono, 52 combo first-line KRAS G12C NSCLC. ORR 78% monotherapy (76.2% TPS<1%, 80% TPS≥1%). ORR 81% combination (71% TPS<1%, 72.7% in TPS 1-49%, 95% in TPS>=50%). Median PFS and DOR immature. 6m PFS rate 68.9% monotherapy, 74.6% combo. 6m DOR rate 77.2% monotherapy, 80.5% combination. ctDNA molecular response 83% mono, 100% combo.Phase 1/2 trial. NCT05410145. N=43 mono, 52 combo first-line KRAS G12C NSCLC. ORR 78% monotherapy (76.2% TPS<1%, 80% TPS≥1%). ORR 81% combination (71% TPS<1%, 72.7% in TPS 1-49%, 95% in TPS>=50%). Median PFS and DOR immature. 6m PFS rate 68.9% monotherapy, 74.6% combo. 6m DOR rate 77.2% monotherapy, 80.5% combination. ctDNA molecular response 83% mono, 100% combo.. (First curated: 2026-07-12)

Changed INCB161734 in Solid Tumours, Non-small cell lung cancer, Pancreatic adenocarcinoma, Colorectal adenocarcinoma, Ovarian cancer, Solid tumour with KRAS G12D: 3

Comments changed: Phase 1. NCT06179160. N=36. INCB161734, a KRAS G12D inhibitor showed promising efficacy in 36 patients with advanced or metastatic solid tumors, with ORR of 30%, and DCR of 85% achieving disease control at doses ≥600 mg qd (PDAC 34%)Phase 1. NCT06179160. N=36. INCB161734, a KRAS G12D inhibitor showed promising efficacy in 36 patients with advanced or metastatic solid tumors, with ORR of 30%, and DCR of 85% achieving disease control at doses ≥600 mg qd (PDAC 34%). (First curated: 2025-10-19)

Changed AMG 337 in Gastric cancer, Gastroesophageal junction adenocarcinoma, Oesophageal adenocarcinoma with MET Amplification: 3

Comments changed: Phase 2. NCT02016534, Cohort 1. ORR was 18% (8/45). Eligibility criteria was MET/CEN-7 ratio ≥2.0 on FISH.Phase 2. NCT02016534, Cohort 1. ORR was 18% (8/45). Eligibility criteria was MET/CEN-7 ratio ≥2.0 on FISH.. (First curated: 2022-01-18)

Changed Crizotinib in Gastric cancer, Gastroesophageal junction adenocarcinoma, Oesophageal adenocarcinoma with MET Amplification: 3

Comments changed: Phase 2. AcSé-Crizotinib. NCT02034981. In chemorefractory patients, the ORR to Crizotinib was 56% (5/9). Response after two cycles were 33%. PFS 3.2 months. MET amplification was determined by copy number >= 6 copies.Phase 2. AcSé-Crizotinib. NCT02034981. In chemorefractory patients, the ORR to Crizotinib was 56% (5/9). Response after two cycles were 33%. PFS 3.2 months. MET amplification was determined by copy number >= 6 copies.. (First curated: 2022-01-18)

Changed Crizotinib in Non-small cell lung cancer with MET Amplification: 3

Comments changed: Phase 2. N=38. ORR 38% for high (8/21, >=4 MET-to-CEP7 ratio on FISH), 14% for medium (2/14, >2.2 to <4 MET-to-CEP7 ratio), and 1 in 3 low (≥1.8 to ≤2.2 MET-to-CEP7 ratio). Median PFS were 6.7 months (high), 1.9 months (medium), and 1.8 months (low).Phase 2. N=38. ORR 38% for high (8/21, >=4 MET-to-CEP7 ratio on FISH), 14% for medium (2/14, >2.2 to <4 MET-to-CEP7 ratio), and 1 in 3 low (≥1.8 to ≤2.2 MET-to-CEP7 ratio). Median PFS were 6.7 months (high), 1.9 months (medium), and 1.8 months (low).. (First curated: 2022-01-12)

Changed Telisotuzumab Adizutecan in Colorectal cancer with MET Overexpression: 3

Comments changed: Phase 1. NCT05029882. N=122. ORR 15.6% (95% CI 9.6-23.2). DOR 5.9 months (95% CI 4.1-10.5). mPFS 4.6 months (95% CI 4.0-5.4). mOS 10.4 months (95% CI 8.9-13.1). In high c-Met expression (≥10%|3+) at ≥2.4 mg/kg, ORR 36%.Phase 1. NCT05029882. N=122. ORR 15.6% (95% CI 9.6-23.2). DOR 5.9 months (95% CI 4.1-10.5). mPFS 4.6 months (95% CI 4.0-5.4). mOS 10.4 months (95% CI 8.9-13.1). In high c-Met expression (≥10%|3+) at ≥2.4 mg/kg, ORR 36%.. (First curated: 2021-06-16)

Changed Luvometinib in Type 1 neurofibromatosis with NF1 Oncogenic mutations (germline): 3

Comments changed: Phase 3. NCT05913037. N=167. Luvometinib vs placebo. Confirmed ORR 43.8% vs 10.9%. Median DOR 15.1 months, 85.2% rate of DOR ≥12 months. Median TTR 3.9 months.Phase 3. NCT05913037. N=167. Luvometinib vs placebo. Confirmed ORR 43.8% vs 10.9%. Median DOR 15.1 months, 85.2% rate of DOR ≥12 months. Median TTR 3.9 months.. (First curated: 2026-06-05)

Changed Alpelisib + Fulvestrant in Breast cancer with PIK3CA C420R, E542K, E545A, E545D, E545G, E545K, Q546E, Q546R, H1047L, H1047R, H1047Y: 3

Comments changed: Phase 2. BYLieve. NCT03056755. N=127 (Cohort A). Alpelisib + fulvestrant met primary endpoint of 6-month PFS (53.8%, 95% CI 44.4–63.0) in PIK3CA-mutated, hormone receptor-positive, HER2-negative advanced breast cancer post CDK4/6 inhibitor. Median PFS 8.0 months, OS 27.3 months. Adverse events included hyperglycaemia (29%) and rash (10%). Original curation: 2021-04-07. Updated 2025-07-30Phase 2. BYLieve. NCT03056755. N=127 (Cohort A). Alpelisib + fulvestrant met primary endpoint of 6-month PFS (53.8%, 95% CI 44.4–63.0) in PIK3CA-mutated, hormone receptor-positive, HER2-negative advanced breast cancer post CDK4/6 inhibitor. Median PFS 8.0 months, OS 27.3 months. Adverse events included hyperglycaemia (29%) and rash (10%). Original curation: 2021-04-07. Updated 2025-07-30. (First curated: 2025-07-30)

Changed Temsirolimus in Endometrial cancer, Solid tumours except Breast Cancer, Colorectal cancer with PIK3CA Oncogenic mutations, H1047R: 3

Comments changed: Phase 2. TAPUR basket trial. N=83. Temsirolimus in PIK3CA-mutated solid tumors. Primary endpoint disease control (DC) defined as OR or SD ≥16 weeks. BC cohort DC rate 9%, Median PFS 8 weeks, Median OS 36 weeks. CRC cohort DC rate 9%, Median PFS 8 weeks, Median OS 37 weeks. UC cohort DC rate 37%, Median PFS 16 weeks, Median OS 37 weeks, Median DOSD 31 weeks. HP cohort DC rate 31%, Median PFS 9 weeks, Median OS 27 weeks, Median DOSD 28 weeks. Overall OR rate 8%. Null hypothesis of 15% DC rate rejected for UC and HP cohorts. H1047R mutation subgroup OR rate 18%. DOR for PR in UC up to 84 weeks. DOR for PR in HP up to 229 weeks ongoing. Antitumor activity demonstrated in UC and HP cohorts but not BC or CRC.Phase 2. TAPUR basket trial. N=83. Temsirolimus in PIK3CA-mutated solid tumors. Primary endpoint disease control (DC) defined as OR or SD ≥16 weeks. BC cohort DC rate 9%, Median PFS 8 weeks, Median OS 36 weeks. CRC cohort DC rate 9%, Median PFS 8 weeks, Median OS 37 weeks. UC cohort DC rate 37%, Median PFS 16 weeks, Median OS 37 weeks, Median DOSD 31 weeks. HP cohort DC rate 31%, Median PFS 9 weeks, Median OS 27 weeks, Median DOSD 28 weeks. Overall OR rate 8%. Null hypothesis of 15% DC rate rejected for UC and HP cohorts. H1047R mutation subgroup OR rate 18%. DOR for PR in UC up to 84 weeks. DOR for PR in HP up to 229 weeks ongoing. Antitumor activity demonstrated in UC and HP cohorts but not BC or CRC.. (First curated: 2026-05-18)

Changed Ipatasertib + Paclitaxel in Triple-negative breast cancer with PIK3CA R88Q, N345K, C420R, E542, E545, Q546, M1043I, H1047, G1049R: 3

Comments changed: LOTUS trial – Ipatasertib + Taxol in TNBCLOTUS trial – Ipatasertib + Taxol in TNBC. (First curated: 2020-05-15)

Changed Nivolumab in Solid tumours with POLE P286R, V411L: 3

Comments changed: Phase 2. AcSé. NCT03012581. N=15 (10 evaluable). Mismatch proficient tumours with POLE exonuclease domain mutations. Responders were seen in three patients with P286R and V411L mutations and in colorectal and cervical cancers. No response in non-pathogenic mutations.Phase 2. AcSé. NCT03012581. N=15 (10 evaluable). Mismatch proficient tumours with POLE exonuclease domain mutations. Responders were seen in three patients with P286R and V411L mutations and in colorectal and cervical cancers. No response in non-pathogenic mutations.. (First curated: 2021-07-02)

Changed VIR-5500 in Prostate cancer with PSMA Protein expression: 3

Comments changed: Phase 1 dose escalation. NCT05997615. N=51. Heavily pretreated mCRPC (including 95% post-taxane). At 3000 µg/kg Q3W: PSA50 91% (10/11), PSA90 55% (6/11), ORR 67% (4/6) in RECIST-evaluable patients; durable PSA responses lasting over one year in select patients.Phase 1 dose escalation. NCT05997615. N=51. Heavily pretreated mCRPC (including 95% post-taxane). At 3000 µg/kg Q3W: PSA50 91% (10/11), PSA90 55% (6/11), ORR 67% (4/6) in RECIST-evaluable patients; durable PSA responses lasting over one year in select patients.. (First curated: 2026-08-02)

Changed Ipatasertib + Paclitaxel in Triple-negative breast cancer with PTEN Oncogenic mutations: 3

Comments changed: LOTUS trial – Ipatasertib + Taxol in TNBCLOTUS trial – Ipatasertib + Taxol in TNBC. (First curated: 2020-05-15)

Changed Cabozantinib in Paraganglioma, Phaeochromocytoma with SDHB Oncogenic mutations (germline): 3

Comments changed: Phase 2. Natalie Trial. NCT02302833. N=17. Cabozantinib achieved ORR of 25% (95% CI 7.3–52.4) in 16 evaluable patients with metastatic phaeochromocytoma/paraganglioma (MPPGs). Note the responses are independent of SDHB pathogenic variants, catecholamine secretion, or noradrenaline transporter expression.Phase 2. Natalie Trial. NCT02302833. N=17. Cabozantinib achieved ORR of 25% (95% CI 7.3–52.4) in 16 evaluable patients with metastatic phaeochromocytoma/paraganglioma (MPPGs). Note the responses are independent of SDHB pathogenic variants, catecholamine secretion, or noradrenaline transporter expression.. (First curated: 2025-07-30)

Changed Acimtamig in Peripheral T-cell lymphoma with TNFRSF8 Protein expression: 3

Comments changed: Phase 2 study. NCT04101331. N=108. In patients with CD30-positive relapsed or refractory peripheral T-cell lymphomas, acimtamig exhibited an ORR of 32.4% with a CD30 positivity determined by Ber-H2 targeted IHC with CD30 expression confirmed in ≥1% of tumor cells, and a median DoR of 2.3 months.Phase 2 study. NCT04101331. N=108. In patients with CD30-positive relapsed or refractory peripheral T-cell lymphomas, acimtamig exhibited an ORR of 32.4% with a CD30 positivity determined by Ber-H2 targeted IHC with CD30 expression confirmed in ≥1% of tumor cells, and a median DoR of 2.3 months.. (First curated: 2025-06-29)

Changed NT-175 in Colorectal adenocarcinoma, Pancreatic adenocarcinoma, Breast cancer, Solid tumours with TP53 R175H: 3

Comments changed: Phase 1. NCT05877599. N=21 infused. NT-175 in TP53 R175H-mutated advanced solid tumors. ORR 47.6% overall, 53.8% in DL3. PR in 10 pts (5/6 PDAC, 2/10 CRC, 2/2 BC, 1 other). DCR 66.7%. 5 of 7 evaluable PR pts with ≥6 months follow-up remain in PR.Phase 1. NCT05877599. N=21 infused. NT-175 in TP53 R175H-mutated advanced solid tumors. ORR 47.6% overall, 53.8% in DL3. PR in 10 pts (5/6 PDAC, 2/10 CRC, 2/2 BC, 1 other). DCR 66.7%. 5 of 7 evaluable PR pts with ≥6 months follow-up remain in PR.. (First curated: 2026-06-03)

Changed Rezatapopt in Ovarian cancer, Solid tumours with TP53 Y220C: 3

Comments changed: Phase 1. PYNNACLE. NCT04585750. N=77. Across all dose groups, rezatapopt established. Overall response rate 20% (30% in KRAS wild-type tumors at ≥1150 mg), including confirmed responses in ovarian and breast cancers; all responders harbored TP53 Y220C and wild-type KRAS.Phase 1. PYNNACLE. NCT04585750. N=77. Across all dose groups, rezatapopt established. Overall response rate 20% (30% in KRAS wild-type tumors at ≥1150 mg), including confirmed responses in ovarian and breast cancers; all responders harbored TP53 Y220C and wild-type KRAS.. (First curated: 2026-02-24)

Changed Atezolizumab in Endometrial cancer, Neuroendocrine carcinoma, Non-small-cell lung cancer, Pancreatic cancer, Sarcoma, Gastrooesophageal carcinoma, Cervical cancer, Cancer of unknown primary, Prostate cancer, Non-melanoma skin cancer with Tumour Mutational Burden High: 3

Comments changed: Phase 2. TAPISTRY trial. NCT04589845. N=150. Atezolizumab showed ORR of 23% (TMB ≥16 mut/Mb) and 20% (TMB ≥13 mut/Mb), with median PFS of 2.8 months and 2.7 months, respectively, in patients with TMB-high solid tumors. TMB was assessed by Foundation One CDx. Tumour types with n>=4 and ORR >=20 are listed. The correlation with MSI-H, dMMR, and PD-L1 status were not reported.Phase 2. TAPISTRY trial. NCT04589845. N=150. Atezolizumab showed ORR of 23% (TMB ≥16 mut/Mb) and 20% (TMB ≥13 mut/Mb), with median PFS of 2.8 months and 2.7 months, respectively, in patients with TMB-high solid tumors. TMB was assessed by Foundation One CDx. Tumour types with n>=4 and ORR >=20 are listed. The correlation with MSI-H, dMMR, and PD-L1 status were not reported.. (First curated: 2024-06-18)

Changed Durvalumab + Tremelimumab in Non-small cell lung cancer with Tumour Mutational Burden High: 3

Comments changed: Phase 3 MYSTIC trial. NCT02453282. N=1118. In patients with blood tumor mutational burden ≥20 mutations per megabase, durvalumab plus tremelimumab demonstrated improved OS (21.9 vs 10.0 months). Overall, durvalumab showed no OS improvement over chemotherapy (16.3 vs 12.9 months) in patients with ≥25% PD-L1 tumor cell expression. Similarly, durvalumab plus tremelimumab did not improve OS or PFS compared to chemotherapy.Phase 3 MYSTIC trial. NCT02453282. N=1118. In patients with blood tumor mutational burden ≥20 mutations per megabase, durvalumab plus tremelimumab demonstrated improved OS (21.9 vs 10.0 months). Overall, durvalumab showed no OS improvement over chemotherapy (16.3 vs 12.9 months) in patients with ≥25% PD-L1 tumor cell expression. Similarly, durvalumab plus tremelimumab did not improve OS or PFS compared to chemotherapy.. (First curated: 2020-04-25)

Changed Ensartinib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: C1156Y, I1171N, V1180L, L1196Q, L1198F, D1203N, S1206F, S1206Y, I1171N and L1198F, F1174L, F1174L, Exon 2–3 deletion, Exon 2-17 deletionC1156Y, I1171N, V1180L, L1196Q, L1198F, D1203N, S1206F, S1206Y, I1171N and L1198F, F1174L, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Zotizalkib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: C1156Y, L1196Q, L1196Q, L1198F, G1202del, S1206F, S1206Y, E1210K, G1269A, G1202R and L1198F, G1202R and G1269A, I1171N and L1198F, F1174L, F1174L, Exon 2–3 deletion, Exon 2-17 deletionC1156Y, L1196Q, L1196Q, L1198F, G1202del, S1206F, S1206Y, E1210K, G1269A, G1202R and L1198F, G1202R and G1269A, I1171N and L1198F, F1174L, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Neladalkib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: G1202R, T1151M, T1151insT, C1156Y, I1171N, I1171S, I1171T, F1174L, V1180L, L1196M, L1196Q, L1196Q, L1198F, G1202del, D1203N, S1206F, S1206Y, E1210K, G1269A, G1202R and T1151M, G1202R and F1174L, G1202R and L1196M, G1202R and L1198F, G1202R and G1269A, I1171N and L1198F, F1174L, F1174L, Exon 2–3 deletion, Exon 2-17 deletionG1202R, T1151M, T1151insT, C1156Y, I1171N, I1171S, I1171T, F1174L, V1180L, L1196M, L1196Q, L1196Q, L1198F, G1202del, D1203N, S1206F, S1206Y, E1210K, G1269A, G1202R and T1151M, G1202R and F1174L, G1202R and L1196M, G1202R and L1198F, G1202R and G1269A, I1171N and L1198F, F1174L, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Alectinib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: T1151M, C1156Y, F1174L, D1203N, S1206F, S1206Y, E1210K, F1174L, Exon 2–3 deletion, Exon 2-17 deletionT1151M, C1156Y, F1174L, D1203N, S1206F, S1206Y, E1210K, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Ceritinib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: T1151M, F1174L, V1180L, L1196M, L1196Q, S1206F, S1206Y, G1269A, F1174L, Exon 2–3 deletion, Exon 2-17 deletionT1151M, F1174L, V1180L, L1196M, L1196Q, S1206F, S1206Y, G1269A, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Crizotinib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: T1151M, F1174L, V1180L, L1198F, G1202del, I1171N and L1198F, F1174L, Exon 2–3 deletion, Exon 2-17 deletionT1151M, F1174L, V1180L, L1198F, G1202del, I1171N and L1198F, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Brigatinib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: T1151M, I1171S, I1171T, F1174L, V1180L, L1196M, L1196Q, G1269A, I1171N and L1198F, F1174L, Exon 2–3 deletion, Exon 2-17 deletionT1151M, I1171S, I1171T, F1174L, V1180L, L1196M, L1196Q, G1269A, I1171N and L1198F, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Lorlatinib in Solid tumours, Non-small cell lung cancer with ALK : 4

Alterations changed: T1151M, T1151insT, C1156Y, F1174L, V1180L, L1196Q, L1198F, G1202del, D1203N, S1206F, S1206Y, E1210K, G1269A, F1174L, Exon 2–3 deletion, Exon 2-17 deletionT1151M, T1151insT, C1156Y, F1174L, V1180L, L1196Q, L1198F, G1202del, D1203N, S1206F, S1206Y, E1210K, G1269A, F1174L, Exon 2–3 deletion, Exon 2-17 deletion. (First curated: 2025-04-30)

Changed Amivantamab in Non-small cell lung cancer with AREG+EGFR AREG:Overexpression and NOT EGFR:Oncogenic mutations: 4

Comments changed: Preclinical study. In 11 EGFRWT NSCLC PDX models, amivantamab tumor growth inhibition (ΔTGI) correlated with AREG RNA levels (Spearman, P<0.05). 5/11 models showed >60% ΔTGI. Fc-silent variant showed similar efficacy (P=0.637). High AREG expression mutually exclusive with EGFR mutations in LUAD (Log2 OR -2.873, q=0.019).Preclinical study. In 11 EGFRWT NSCLC PDX models, amivantamab tumor growth inhibition (ΔTGI) correlated with AREG RNA levels (Spearman, P<0.05). 5/11 models showed >60% ΔTGI. Fc-silent variant showed similar efficacy (P=0.637). High AREG expression mutually exclusive with EGFR mutations in LUAD (Log2 OR -2.873, q=0.019).. (First curated: 2026-07-19)

Changed Naporfenib in Solid tumours with BRAF Exon 12 deletion: 4

Comments changed: Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivitywith RAF inhibitors.Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivitywith RAF inhibitors.. (First curated: 2024-07-31)

Changed Sorafenib in Solid tumours with BRAF L485_P490delinsF, L485_P490delinsY: 4

Comments changed: Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivity with RAF inhibitors.Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivity with RAF inhibitors.. (First curated: 2024-07-31)

Changed Encorafenib, Dabrafenib in Solid tumours with BRAF N486_P490del, V487_P492delinsA: 4

Comments changed: Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivitywith RAF inhibitors.Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivitywith RAF inhibitors.. (First curated: 2024-07-31)

Changed Vemurafenib in Melanoma with BRAF T599_V600insT: 4

Comments changed: Phase 2. AcSé vemurafenib basket study. NCT01895643. One responder seen in melanoma harbouring T599dupPhase 2. AcSé vemurafenib basket study. NCT01895643. One responder seen in melanoma harbouring T599dup. (First curated: 2023-12-22)

Changed Atezolizumab + Docetaxel + Cisplatin + Fluorouracil in Anal cancer with CD274 Protein expression: 4

Comments changed: Phase 2. SCARCE C17-02 PRODIGE 60. NCT03519295. N=97 (64 in Atezolizumab + mDCF vs 33 in mDCF alone). 12-month PFS 45% (90% CI 35-55) vs 43% (29-58) in group A and B; in PD-L1 CPS ≥5, 70% vs 40% (interaction p=0.051). Higher grade 3-4 adverse events in group A (61% vs 42%), primary endpoint not met.Phase 2. SCARCE C17-02 PRODIGE 60. NCT03519295. N=97 (64 in Atezolizumab + mDCF vs 33 in mDCF alone). 12-month PFS 45% (90% CI 35-55) vs 43% (29-58) in group A and B; in PD-L1 CPS ≥5, 70% vs 40% (interaction p=0.051). Higher grade 3-4 adverse events in group A (61% vs 42%), primary endpoint not met.. (First curated: 2025-07-30)

Changed Nivolumab in Hepatocellular carcinoma with CD274 Protein expression: 4

Comments changed: Phase 1/2. CheckMate 040 trial. N=234 (80 sorafenib-naive, 154 sorafenib-experienced). ORR was 20% and 14% in sorafenib-naive and sorafenib-experienced groups, respectively. Median OS were 26.6 months and 15.1 months, respectively. Higher ORR and extended OS were observed with baseline PD-L1 ≥1% vs <1%, more pronounced in the sorafenib-experienced group.Phase 1/2. CheckMate 040 trial. N=234 (80 sorafenib-naive, 154 sorafenib-experienced). ORR was 20% and 14% in sorafenib-naive and sorafenib-experienced groups, respectively. Median OS were 26.6 months and 15.1 months, respectively. Higher ORR and extended OS were observed with baseline PD-L1 ≥1% vs <1%, more pronounced in the sorafenib-experienced group.. (First curated: 2025-02-16)

Changed Sacituzumab Tirumotecan + Pembrolizumab in Non-small cell lung cancer with CD274 Protein expression: 4

Comments changed: Phase 3 OptiTROP-Lung05. NCT06448312. N=413. Sac-TMT plus pembrolizumab significantly improved PFS over pembrolizumab (median not reached vs 5.7 months; HR 0.35). ORR was 70.2% vs 42.0%. In PD-L1 TPS 1-49% subgroup, PFS HR 0.28; in TPS ≥50% subgroup, PFS HR 0.47. In non-squamous histology, PFS HR 0.28; in squamous, PFS HR 0.44. OS trend favored sac-TMT plus pembrolizumab (HR 0.55).Phase 3 OptiTROP-Lung05. NCT06448312. N=413. Sac-TMT plus pembrolizumab significantly improved PFS over pembrolizumab (median not reached vs 5.7 months; HR 0.35). ORR was 70.2% vs 42.0%. In PD-L1 TPS 1-49% subgroup, PFS HR 0.28; in TPS ≥50% subgroup, PFS HR 0.47. In non-squamous histology, PFS HR 0.28; in squamous, PFS HR 0.44. OS trend favored sac-TMT plus pembrolizumab (HR 0.55).. (First curated: 2026-06-08)

Changed Pembrolizumab + Cisplatin + Gemcitabine, Pembrolizumab + Carboplatin + Gemcitabine in Urothelial carcinoma with CD274 Protein expression: 4

Comments changed: Phase 3 KEYNOTE-361 trial. NCT02853305. N=993. Primary endpoints of PFS (HR 0.78, P=0.0033) and OS (HR 0.86, P=0.0407) were not met for pembrolizumab plus chemotherapy versus chemotherapy. TMB as a continuous variable was significantly associated with improved ORR, PFS, and OS in pembrolizumab monotherapy (one-sided P<0.001, P<0.001, P=0.007), with highest benefits observed in patients with TMB ≥175 mutations/exome and PD-L1 CPS ≥10 versus chemotherapy alone. Cutoffs of 175 mutations/exome (TMB) and CPS 10 (PD-L1) were prespecified.Phase 3 KEYNOTE-361 trial. NCT02853305. N=993. Primary endpoints of PFS (HR 0.78, P=0.0033) and OS (HR 0.86, P=0.0407) were not met for pembrolizumab plus chemotherapy versus chemotherapy. TMB as a continuous variable was significantly associated with improved ORR, PFS, and OS in pembrolizumab monotherapy (one-sided P<0.001, P<0.001, P=0.007), with highest benefits observed in patients with TMB ≥175 mutations/exome and PD-L1 CPS ≥10 versus chemotherapy alone. Cutoffs of 175 mutations/exome (TMB) and CPS 10 (PD-L1) were prespecified.. (First curated: 2025-06-29)

Changed SKB500 in Small cell lung cancer, Oesophageal squamous cell carcinoma with CD276 Overexpression: 4

Comments changed: Phase 1 FIH study of SKB500 (B7-H3 ADC). NCT06736327. N=150. RP2D established 12 mg/kg. ORR 54.5% (30/55) DCR 92.7% (51/55) at 12mg/kg at ≥6 weeks follow-up. SCLC cohort ORR 71.4% (15/21) DCR 100%. ESCC cohort ORR 55.6% (10/18) DCR 88.9%. Response seen across B7-H3 expression level. Relationship between B7-H3 expression level and ORR not established.Phase 1 FIH study of SKB500 (B7-H3 ADC). NCT06736327. N=150. RP2D established 12 mg/kg. ORR 54.5% (30/55) DCR 92.7% (51/55) at 12mg/kg at ≥6 weeks follow-up. SCLC cohort ORR 71.4% (15/21) DCR 100%. ESCC cohort ORR 55.6% (10/18) DCR 88.9%. Response seen across B7-H3 expression level. Relationship between B7-H3 expression level and ORR not established.. (First curated: 2026-06-05)

Changed FOR46 in Prostate cancer with CD46 Overexpression: 4

Comments changed: Phase I. FOR46 (FG-3246). NCT03575819. N=56. In patients with progressive mCRPC after ≥one androgen signaling inhibitors, median radiographic PFS was 8.7 months in efficacy evaluable subset (n=40). Confirmed ORR was 20% (5/25 RECIST-evaluable). PSA50 response was 36% (14/39). Median DOR was 7.5 months. Responders associated with higher on-treatment circulating effector CD8+ T cells. Note, Response was not clearly associated with CD46 expression despite mechanism of action.Phase I. FOR46 (FG-3246). NCT03575819. N=56. In patients with progressive mCRPC after ≥one androgen signaling inhibitors, median radiographic PFS was 8.7 months in efficacy evaluable subset (n=40). Confirmed ORR was 20% (5/25 RECIST-evaluable). PSA50 response was 36% (14/39). Median DOR was 7.5 months. Responders associated with higher on-treatment circulating effector CD8+ T cells. Note, Response was not clearly associated with CD46 expression despite mechanism of action.. (First curated: 2026-03-04)

Changed Precemtabart tocentecan in Colorectal cancer with CEACAM5 Protein expression: 4

Comments changed: Phase 1. PROCEADE-CRC-01. NCT05464030. N=40. Heavily pretreated irinotecan-refractory metastatic colorectal cancer. Precemtabart tocentecan. Confirmed ORR 7.5% (3/40), unconfirmed 15.0% (6/40), all at dose levels ≥2.4 mg/kg. Median PFS 5.9 months (95% CI: 4.6–7.2); at dose levels ≥2.4 mg/kg (n=34), median PFS 6.7 months (95% CI: 4.6–8.8).Phase 1. PROCEADE-CRC-01. NCT05464030. N=40. Heavily pretreated irinotecan-refractory metastatic colorectal cancer. Precemtabart tocentecan. Confirmed ORR 7.5% (3/40), unconfirmed 15.0% (6/40), all at dose levels ≥2.4 mg/kg. Median PFS 5.9 months (95% CI: 4.6–7.2); at dose levels ≥2.4 mg/kg (n=34), median PFS 6.7 months (95% CI: 4.6–8.8).. (First curated: 2026-05-18)

Changed EBC-129 in Gastric cancer, Gastroesophageal adenocarcinoma with CEACAM5 Protein expression, Overexpression: 4

Comments changed: Phase 1. NCT05701527. N=21 (17 evaluable). Overall ORR 29.4%, DCR 82.4%, median PFS 17.86 weeks in IHC ≥20% at IHC 2+/3+. In IHC ≥50% subgroup, ORR 50%, DCR 90%, median PFS 21.4 weeks. At 1.8 mg/kg with IHC ≥50%, ORR 50%, DCR 100%, median PFS 29.2 weeks.Phase 1. NCT05701527. N=21 (17 evaluable). Overall ORR 29.4%, DCR 82.4%, median PFS 17.86 weeks in IHC ≥20% at IHC 2+/3+. In IHC ≥50% subgroup, ORR 50%, DCR 90%, median PFS 21.4 weeks. At 1.8 mg/kg with IHC ≥50%, ORR 50%, DCR 100%, median PFS 29.2 weeks.. (First curated: 2026-06-07)

Changed EBC-129 in Gastroesophageal adenocarcinoma with CEACAM5 Protein expression, Overexpression: 4

Comments changed: Phase 1. NCT05701527. N=21 (17 evaluable). Overall ORR 29.4%, DCR 82.4%, median PFS 17.86 weeks in IHC ≥20% cohort. In IHC ≥50% subgroup, ORR 50%, DCR 90%, median PFS 21.4 weeks. At 1.8 mg/kg with IHC ≥50%, ORR 50%, DCR 100%, median PFS 29.2 weeks. Protein expression at IHC 2+ and/or 3+Phase 1. NCT05701527. N=21 (17 evaluable). Overall ORR 29.4%, DCR 82.4%, median PFS 17.86 weeks in IHC ≥20% cohort. In IHC ≥50% subgroup, ORR 50%, DCR 90%, median PFS 21.4 weeks. At 1.8 mg/kg with IHC ≥50%, ORR 50%, DCR 100%, median PFS 29.2 weeks. Protein expression at IHC 2+ and/or 3+. (First curated: 2021-06-16)

Changed BNT142 in Ovarian cancer, Solid tumours with CLDN6 Protein expression: 4

Comments changed: Phase 1/2 BNT142-01 trial. NCT05262530. N=65. BNT142 showed anti-tumor activity with 7 partial responses in ovarian cancer and a disease control rate of 58% across all dose levels in CLDN6+ advanced solid tumors. CLDN6 positivity is defined as ≥ membrane positivity in 10% of cell. No clear relationship beween CLDN6 expression level versus response seen.Phase 1/2 BNT142-01 trial. NCT05262530. N=65. BNT142 showed anti-tumor activity with 7 partial responses in ovarian cancer and a disease control rate of 58% across all dose levels in CLDN6+ advanced solid tumors. CLDN6 positivity is defined as ≥ membrane positivity in 10% of cell. No clear relationship beween CLDN6 expression level versus response seen.. (First curated: 2025-06-01)

Changed FOG-001 in Solid tumors, Desmoid tumors, Ameloblastoma, Adamantinomatous craniopharyngioma, Salivary gland carcinoma with CTNNB1 Oncogenic mutation: 4

Comments changed: Phase 1/2. NCT05919264. N=83. FOG-001 monotherapy in patients with solid tumors bearing Wnt pathway-activating mutations (WPAM+). In Wnt-β-catenin driven solid tumors (N=14), ORR was 43% and DCR 79%. In desmoid tumors (N=5), ORR and DCR were 60% and 100%, respectively. In MSS CRC, DCR was 50% at higher dose levels (240–480 mg/m2) with molecular responses (≥50% ctDNA reduction) in 60% of pts.Phase 1/2. NCT05919264. N=83. FOG-001 monotherapy in patients with solid tumors bearing Wnt pathway-activating mutations (WPAM+). In Wnt-β-catenin driven solid tumors (N=14), ORR was 43% and DCR 79%. In desmoid tumors (N=5), ORR and DCR were 60% and 100%, respectively. In MSS CRC, DCR was 50% at higher dose levels (240–480 mg/m2) with molecular responses (≥50% ctDNA reduction) in 60% of pts.. (First curated: 2026-05-17)

Changed TQB6411 in Non-small cell lung cancer with EGFR Exon 19 deletion, L858R: 4

Comments changed: Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%.Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%.. (First curated: 2026-06-07)

Changed TQB6411 in Non-small cell lung cancer, Oesophageal adenocarcinoma, Gastroesophageal adenocarcinoma, Colorectal cancer with EGFR Protein expression, Overexpression: 4

Comments changed: Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%. Median PFS and duration of response not reported. Not biomarker pre-selected.Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%. Median PFS and duration of response not reported. Not biomarker pre-selected.. (First curated: 2021-06-16)

Changed Gefitinib + Capmatinib in Non-small cell lung cancer with EGFR+MET EGFR:Oncogenic mutations and MET:amplification and NOT EGFR:T790M: 4

Comments changed: Phase Ib/II study. Capmatinib plus gefitinib showed clinical activity in patients with EGFR-mutated, MET-dysregulated NSCLC who progressed on EGFR-TKI, particularly in those with high MET-amplified tumors (ORR 47% with MET gene copy number ≥ 6), addressing a predominant EGFR-TKI resistance mechanism.Phase Ib/II study. Capmatinib plus gefitinib showed clinical activity in patients with EGFR-mutated, MET-dysregulated NSCLC who progressed on EGFR-TKI, particularly in those with high MET-amplified tumors (ORR 47% with MET gene copy number ≥ 6), addressing a predominant EGFR-TKI resistance mechanism.. (First curated: 2020-06-23)

Changed Trastuzumab + Pertuzumab + Paclitaxel with ERBB2 Overexpression: 4

Cancer type(s) changed: Extramammary Paget’s diseaseExtramammary Paget’s disease (First curated: 2023-12-26)

Changed VVD-159642 in Solid tumours with ERBB2 Overexpression: 4

Comments changed: Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors.Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors.. (First curated: 2026-06-16)

Changed GQ1001 in Solid tumour with ERBB2 Overexpression, Amplification: 4

Comments changed: Phase Ia study. NCT04450732. GQ1001, a HER2-targeting ADC, showed antitumor activity in HER2-positive advanced solid tumors, with 6 out of 15 evaluable subjects achieving confirmed partial response at doses ≥ 7.2 mg/kg, and a median progression-free survival of 4.8 months.Phase Ia study. NCT04450732. GQ1001, a HER2-targeting ADC, showed antitumor activity in HER2-positive advanced solid tumors, with 6 out of 15 evaluable subjects achieving confirmed partial response at doses ≥ 7.2 mg/kg, and a median progression-free survival of 4.8 months.. (First curated: 2025-05-28)

Changed Lapatinib + Capecitabine with ERBB2 S310F: 4

Cancer type(s) changed: Extramammary Paget’s diseaseExtramammary Paget’s disease (First curated: 2020-06-09)

Changed Trastuzumab + Carboplatin with ERBB2 S310F: 4

Cancer type(s) changed: Extramammary Paget’s diseaseExtramammary Paget’s disease (First curated: 2020-06-09)

Changed Tazemetostat with EZH2 Oncogenic mutations, A677G, Y641N, Y641C, Y641H, Y641S, Y641F, Y646, A687V: 4

Cancer type(s) changed: Non-Hodgkin’s lymphomaNon-Hodgkin’s lymphoma (First curated: 2020-06-15)

Changed ALK201 in Solid tumours with FGFR2 FGFR2b Overexpression, FGFR2-IIIb Overexpression: 4

Comments changed: Phase 1/2. NCT06656390. N=38. ALK201 showed ORR of 24% and DCR of 68% in evaluable patients (n=25); at ≥7.2 mg/kg, ORR was 35.7% and DCR was 100%. In IHC2+/3+ in >=5% of cells, ORR was 27%.(n=11)Phase 1/2. NCT06656390. N=38. ALK201 showed ORR of 24% and DCR of 68% in evaluable patients (n=25); at ≥7.2 mg/kg, ORR was 35.7% and DCR was 100%. In IHC2+/3+ in >=5% of cells, ORR was 27%.(n=11). (First curated: 2026-06-07)

Changed LY4170156 in Ovarian cancer, Peritoneal serous carcinoma, Fallopian tube carcinoma with FOLR1 Protein expression: 4

Comments changed: Phase 1a/b study. NCT06400472. LY4170156, an ADC targeting folate receptor alpha, showed a preliminary ORR of 38% (5/13) in HGSOC patients with varying FRα expression levels and prior mirvetuximab soravtansin treatment.Phase 1a/b study. NCT06400472. LY4170156, an ADC targeting folate receptor alpha, showed a preliminary ORR of 38% (5/13) in HGSOC patients with varying FRα expression levels and prior mirvetuximab soravtansin treatment.. (First curated: 2025-06-09)

Changed Cisplatin in Breast cancer with Homologous Recombination Deficiency Score High: 4

Comments changed: Preclinical and clinical study. Homologous recombination deficiency (HRD) score, defined as HRD score ≥42 or BRCA1/2 mutation, predicts response to platinum-containing neoadjuvant chemotherapy in triple-negative breast cancer patients, including those with BRCA1/2 nonmutated tumors with high HRD scores.Preclinical and clinical study. Homologous recombination deficiency (HRD) score, defined as HRD score ≥42 or BRCA1/2 mutation, predicts response to platinum-containing neoadjuvant chemotherapy in triple-negative breast cancer patients, including those with BRCA1/2 nonmutated tumors with high HRD scores.. (First curated: 2020-04-16)

Changed VVD-159642 in Solid tumours with HRAS G12C, G12V: 4

Comments changed: Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors.Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors.. (First curated: 2026-06-16)

Changed BBO-11818 + Cetuximab in Colorectal adenocarcinoma with KRAS G12D: 4

Comments changed: Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.. (First curated: 2026-03-11)

Changed BBO-11818 in Solid tumours with KRAS G12D, G12V, G12C, G12A, G12S, G13D, Amplification and NOT Oncogenic mutation: 4

Comments changed: Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.. (First curated: 2026-03-11)

Changed BBO-11818 in Colorectal cancer, Pancreatic cancer, Lung cancer with KRAS G12D, G12V, G12C, Oncogenic mutations: 4

Comments changed: Preclinical study. BBO-11818, a noncovalent pan-KRAS inhibitor, showed inhibition of MAPK signaling and cellular viability in KRAS-driven lines and tumor regressions in KRAS-mutant xenograft models. Combination with anti-PD-1, anti-EGFR antibodies, and a RAS:PI3Kα breaker showed enhanced efficacy.Preclinical study. BBO-11818, a noncovalent pan-KRAS inhibitor, showed inhibition of MAPK signaling and cellular viability in KRAS-driven lines and tumor regressions in KRAS-mutant xenograft models. Combination with anti-PD-1, anti-EGFR antibodies, and a RAS:PI3Kα breaker showed enhanced efficacy.. (First curated: 2021-06-16)

Changed VVD-159642 in Solid tumours with KRAS G12R, G12C, G12E, G12A, G12V, Q61H, Q61K, G13C, Q61R, Q61L, Amplification, Oncogenic mutations: 4

Comments changed: Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors.Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors.. (First curated: 2026-06-16)

Changed Telisotuzumab Adizutecan in Colorectal cancer with MET Protein expression: 4

Comments changed: Phase 1. NCT05029882. N=122. ORR 15.6% (95% CI 9.6-23.2). DOR 5.9 months (95% CI 4.1-10.5). mPFS 4.6 months (95% CI 4.0-5.4). mOS 10.4 months (95% CI 8.9-13.1). In high c-Met expression (≥10%|3+) at ≥2.4 mg/kg, ORR 36%.Phase 1. NCT05029882. N=122. ORR 15.6% (95% CI 9.6-23.2). DOR 5.9 months (95% CI 4.1-10.5). mPFS 4.6 months (95% CI 4.0-5.4). mOS 10.4 months (95% CI 8.9-13.1). In high c-Met expression (≥10%|3+) at ≥2.4 mg/kg, ORR 36%.. (First curated: 2021-06-16)

Changed TQB6411 in Non-small cell lung cancer, Oesophageal adenocarcinoma, Gastroesophageal adenocarcinoma, Colorectal cancer with MET Protein expression, Overexpression: 4

Comments changed: Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%. Median PFS and duration of response not reported. Not biomarker pre-selected.Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%. Median PFS and duration of response not reported. Not biomarker pre-selected.. (First curated: 2021-06-16)

Changed HRO761 in Colorectal adenocarcinoma with Microsatellite Instability High: 4

Comments changed: Phase I/Ib. HRO761. NCT05838768. N=47 (19 CRC). ORR 8.6% (10.5% in CRC), DCR 68.6% (84.2% in CRC), median PFS 5.6 months; 9-mo PFS rate 68.6% (95% CI 30.5–88.7) at 200 mg daily. ctDNA clearance observed in 6/14 pts with detectable baseline ctDNA, median treatment duration 9.3 months in responders.Phase I/Ib. HRO761. NCT05838768. N=47 (19 CRC). ORR 8.6% (10.5% in CRC), DCR 68.6% (84.2% in CRC), median PFS 5.6 months; 9-mo PFS rate 68.6% (95% CI 30.5–88.7) at 200 mg daily. ctDNA clearance observed in 6/14 pts with detectable baseline ctDNA, median treatment duration 9.3 months in responders.. (First curated: 2025-10-18)

Changed AG-270 in Solid tumours with MTAP Deletion: 4

Comments changed: Phase 1 trial. NCT03435250. N=40. AG-270/S095033, a MAT2A inhibitor, achieved 2 partial responses and 5 patients with stable disease ≥16 weeks in patients with advanced MTAP-deleted malignancies. First curated: 2020-11-23Phase 1 trial. NCT03435250. N=40. AG-270/S095033, a MAT2A inhibitor, achieved 2 partial responses and 5 patients with stable disease ≥16 weeks in patients with advanced MTAP-deleted malignancies. First curated: 2020-11-23. (First curated: 2025-05-27)

Changed T-025 in Solid tumours with MYC Amplification: 4

Comments changed: Cell line study. CLK inhibitor showed stronger anti‐proliferative effects for cell lines of MYC‐amplified solid tumours than non‐amplified counterparts.Cell line study. CLK inhibitor showed stronger anti‐proliferative effects for cell lines of MYC‐amplified solid tumours than non‐amplified counterparts.. (First curated: 2022-02-27)

Changed ADRX-0706 in Solid tumours with NECTIN4 Protein expression: 4

Comments changed: Phase 1 trial. NCT06036121. N=53. ADRX-0706, a Nectin-4 targeting antibody-drug conjugate (ADC), showed anti-tumor activity in 30 response-evaluable subjects treated at doses ≥8 mg/kg, with a confirmed complete response in a cervical cancer patient. The study reported an ORR of 17%, including 5 objective responses, and a DCR of 47%, with 9 patients experiencing stable disease. Nectin-4 expression is retrospective analysis criteria and not prospectively assessed.Phase 1 trial. NCT06036121. N=53. ADRX-0706, a Nectin-4 targeting antibody-drug conjugate (ADC), showed anti-tumor activity in 30 response-evaluable subjects treated at doses ≥8 mg/kg, with a confirmed complete response in a cervical cancer patient. The study reported an ORR of 17%, including 5 objective responses, and a DCR of 47%, with 9 patients experiencing stable disease. Nectin-4 expression is retrospective analysis criteria and not prospectively assessed.. (First curated: 2025-06-09)

Changed STX-478 in Solid tumours with PIK3CA H1047R, H1047L, H1047Y, H1047A, M1043I, M1043L, M1043Y, M1043A, G1049R: 4

Comments changed: Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated activities in PI3Kalpha-mutant xenografts.Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated activities in PI3Kalpha-mutant xenografts.. (First curated: 2026-06-15)

Changed GDC-0077 in Breast cancer with PIK3CA Oncogenic mutations: 4

Comments changed: Phase 1a dose escalation study. NCT03006172. N=20. GDC-0077, a p110α-selective and mutant-degrading PI3K inhibitor, showed manageable safety profile, linear PK, and preliminary anti-tumor activity with 25% partial response rate and 45% clinical benefit rate in patients with PIK3CA-mutant solid tumors.Phase 1a dose escalation study. NCT03006172. N=20. GDC-0077, a p110α-selective and mutant-degrading PI3K inhibitor, showed manageable safety profile, linear PK, and preliminary anti-tumor activity with 25% partial response rate and 45% clinical benefit rate in patients with PIK3CA-mutant solid tumors.. (First curated: 2020-04-16)

Changed STX-478, STX-478 + Fulvestrant, STX-478 + Palbociclib, STX-478 + Fulvestrant + Palbociclib in Breast cancer, Head and neck squamous cell carcinoma, Gynaecological cancer, Colon cancer, Lung cancer with PIK3CA Oncogenic mutations, H1047R, H1047L, E542K, E545K: 4

Comments changed: Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated robust efficacy in PI3Kα-mutant xenografts: 82% TGI in CAL-33 HNSCC; tumor regressions in 50% of GP2d colon and 5/9 Detroit 562 HNSCC; 100% regression in T47D breast at 100 mg/kg; durable tumor suppression to day 94 in ST1056 PDX with STX-478 plus fulvestrant, followed by modest regrowth off treatment.Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated robust efficacy in PI3Kα-mutant xenografts: 82% TGI in CAL-33 HNSCC; tumor regressions in 50% of GP2d colon and 5/9 Detroit 562 HNSCC; 100% regression in T47D breast at 100 mg/kg; durable tumor suppression to day 94 in ST1056 PDX with STX-478 plus fulvestrant, followed by modest regrowth off treatment.. (First curated: 2026-07-19)

Changed 212Pb-VMT-alpha-NET in Neuroendocrine tumour with SSTR2 Protein expression: 4

Comments changed: Phase 1/2a study. NCT05636618. [212Pb]VMT-α-NET. 3/7 patients achieving partial responses at 185 MBq dose level in SSTR2-expressing neuroendocrine tumors. DOTATATE-positivePhase 1/2a study. NCT05636618. [212Pb]VMT-α-NET. 3/7 patients achieving partial responses at 185 MBq dose level in SSTR2-expressing neuroendocrine tumors. DOTATATE-positive. (First curated: 2025-05-31)

Changed Xaluritamig in Prostate cancer with STEAP1 Protein expression: 4

Comments changed: Phase 1 study. Xaluritamig, a STEAP1-targeted T-cell engager, showed responses (49% PSA50; 24% ORR) in patients with metastatic castration-resistant prostate cancer, with greater frequency at target doses ≥0.75 mg (59% PSA50; 41% ORR). Note relationship between STEAP1 expression and response was not prospectively assessed in this study.Phase 1 study. Xaluritamig, a STEAP1-targeted T-cell engager, showed responses (49% PSA50; 24% ORR) in patients with metastatic castration-resistant prostate cancer, with greater frequency at target doses ≥0.75 mg (59% PSA50; 41% ORR). Note relationship between STEAP1 expression and response was not prospectively assessed in this study.. (First curated: 2025-06-09)

Changed Atezolizumab in Breast cancer, Hepatobiliary cancers, Solid Tumours with Tumour Mutational Burden High: 4

Comments changed: Phase 2. TAPISTRY trial. NCT04589845. N=150. Atezolizumab showed ORR of 23% (TMB ≥16 mut/Mb) and 20% (TMB ≥13 mut/Mb), with median PFS of 2.8 months and 2.7 months, respectively, in patients with TMB-high solid tumors. TMB was assessed by Foundation One CDx. Tumour types with n>=4 are identifed; no objective responses were seen in breast and hepatobiliary cancers.Phase 2. TAPISTRY trial. NCT04589845. N=150. Atezolizumab showed ORR of 23% (TMB ≥16 mut/Mb) and 20% (TMB ≥13 mut/Mb), with median PFS of 2.8 months and 2.7 months, respectively, in patients with TMB-high solid tumors. TMB was assessed by Foundation One CDx. Tumour types with n>=4 are identifed; no objective responses were seen in breast and hepatobiliary cancers.. (First curated: 2024-06-18)

Changed Pembrolizumab + Cisplatin + Gemcitabine, Pembrolizumab + Carboplatin + Gemcitabine in Urothelial carcinoma with Tumour Mutational Burden High: 4

Comments changed: Phase 3 KEYNOTE-361 trial. NCT02853305. N=993. Primary endpoints of PFS (HR 0.78, P=0.0033) and OS (HR 0.86, P=0.0407) were not met for pembrolizumab plus chemotherapy versus chemotherapy. TMB as a continuous variable was significantly associated with improved ORR, PFS, and OS in pembrolizumab monotherapy (one-sided P<0.001, P<0.001, P=0.007), with highest benefits observed in patients with TMB ≥175 mutations/exome and PD-L1 CPS ≥10 versus chemotherapy alone. Cutoffs of 175 mutations/exome (TMB) and CPS 10 (PD-L1) were prespecified.Phase 3 KEYNOTE-361 trial. NCT02853305. N=993. Primary endpoints of PFS (HR 0.78, P=0.0033) and OS (HR 0.86, P=0.0407) were not met for pembrolizumab plus chemotherapy versus chemotherapy. TMB as a continuous variable was significantly associated with improved ORR, PFS, and OS in pembrolizumab monotherapy (one-sided P<0.001, P<0.001, P=0.007), with highest benefits observed in patients with TMB ≥175 mutations/exome and PD-L1 CPS ≥10 versus chemotherapy alone. Cutoffs of 175 mutations/exome (TMB) and CPS 10 (PD-L1) were prespecified.. (First curated: 2025-06-29)

Changed Niraparib in Cholangiocarcinoma, Uveal melanoma, Mesothelioma, Clear cell renal cell carcinoma with BAP1 Oncogenic mutations; Loss-of-function mutations; Deletion: R2

Comments changed: NCT03207347. Phase 2. Cohort A. ORR 6% (1/18) failed to meet the primary endpoint and stopped at the first stage of Simon’s design.NCT03207347. Phase 2. Cohort A. ORR 6% (1/18) failed to meet the primary endpoint and stopped at the first stage of Simon’s design.. (First curated: 2023-03-08)

Changed Encorafenib, Dabrafenib in Solid tumours with BRAF L485_P490delinsF, L485_P490delinsY, L485delinsFS: R2

Comments changed: Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivitywith RAF inhibitors.Preclinical study. BRAFΔβ3-αC in-frame deletion mutants reveals differences in sensitivitywith RAF inhibitors.. (First curated: 2024-07-31)

Changed Vemurafenib in Non-small cell lung cancer with BRAF Oncogenic mutations AND NOT V600: R2

Comments changed: Phase 2. AcSé. NCT02304809. BRAF(V600) mutated NSCLC patients treated with Vemurafenib showed an ORR of 44.9% and median PFS of 5.2 months, while BRAF(nonV600) mutated patients had an ORR of 0%.Phase 2. AcSé. NCT02304809. BRAF(V600) mutated NSCLC patients treated with Vemurafenib showed an ORR of 44.9% and median PFS of 5.2 months, while BRAF(nonV600) mutated patients had an ORR of 0%.. (First curated: 2021-11-10)

Changed BBO-11818 in Solid tumours with BRAF V600E: R2

Comments changed: Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.. (First curated: 2026-03-11)

Changed Atezolizumab in Hepatocellular carcinoma with CRKL Amplification, Overexpression: R2

Comments changed: Preclinical study. CRKL overexpression attenuates anti-PD-1 efficacy by mobilizing tumor-associated neutrophils in HCC. Blocking CRKL/β-catenin/VEGF alpha and CXCL1 axis using bevacizumab or lenvatinib overcomes anti-PD-1 resistance.Preclinical study. CRKL overexpression attenuates anti-PD-1 efficacy by mobilizing tumor-associated neutrophils in HCC. Blocking CRKL/β-catenin/VEGF alpha and CXCL1 axis using bevacizumab or lenvatinib overcomes anti-PD-1 resistance.. (First curated: 2024-11-04)

Changed Pembrolizumab in Non-small cell lung cancer with EGFR+CD274 CD274:Protein expression and EGFR:Oncogenic mutations: R2

Comments changed: NCT02879994. Phase 2. The ORR was <9% in in EGFR-Mutant, TKI naive patients treated with pembrolizumab. including PD-L1 expression ≥50%.NCT02879994. Phase 2. The ORR was <9% in in EGFR-Mutant, TKI naive patients treated with pembrolizumab. including PD-L1 expression ≥50%.. (First curated: 2023-02-28)

Changed Trastuzumab with ERBB2+PTEN ERBB2:Oncogenic mutations and PTEN:Loss of protein expression, ERBB2:Oncogenic mutations and PTEN:Loss-of-function mutations, ERBB2:Oncogenic mutations and PTEN:Oncogenic mutations, ERBB2:Oncogenic mutations and PTEN:Deletion: R2

Cancer type(s) changed: Extramammary Paget’s diseaseExtramammary Paget’s disease (First curated: 2025-02-16)

Changed Trastuzumab with ERBB3 A232V: R2

Cancer type(s) changed: Extramammary Paget’s diseaseExtramammary Paget’s disease (First curated: 2020-06-09)

Changed Binimetinib in Low-grade serous ovarian cancer with ERBB3 Amplification: R2

Comments changed: Case series. KRAS-mutated LGSOC patient with MEK inhibitor resistance developed aggressive brain metastases associated with ERBB3 amplification and aberrant ERBB3–MYC signaling, suggesting potential resistance mechanisms and need for combinatorial strategies.Case series. KRAS-mutated LGSOC patient with MEK inhibitor resistance developed aggressive brain metastases associated with ERBB3 amplification and aberrant ERBB3–MYC signaling, suggesting potential resistance mechanisms and need for combinatorial strategies.. (First curated: 2025-07-01)

Changed Ivosidenib in Acute myeloid leukaemia with IDH1 S280F, R119P, G131A, D279N, G289D, H315D: R2

Comments changed: 2-HG restoration as a result of mutations preventing drug/cofactor binding and/or emergence of an IDH2 mutation represents a mechanism of secondary resistance2-HG restoration as a result of mutations preventing drug/cofactor binding and/or emergence of an IDH2 mutation represents a mechanism of secondary resistance. (First curated: 2023-01-12)

Changed Ivosidenib in Acute myeloid leukaemia with IDH2 R140Q, R172K: R2

Comments changed: 2-HG restoration as a result of mutations preventing drug/cofactor binding and/or emergence of an IDH2 mutation represents a mechanism of secondary resistance2-HG restoration as a result of mutations preventing drug/cofactor binding and/or emergence of an IDH2 mutation represents a mechanism of secondary resistance. (First curated: 2023-01-12)

Changed BBO-11818 in Solid tumours with KRAS G12R, Q61R, Q61: R2

Comments changed: Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.. (First curated: 2026-03-11)

Changed Paclitaxel in Oesophageal squamous cell carcinoma with LGALS1 Protein expression: R2

Comments changed: Preclinical study. Galectin-1 is a key mediator of paclitaxel resistance in esophageal squamous cell carcinoma, acting through the interaction with β-catenin and enhancing MDR1 transcription, thereby increasing resistance to paclitaxel.Preclinical study. Galectin-1 is a key mediator of paclitaxel resistance in esophageal squamous cell carcinoma, acting through the interaction with β-catenin and enhancing MDR1 transcription, thereby increasing resistance to paclitaxel.. (First curated: 2025-06-13)

Changed Trastuzumab with MET Amplification: R2

Cancer type(s) changed: Extramammary Paget’s diseaseExtramammary Paget’s disease (First curated: 2020-06-09)

Changed BBO-11818 in Solid tumours with NRAS Oncogenic mutations: R2

Comments changed: Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.Preclinical study. BBO-11818. Potent noncovalent pan-KRAS inhibitor targeting ON and OFF states of KRAS G12D, G12V, and G12C. Potently inhibited MAPK signaling and cellular viability in KRAS-driven cell lines. Produced tumor regressions in KRAS-mutant xenograft models. Enhanced efficacy observed in combination with anti-PD-1, anti-EGFR antibodies, and RAS:PI3Kα breaker.. (First curated: 2026-03-11)

Changed STX-478 in Solid tumours with PIK3CA E542K, E545K, Helical domain mutation, Wildtype: R2

Comments changed: Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated activities in PI3Kalpha-mutant xenografts.Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated activities in PI3Kalpha-mutant xenografts.. (First curated: 2026-06-15)

Changed LOXO-783, LOXO-783 + Fulvestrant, LOXO-783 + Letrozole, LOXO-783 + Anaztrozole, LOXO-783 + Paclitaxel in Solid tumours with PIK3CA H1047R: R2

Comments changed: Phase 1a/b PIKASSO-01 trial. NCT05307705. LOXO-783, a PI3Kα H1047R inhibitor, demonstrated mutant selectivity and reduced hyperglycemia, with objective response rates (ORR) and clinical benefit rates (CBR) of 3%/17% in monotherapy, 5%/19% with endocrine therapy, and 19%/25% when combined with paclitaxel, though limited by high rates of diarrhea.Phase 1a/b PIKASSO-01 trial. NCT05307705. LOXO-783, a PI3Kα H1047R inhibitor, demonstrated mutant selectivity and reduced hyperglycemia, with objective response rates (ORR) and clinical benefit rates (CBR) of 3%/17% in monotherapy, 5%/19% with endocrine therapy, and 19%/25% when combined with paclitaxel, though limited by high rates of diarrhea.. (First curated: 2022-06-20)

Changed Temsirolimus in Breast cancer, Colorectal cancer with PIK3CA Oncogenic mutations: R2

Comments changed: Phase 2. TAPUR basket trial. N=83. Temsirolimus in PIK3CA-mutated solid tumors. Primary endpoint disease control (DC) defined as OR or SD ≥16 weeks. BC cohort DC rate 9%, Median PFS 8 weeks, Median OS 36 weeks. CRC cohort DC rate 9%, Median PFS 8 weeks, Median OS 37 weeks. UC cohort DC rate 37%, Median PFS 16 weeks, Median OS 37 weeks, Median DOSD 31 weeks. HP cohort DC rate 31%, Median PFS 9 weeks, Median OS 27 weeks, Median DOSD 28 weeks. Overall OR rate 8%. Null hypothesis of 15% DC rate rejected for UC and HP cohorts. H1047R mutation subgroup OR rate 18%. DOR for PR in UC up to 84 weeks. DOR for PR in HP up to 229 weeks ongoing. Antitumor activity demonstrated in UC and HP cohorts but not BC or CRC.Phase 2. TAPUR basket trial. N=83. Temsirolimus in PIK3CA-mutated solid tumors. Primary endpoint disease control (DC) defined as OR or SD ≥16 weeks. BC cohort DC rate 9%, Median PFS 8 weeks, Median OS 36 weeks. CRC cohort DC rate 9%, Median PFS 8 weeks, Median OS 37 weeks. UC cohort DC rate 37%, Median PFS 16 weeks, Median OS 37 weeks, Median DOSD 31 weeks. HP cohort DC rate 31%, Median PFS 9 weeks, Median OS 27 weeks, Median DOSD 28 weeks. Overall OR rate 8%. Null hypothesis of 15% DC rate rejected for UC and HP cohorts. H1047R mutation subgroup OR rate 18%. DOR for PR in UC up to 84 weeks. DOR for PR in HP up to 229 weeks ongoing. Antitumor activity demonstrated in UC and HP cohorts but not BC or CRC.. (First curated: 2026-05-18)

Changed Alisertib + Pembrolizumab in Head and neck squamous cell carcinoma with RB1 Deletion, Oncogenic mutations, Loss of protein expression: R2

Comments changed: Phase 1/2 trial. Alisertib + Pembrolizumab demonstrated no objective responses but achieved prolonged stable disease in several patients. Among 15 HPV-positive patients, 4 experienced stable disease ≥6 months. Median overall survival was 16.8 months and median progression-free survival was 1.4 months.Phase 1/2 trial. Alisertib + Pembrolizumab demonstrated no objective responses but achieved prolonged stable disease in several patients. Among 15 HPV-positive patients, 4 experienced stable disease ≥6 months. Median overall survival was 16.8 months and median progression-free survival was 1.4 months.. (First curated: 2025-06-24)

12 August, 2026 (Version: 20260812AU)

New AZD4956 + Saruparib in Ovarian cancer, Breast cancer, Pancreatic cancer, Prostate cancer with BRCA1 Loss-of-function mutations: 4

Preclinical study. AZD4956 combined with saruparib drove sustained regression of HRR-deficient BRCA2-/- DLD-1 xenografts, superior to monotherapies with PARP inhibition. References: 10.1158/1538-7445.AM2026-5745

New AZD4956 + Saruparib in Ovarian cancer, Breast cancer, Pancreatic cancer, Prostate cancer with BRCA2 Loss-of-function mutations: 4

Preclinical study. AZD4956 combined with saruparib drove sustained regression of HRR-deficient BRCA2-/- DLD-1 xenografts, superior to monotherapies with PARP inhibition. References: 10.1158/1538-7445.AM2026-5745

New Nivolumab in Non-small cell lung cancer with CD274 Amplification: 4

Prospective cohort study. N=194. PD-L1 amplification (2.6%) had ORR 80% vs polysomy 18.5% and disomy 17.9%. Median DOR not reached for amplification vs 14.9 and 16.8 months for polysomy and disomy. PFS HR 0.10 for amplification vs disomy; polysomy no benefit. 1-year OS 100% for amplification. PD-L1 TPS not correlated with copy number. Amplification but not polysomy predicts durable benefit from nivolumab. References: 32955570

New Patritumab deruxtecan in Breast cancer with ERBB3 Protein expression: 4

Phase 1/2 U31402-A-J101. NCT02980341. N=182. HER3-DXd in HER3-expressing metastatic breast cancer: HR+/HER2- (n=113) ORR 30.1%, mPFS 7.4 months, mOS 14.6 months, mDOR 7.2 months; TNBC (n=53) ORR 22.6%, mPFS 5.5 months, mOS 14.6 months, mDOR 5.9 months; HER2+ (n=14) ORR 42.9%, mPFS 11.0 months, mOS 19.5 months, mDOR 8.3 months; responses observed across HER3 expression levels. References: 37801674

New Bisantrene in Solid tumour with MYC Overexpression: 4

Preclinical study. (E,E)-bisantrene stabilized c-MYC promoter G-quadruplex and silenced c-MYC expression in multiple cancer cell lines, also decreasing expression of MET, TERT, VEGFA, ATF4, MDM2. No clinical efficacy endpoints reported. References: 10.1158/1538-7445.AM2026-5751

New Daraxonrasib in Pancreatic adenocarcinoma with ARAF N217K, S214C, S214F, S214T, S214Y: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with BRAF G466A, G469R, T599dup, BRAF-AGK fusion, BRAF-IGF1R fusion, BRAF-LRGUK fusion: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with ERBB2 Amplification: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Trastuzumab deruxtecan in Breast cancer with ERBB2 Loss of protein expression, V597M, P593R: R2

Translational study (paired patient specimens and isogenic models). 49% of cases had major decreases in HER2 expression after progression on T-DxD (52% of those had complete loss). ERBB2 mutations (V597M, P593R) promoted resistance. References: 41212147

New Daraxonrasib in Pancreatic adenocarcinoma with FGFR1 FGFR1-KAT6A: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with KRAS Amplification AND Oncogenic mutation: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with MAP2K1 G128D, I103N: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with MET Y1230C (Y1248C), MET-CREB3L2: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with MYC Amplification: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with NF1 Truncating mutations: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with PIK3CA E542K, E545K: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with PIK3R1 Loss-of-function mutations: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with RAF1 P261R, S259F: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with RICTOR Amplification: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

New Daraxonrasib in Pancreatic adenocarcinoma with RIT1 F82L: R2

Translational and preclinical studies. Analysis of acquired resistance to daraxonrasib via paired targeted sequencing and end-of-treatment ctDNA from 44 patients revealed treatment-emergent RAS pathway alterations in 59% (26/44), comprising mutant KRAS amplifications (36%, 16/44), MAPK alterations (25%, 11/44), RTK alterations (9%, 4/44), and PI3K alterations (9%, 4/44). No acquired secondary KRAS mutations were observed. Preclinical PDAC models corroborated these mechanisms and further identified MYC amplification and RTK upregulation. References: 10.1038/s41591-026-04537-w

02 August, 2026 (Version: 20260802AU)

New Brigatinib in Solid tumors except Non-small cell lung cancer with ALK Fusions: 3

Phase 2 ALLBREAK basket trial. jRCT2041210148. N=27. Brigatinib in ALK fusion-positive non-NSCLC solid tumors. ORR 63%. DCR 92.6%. Median PFS 9.7 months. Median DOR 14.4 months. Median OS 19.5 months. References: 10.1200/JCO.2026.44.16_suppl.3105

New Cesnicabtagene autoleucel in Multiple myeloma with BCMA Protein expression: 3

Long-term follow-up of ARI0002h (cesnicabtagene autoleucel) in 60 patients with RRMM (NCT04309981). ORR 95%, CR 58% (sCR 55%). MRD-negative rates 98% (day 28) and 96% (day 100). Median PFS 20 months (95% CI 13.2-26.8). Median OS not reached; 24-month OS rate 63%. References: 10.1200/JCO.2024.42.16_suppl.7544

New Palbociclib in Head and neck squamous cell carcinoma with CDKN2A Deletion, Oncogenic mutations, Loss of protein expression: 3

Phase 2 single-arm trial. N=26. Palbociclib before chemoradiotherapy in HPV-negative locally advanced HNSCC. ORR with palbociclib before chemoradiotherapy was 41.7% (95% CI, 22.1 to 63.4). ORR was 66.7% (10/15) in CDKN2A-altered vs 0% (0/9) in wild-type (P=.002). Relapse occurred in 13.3% (2/15) with CDKN2A alterations vs 70% (7/10) without (P=.009). Median follow-up 33.9 months. References: 40403207

New Sonesitatug vedotin in Gastric cancer, Gastroesophageal junction cancer with CLDN18 Protein expression: 3

Phase 2 CLARITY-PanTumor01. NCT06219941. N=67. Sonesitatug vedotin 2.2 mg/kg monotherapy in CLDN18.2+ advanced gastric/GEJ cancers. ORR 28.4% (RC 26.7%, PBC 29.0%). Median PFS 4.2 months (RC 4.2 months, PBC 3.1 months). 6-month PFS 39.9%. Median DoR not reached. 58.8% of evaluable patients had at least partial ctDNA molecular response. References: 10.1200/JCO.2026.44.16_suppl.4023

New ZL-1310 in Small-cell lung cancer with DLL3 Protein expression: 3

Phase 1 trial. NCT06179069. N=28. ZL-1310 in r/r ES-SCLC. ORR 68% (19/28). DCR 93%. Brain metastases response rate 80%, DCR 100%. 74% responders remain on study. Responses included prior tarlatamab patient. Note responses is across all dose levels and DLL3 expression levels (H-score 0-260). References: 10.1200/JCO.2025.43.16_suppl.3041

New CADI-05 in Head and neck squamous cell carcinoma with DSC3 Protein expression, Overexpression: 3

Phase 2 single-arm study. Desmocollin-3 (DSC3)-directed immunotherapy in R/M HNSCC. N=20. ORR 35% (2 CR, 5 PR). Disease control rate 45%. Median PFS 115 days. Median OS 155 days. Median duration of response 332 days. Responders had higher mean DSC3 expression than non-responders (50% vs 29%). ORR higher in Stage IVA (57%) vs IVC (20%). References: 10.1200/JCO.2026.44.16_suppl.2503

New Pemigatinib in Cholangiocarcinoma with FGFR2 Fusion: 3

Phase 3 FIGHT-302. NCT03656536. N=167. Pemigatinib improved PFS over chemotherapy (8.3 vs 6.8 months; HR 0.58). ORR was 47% (chemotherapy 15.5%). Median DoR was 14.2 months (chemotherapy 6.3 months). Median OS was similar (24.4 vs 25.0 months). Crossover pemigatinib mPFS was 8.1 months. References: 10.1200/JCO.2026.44.16_suppl.4017

New Bevacizumab + Erlotinib in FH-deficient renal cell carcinoma with FH Oncogenic mutations, Oncogenic mutations (germline): 3

Phase 2 BRISK. NCT05904457. N=35. Bevacizumab + erlotinib in Krebs cycle gene-mutated solid tumors. ORR 37.1% (1 CR, 12 PR). DCR 85.7%. Median PFS 8.3 months. Subgroup ORRs: FH-deficient RCC 80.0%, biliary tract cancer 36.8%, brain tumors 28.6%. References: 41231120

New PHI-101 in Acute myeloid leukaemia with FLT3 Internal tandem duplication, D835E, N676K: 3

Phase Ia/Ib trial. NCT04842370. In R/R AML, PHI-101 yielded clinical responses in 92% (12/13) of evaluable patients including 4 clinical CR; responses in 88% of prior FLT3 inhibitor-treated patients, and all 5 gilteritinib-resistant patients (2 CRc); at 160 mg dose, 4/7 (57.1%) responded (2 CRi, 1 MLFS, 1 PR). References: 10.1182/blood-2023-185606

New IMA401, IMA401 + Pembrolizumab in Solid tumors, Head and neck squamous cell carcinoma, Melanoma, Squamous non-small cell lung cancer with HLA-A+MAGEA4+MAGEA8 HLA-A:A*02:01 and MAGEA4:Protein expression and MAGEA8:Protein expression: 3

Phase 1a/b IMA401-101. NCT05359445. N=55 (38 efficacy evaluable). cORR 25% (2/8) in head and neck cancer, 29% (2/7) in melanoma, duration of all confirmed responses beyond 6 months. DCR 63% in HN, 57% in melanoma. Updated cORR 33% (4/12) in HN cancer. In sqNSCLC (n=3): 1 PR, 1 SD (OS ~16 months), 1 PD with reduction in liver lesions. References: 10.1200/JCO.2026.44.16_suppl.2507

New Bevacizumab + Erlotinib in Cholangiocarcinoma, Glioma with IDH1 Oncogenic mutations: 3

Phase 2 BRISK. NCT05904457. N=35. Bevacizumab + erlotinib in Krebs cycle gene-mutated solid tumors. ORR 37.1% (1 CR, 12 PR). DCR 85.7%. Median PFS 8.3 months. Subgroup ORRs: FH-deficient RCC 80.0%, biliary tract cancer 36.8%, brain tumors 28.6%. References: 41231120

New Bevacizumab + Erlotinib in Cholangiocarcinoma with IDH2 Oncogenic mutations: 3

Phase 2 BRISK. NCT05904457. N=35. Bevacizumab + erlotinib in Krebs cycle gene-mutated solid tumors. ORR 37.1% (1 CR, 12 PR). DCR 85.7%. Median PFS 8.3 months. Subgroup ORRs: FH-deficient RCC 80.0%, biliary tract cancer 36.8%, brain tumors 28.6%. References: 41231120

New CBL0137 in Acute lymphoblastic leukaemia, Acute myeloid leukaemia with KMT2A Rearrangement: 3

Preclinical study. CBL0137 decreased viability of MLL-rearranged leukaemia cell lines (n=12) and xenograft cells (n=3) with submicromolar IC50s. Significantly reduced leukaemia burden in subcutaneous leukaemia AML model and patient-derived xenograft models of MLL-rearranged ALL (n=5). References: 31325323

New VIR-5500 in Prostate cancer with PSMA Protein expression: 3

Phase 1 dose escalation. NCT05997615. N=51. Heavily pretreated mCRPC (including 95% post-taxane). At 3000 µg/kg Q3W: PSA50 91% (10/11), PSA90 55% (6/11), ORR 67% (4/6) in RECIST-evaluable patients; durable PSA responses lasting over one year in select patients. References: 10.1200/JCO.2026.44.7_suppl.17

New AZD0120 in Multiple myeloma with TNFRSF17 Protein expression: 3

Phase 1b/2 DURGA-1 trial. NCT05850234. Preliminary results in relapsed/refractory multiple myeloma (3+ prior lines, triple-class refractory). AZD0120 (BCMA/CD19 dual-targeting CAR T) yielded ORR 100% (sCR 33%, VGPR 47%, PR 20%) in evaluable patients. CR rates: 30% (DL1) and 40% (DL2). All MRD-evaluable patients achieved MRD negativity at 10^-5; 3 patients maintained MRD negativity for >=12 months. Biomarker not required. References: 10.1182/blood-2025-269

New GSK5471713 in Prostate cancer with AR Amplification, Ligand-binding domain mutation, Splice variants: 4

Preclinical study. GSK5471713, the oral AR degrader showing activities in full-length AR, including wild-type, LBD mutants, amplified, in prostate cancer cell lines, downregulates AR-dependent genes and inhibits cell growth. References: 10.1158/1538-7445.AM2026-4608

New ICP-248 in Chronic lymphocytic leukaemia, Small lymphocytic lymphoma, Mantle cell lymphoma with BCL2 Protein expression, Overexpression: 4

Phase 1. NCT05728658. N=55. In r/r CLL/SLL (n=20) at >=100mg: ORR 80%, CRR 15%, uMRD 10%. In r/r MCL (n=19): ORR 78.9%, CRR 42.1%, uMRD 15.8%. In BTKi-refractory MCL (n=10): ORR 80%, CRR 30%. In BTKi-failure CLL/SLL (n=11): ORR 81.8%, CRR 18.2%. References: 10.1200/JCO.2025.43.16_suppl.7038

New Saruparib in Breast cancer with BRCA1 Oncogenic mutations: 4

Preclinical and Phase 1 PETRA study. NCT04644068. Saruparib had extended PARP1 residence time (>5 days) and >90% PAR inhibition for up to 7 days after dosing cessation in vitro/in vivo and clinic (single dose). In BRCA1-mutant MDA-MB-436 model, intermittent schedules (1wk on, 2wk off) at 1mg/kg produced durable regressions, but not at the lower dose level of 0.1mg/kg where activity was lost. References: 10.1158/1538-7445.AM2026-254

New ZE94-0605 in Ovarian cancer, Glioblastoma with CCNE1 Amplification: 4

Preclinical study. Discovery of novel selective brain-penetrant CDK2 inhibitor ZE94-0605. Sub-nanomolar CDK2 inhibition (0.38 nM) was seen with selectivity over CDK1/4/6/9 with cytotoxicity seen in in breast, ovarian, and glioblastoma cells with aberrant CDK2 signaling. References: 10.1158/1535-7163.TARG-25-C114

New NTX1088, NTX1088 + Pembrolizumab in Solid tumours with CD155+CD274 CD155:Protein expression and CD274:Protein expression: 4

Phase 1 NTX1088-01 trial. NCT05378425. N=81 monotherapy (24) and combination (57). At active dose levels in combination with pembrolizumab, All responders had prior CPI, ORR was 17% (6/35 confirmed PRs in gastric, bladder, NSCLC, HNSCC, melanoma). ORR 32% with high PVR H-Score >100 and PD-L1 CPS >= 5. References: 10.1200/JCO.2026.44.16_suppl.2518

New ARC-02 in Non-Hodgkin lymphoma with CD79B Protein expression: 4

Preclinical study. ARC-02 (CD79b-targeting ADC) achieved complete tumor regression at about half the Polivy payload dose in Granta-519 and Ramos NHL models. References: 10.1182/blood-2022-160056

New HRS-6209 in Breast cancer with ESR1+ERBB2 ESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 4

Phase 1. HRS-6209 (CDK4 inhibitor) in advanced solid tumors. in HR+/HER2- breast cancer (n=48): ORR 6.3% (3/48), CBR 43.8% (21/48), median PFS 5.5 months. At 50, 75, 100 mg BID: PFS 1.8, 7.4, 9.1 months respectively. References: 10.1158/1538-7445.AM2026-CT117

New OP-3136, OP-3136 + Fulvestrant, OP-3136 + Palazestrant in Breast cancer with ESR1+ERBB2 ESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 4

Phase 1 first-in-human NCT06784193. OP-3136 monotherapy in advanced solid tumors and combination with fulvestrant in ER+ HER2- ABC. N=32. Median prior therapies for ABC was 3 lines. 64% target lesion reduction among 14 evaluable patients with measurable disease. 2 unconfirmed partial responses (1 ABC, 1 mCRPC). 10 stable disease among 17 patients with evaluable disease. References: 10.1200/JCO.2026.44.16_suppl.3088

New ZE94-0605 in Breast cancer with ESR1+ERBB2 ESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 4

Preclinical study. Discovery of novel selective brain-penetrant CDK2 inhibitor ZE94-0605. Sub-nanomolar CDK2 inhibition (0.38 nM) was seen with selectivity over CDK1/4/6/9 with cytotoxicity seen in in breast, ovarian, and glioblastoma cells with aberrant CDK2 signaling. References: 10.1158/1535-7163.TARG-25-C114

New 177Lu-FAP-2286 in Solid tumours with FAP Protein expression: 4

Retrospective study. N=17. [177Lu]Lu-FAP-2286 for pleural metastases. DCR 59%. Median OS 17.3 mo. Median PFS 4.1 mo. Patients with disease control had longer OS (20.3 v 6.4 mo). References: 41571431

New DS-1001 in Glioma with IDH1 R132H, R132L: 4

Phase I trial. NCT03030066. N=47. DS-1001 in recurrent and progressive IDH1-mutant gliomas. ORR 17.1% (enhancing) and 33.3% (non-enhancing). Median PFS 10.4 months (enhancing) and not reached (non-enhancing). D-2-HG levels reduced in on-treatment tumors. Ongoing phase II in treatment-naive grade 2 gliomas. References: 35722822

New ZE74-0282 in Myeloproliferative disorders with JAK2 V617F: 4

Preclinical study. ZE74-0282 demonstrated 500-fold selectivity for JAK2 V617F over WT JH2 cell lines. In BaF3 JAK2 V617F cells, growth inhibition IC50 40.6 nM vs ruxolitinib 19.5 nM. In murine colony assays, selectively suppressed mutant progenitors without affecting WT. References: 10.1182/blood-2025-1988

New VVD-133214 in Solid tumours, Colorectal cancer with Microsatellite Instability High: 4

Preclinical study. VVD-133214, a covalent allosteric inhibitor of WRN, induced robust tumour regression in multiple MSI-H colorectal cancer cell lines and patient-derived xenograft models. References: 38658751, 38961306

New Lu-177 rosopatamab tetraxetan, Lu-177 rosopatamab tetraxetan + Abiraterone, Lu-177 rosopatamab tetraxetan + Enzalutamide, Lu-177 rosopatamab tetraxetan + Docetaxel in Prostate cancer with PSMA Protein expression: 4

Phase 3 ProstACT Global (NCT06520345) Part 1 lead-in. 177Lu-rosopatamab plus SoC in PSMA+ mCRPC. Efficacy endpoints not reported in this abstract; ORR, PFS, OS, DOR not provided. References: 10.1200/JCO.2026.44.17_suppl.LBA5009

New Trastuzumab deruxtecan in Gastric cancer with MUC3A Overexpression: R2

Translational study of single-arm phase II DESTINY-Gastric06 trial (NCT04989816). N=95 HER2-positive advanced gastric cancer. T-DXd ORR 28.8%. MUC3A high expression associated with shorter PFS in T-DXd-treated patients (IHC cohort n=29, median PFS not reported, P=0.021) and in trastuzumab-treated cohort (PFS<12 months vs >= months, P=0.032). MUC3A knockdown enhanced T-DXd sensitivity in vitro; CST3 upregulation linked to acquired resistance. References: 41625230

Changed Vorasidenib with IDH2 R172K: 4

Cancer type(s) changed: Intrahepatic cholangiocarcinoma (First curated: 2021-06-16)

27 July, 2026 (Version: 20260727AU)

Removed Daraxonrasib in Pancreatic adenocarcinoma with KRAS alterations G12, G12D, G12V, G12R, G12A, G12L, G12S, G13, Q61, Oncogenic mutations: Tier 3   (First curated: 2026-05-31)

Removed TSN1611 in Non-small cell lung cancer with KRAS alterations G12D: Tier 3   (First curated: 2026-06-03)

Changed Daraxonrasib in Pancreatic ductal adenocarcinoma with KRAS G12, G12D, G12V, G12R, G12A, G12L, G12S, G13, Q61, Q61H, Oncogenic mutations: 3

Comments changed: Phase 1-2 study. NCT05379985. N=168. Daraxonrasib 300 mg in previously treated RAS-mutated PDAC. RAS G12 second-line subgroup ORR 35% (95% CI, 17 to 56). Median duration of response 8.2 months. Median PFS 8.5 months. Median OS 13.1 months. All RAS G12, G13, or Q61 mutations subgroup ORR 29%. Median PFS 8.1 months. Median OS 15.6 months. Supports ongoing Phase 3 RASolute 302 trial (NCT06625320).. (First curated: 2026-05-07)

23 July, 2026 (Version: 20260723AU)

Changed Amivantamab in Non-small cell lung cancer with EGFR Exon 20 insertion: 1

Comments changed: PBS listed. FDA accelerated approval 2021-05-21. Median PFS 8.3 months. Phase 1 CHRYSALIS trial. N=81. Amivantamab, an EGFR-MET bispecific antibody, showed an ORR of 40% (3 complete responses) and median DOR of 11.1 months in patients with EGFR Exon20ins NSCLC progressing on platinum chemotherapy, with a median PFS of 8.3 months.PBS listed. FDA accelerated approval 2021-05-21. Median PFS 8.3 months. "Phase 1 CHRYSALIS trial. N=81. Amivantamab, an EGFR-MET bispecific antibody, showed an ORR of 40% (3 complete responses) and median DOR of 11.1 months in patients with EGFR Exon20ins NSCLC progressing on platinum chemotherapy, with a median PFS of 8.3 months.. (First curated: 2021-05-22)

Changed Amivantamab + Lazertinib in Non-small cell lung cancer with EGFR : 3

Alterations changed: Exon 18 mutation, Exon 21 mutation except L858R, G719, L861, Exon 20 mutation, S768, E709K, E709A, L833V, R776C, R776H, R831H, V744M, V769L, V774M, P-loop mutations, Alpha-c-helix mutations, T790M, T790M-like mutationsExon 19 deletion, L858R, Exon 21 mutation. (First curated: 2026-03-03)

22 July, 2026 (Version: 20260722AU)

New VRN110755 in Non-small cell lung cancer with EGFR Oncogenic mutations, C797S: 4

Phase 1a dose-escalation. VRN110755. N=7 evaluable patients with EGFR C797S-positive NSCLC. Confirmed ORR of 85.7% (6/7 partial responses). ctDNA reduction in all 5 evaluable patients; complete ctDNA clearance in 4. No dose-limiting toxicities up to 480 mg. References: 10.1158/1538-7445.AM2026-LB336

New GFH276 in Solid tumours with HRAS Oncogenic mutations, Q61H: 4

Preclinical study. GFH276 is a molecular glue panRAS(on) inhibitor. Suppressed p-ERK in KRAS G12C, G12D, G12V cells with IC50s <1 nM. Potent anti-proliferative activity against cell lines with KRAS (G12A, G12C, G12V, G12R, G12S, G13D, Q61K), NRAS (G12D), or HRAS (Q61H) mutations with IC50s 0.07-73 nM. Active in EGFR or FGFR2/3-altered cell lines. Induced dose-dependent tumor regression at 1 mg/kg QD in KRAS-mutated xenograft models. Not susceptible to upstream RTK-reactivation by EGF. Remained effective against cell lines with second KRAS mutations, RTK alterations, or induced Sotorasib resistance. References: 10.1158/1538-7445.AM2025-389

New GFH276 in Solid tumours with KRAS Oncogenic mutations, G12C, G12D, G12V, G12A, G12R, G12S, G13D, Q61K: 4

Preclinical study. GFH276 is a molecular glue panRAS(on) inhibitor. Suppressed p-ERK in KRAS G12C, G12D, G12V cells with IC50s <1 nM. Potent anti-proliferative activity against cell lines with KRAS (G12A, G12C, G12V, G12R, G12S, G13D, Q61K), NRAS (G12D), or HRAS (Q61H) mutations with IC50s 0.07-73 nM. Active in EGFR or FGFR2/3-altered cell lines. Induced dose-dependent tumor regression at 1 mg/kg QD in KRAS-mutated xenograft models. Not susceptible to upstream RTK-reactivation by EGF. Remained effective against cell lines with second KRAS mutations, RTK alterations, or induced Sotorasib resistance. References: 10.1158/1538-7445.AM2025-389

New LM-364 in Bladder cancer, Triple-negative breast cancer, Urothelial carcinoma, Esophageal cancer, Cervical cancer with NECTIN4 Protein expression: 4

Preclinical study. LM-364TME, a conditionally active anti-Nectin-4 ADC with ANP-dependent binding, demonstrated TGI of 119.1% in MDA-MB-468, 107.46% in urothelial carcinoma PDX, 86.73% in esophageal cancer PDX, and 168.79% in cervical cancer PDX models. Binding EC50 0.02 nM to huNectin4; negligible binding without ANP. References: 10.1158/1538-7445.AM2026-4433

New GFH276 in Solid tumours with NRAS Oncogenic mutations, G12D: 4

Preclinical study. GFH276 is a molecular glue panRAS(on) inhibitor. Suppressed p-ERK in KRAS G12C, G12D, G12V cells with IC50s <1 nM. Potent anti-proliferative activity against cell lines with KRAS (G12A, G12C, G12V, G12R, G12S, G13D, Q61K), NRAS (G12D), or HRAS (Q61H) mutations with IC50s 0.07-73 nM. Active in EGFR or FGFR2/3-altered cell lines. Induced dose-dependent tumor regression at 1 mg/kg QD in KRAS-mutated xenograft models. Not susceptible to upstream RTK-reactivation by EGF. Remained effective against cell lines with second KRAS mutations, RTK alterations, or induced Sotorasib resistance. References: 10.1158/1538-7445.AM2025-389

21 July, 2026 (Version: 20260721AU)

New AN9025 in Solid tumours with KRAS Oncogenic mutations, G12C, G12D, G12V, G12R, G12A, G13C: 4

Preclinical study. AN9025, an oral pan-RAS(ON) inhibitor, demonstrated picomolar potency against RAS-dependent tumor cell lines, deep tumor regression in KRASG12D xenograft models, and activity in models resistant to KRAS(OFF) G12C inhibitors. References: 10.1158/1538-7445.AM2025-4377

New AN9025 in Solid tumours with NRAS Q61H, Q61L, Q61K: 4

Preclinical study. AN9025, an oral pan-RAS(ON) inhibitor, demonstrated picomolar potency against RAS-dependent tumor cell lines, deep tumor regression in KRASG12D xenograft models, and activity in models resistant to KRAS(OFF) G12C inhibitors. References: 10.1158/1538-7445.AM2025-4377

20 July, 2026 (Version: 20260720AU)

New Atebimetinib + Gemcitabine + Nab-paclitaxel in Pancreatic adenocarcinoma with KRAS Oncogenic mutation: 4

Phase 2a. NCT05585320. Atebimetinib + mGnP in advanced/metastatic PDAC. ORR 42%. DCR 84%. Median PFS 8.3 months. 6-month OS 88%. 9-month OS 79%. Median OS not reached. KRAS implicated but not prespecified. References: 10.1200/JCO.2026.44.17_suppl.4013

Changed STX-478, STX-478 + Fulvestrant, STX-478 + Palbociclib, STX-478 + Fulvestrant + Palbociclib with PIK3CA Oncogenic mutations, H1047R, H1047L, E542K, E545K: 4

Cancer type(s) changed: Breast cancer, Head and neck squamous cell carcinoma, Gynaecological cancer, Colon cancer, Lung cancerBreast cancer, Head and neck squamous cell carcinoma, Gynecologic cancer, Colon cancer, Lung cancer (First curated: 2026-07-19)

19 July, 2026 (Version: 20260719AU)

New Trastuzumab deruxtecan + Durvalumab in Breast cancer with ERBB2 Overexpression, Amplification: 2

Phase 1b/2 DESTINY-Breast07. NCT04538742. N=64. T-DXd + durvalumab in 1L HER2+ mBC. cORR 82.8%. mDOR 36.1 months. mPFS 37.7 months. PFS rate at 24 months 75.5%. mOS not evaluable. mPFS2 not evaluable. References: 10.1200/JCO.2026.44.16_suppl.1012

New Datopotamab Deruxtecan in Triple-negative breast cancer with ESR1+ERBB2 NOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 2

Phase 3 TROPION-Breast02. NCT05374512. N=644. Dato-DXd vs chemotherapy in first-line metastatic TNBC (immunotherapy not an option). OS HR 0.79, PFS HR 0.57, median PFS and OS >= 5 months longer vs investigator choice of chemotherapy. PFS2 15.6 vs 11.8 months (HR 0.61); TFST 10.9 vs 5.6 months (HR 0.49); TSST 16.7 vs 12.6 months (HR 0.67). References: 10.1200/JCO.2026.44.16_suppl.1002

New XNW27011 in Gastric cancer, Gastroesophageal junction adenocarcinoma with CLDN18 Protein expression: 3

Phase 2. NCT06792435. N=26 evaluable at 3.0 mg/kg. cORR 65.4%, cDCR 84.6%. mPFS 5.7 months (6.8 months in ≥2 prior lines). mOS 11.7 months (11.9 months in ≥2 prior lines). Noted durable PFS of 11.3 months in one patient with prior CLDN18.2-targeted therapy. Phase 3 study ongoing. References: 10.1200/JCO.2026.44.16_suppl.3036

New XNW27011 in Pancreatic adenocarcinoma with CLDN18 Protein expression, Overexpression: 3

Phase 2 trial. NCT06792435. N=48 (30 evaluable at 3.0 mg/kg). ORR 26.7%, DCR 83.3%, mPFS 4.1 months, mOS 10.0 months. In patients with one prior line: ORR 46.2%, DCR 100%, mPFS 4.4 months, mOS 10.1 months. In TOP1i pretreated: mPFS 5.2 months, mOS 10.0 months. References: 10.1200/JCO.2026.44.16_suppl.3039

New IBI354 in Ovarian cancer with ERBB2 Protein expression, Overexpression, Amplification: 3

Phase 1 IBI354 trial. NCT05636215. N=92. In efficacy-evaluable patients at 12 mg/kg Q3W (n=40), ORR 55.0%, DCR 90.0%, median DoR not reached, 9-month DoR rate 58.1%, median PFS 7.1 months, 9-month OS rate 70.7%. In HER2 IHC 1+ subgroup (n=27), ORR 55.6%, DCR 88.9%. References: 10.1200/JCO.2025.43.16_suppl.5565

New Tersolisib, Tersolisib + Fulvestrant, Tersolisib + Fulvestrant + Palbociclib, Tersolisib + Fulvestrant + Ribociclib, Tersolisib + Fulvestrant + Abemaciclib in Breast cancer with ESR1+ERBB2+PIK3CA ESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression and PIK3CA:Oncogenic mutations: 3

Phase 1/2 PIKALO-1. NCT05768139. N=193. ORR Tersolisib alone 19%, Tersolisib+Fulvestrant 35%, Tersolisib+Fulvestrant+CDK4/6i 27%. References: 10.1200/JCO.2026.44.16_suppl.1072

New Zenocutuzumab in Cholangiocarcinoma with NRG1 Fusions, ATP1B1-NRG1 fusion, RBPMS-NRG1 fusion, VTCN1-NRG1 fusion, ALB-NRG1 fusion, CFH-NRG1 fusion, FBLN2-NRG1 fusion, FN1-NRG1 fusion, NOTCH2-NRG1 fusion, SDC4-NRG1 fusion, TNC-NRG1 fusion, TNFSF15-NRG1 fusion: 3

Phase 2 eNRGy trial. N=22 (19 evaluable). Zenocutuzumab in advanced NRG1+ cholangiocarcinoma. ORR 36.8%. Median DOR 7.4 months. Median PFS 9.2 months. Clinical benefit rate 57.9%. References: 42385125

New JK06 in Non-small cell lung cancer, Breast cancer with TPBG Protein expression, Overexpression: 3

Phase 1b/2 study of JK06 (5T4-targeted ADC). NCT06667960. N=80. In 19 response-evaluable NSCLC patients, ORR 32% (1 cCR, 4 cPR, 1 uPR; one CNS response, longest therapy 51 weeks). In 7 evaluable breast cancer patients, ORR 14% (1 cPR, >27 weeks on treatment). References: 10.1200/JCO.2026.44.16_suppl.3038

New Amivantamab in Non-small cell lung cancer with AREG+EGFR AREG:Overexpression and NOT EGFR:Oncogenic mutations: 4

Preclinical study. In 11 EGFRWT NSCLC PDX models, amivantamab tumor growth inhibition (ΔTGI) correlated with AREG RNA levels (Spearman, P<0.05). 5/11 models showed >60% ΔTGI. Fc-silent variant showed similar efficacy (P=0.637). High AREG expression mutually exclusive with EGFR mutations in LUAD (Log2 OR -2.873, q=0.019). References: 39242834

New BC3195 in Solid tumours with CDH3 Protein expression: 4

Phase 1 BC3195-102/101. NCT06548672. N=16 evaluable. 3 partial responses (HER+ breast cancer, prostate cancer, fibrosarcoma) at 1.8 mg/kg dose level. Dose escalation ongoing with convergence on 2.1 mg/kg. Preliminary antitumor activity observed in heavily pretreated advanced solid malignancies. References: 10.1200/JCO.2026.44.16_suppl.3035

New STX-478, STX-478 + Fulvestrant, STX-478 + Palbociclib, STX-478 + Fulvestrant + Palbociclib in Breast cancer, Head and neck squamous cell carcinoma, Gynecologic cancer, Colon cancer, Lung cancer with PIK3CA Oncogenic mutations, H1047R, H1047L, E542K, E545K: 4

Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated robust efficacy in PI3Kα-mutant xenografts: 82% TGI in CAL-33 HNSCC; tumor regressions in 50% of GP2d colon and 5/9 Detroit 562 HNSCC; 100% regression in T47D breast at 100 mg/kg; durable tumor suppression to day 94 in ST1056 PDX with STX-478 plus fulvestrant, followed by modest regrowth off treatment. References: 37623743

New XNW28012 in Pancreatic adenocarcinoma with TF Overexpression: 4

Phase 1/2 NCT06799637. N=313. XNW28012 is a tissue factor ADC with TOP1i payload. In PDAC dose expansion (2.0 and 2.4 mg/kg), first line patients had ORR 28.0% and 47.6%, subsequent line with ORR 15.0% and 25.9%; 1L mPFS 4.2 and 6.4 months, 2L+ mPFS 4.5 and 5.2 months; 1L mOS not calculable and 14.6 months, 2L+ mOS 10.7 and 9.0 months. References: 10.1200/JCO.2026.44.16_suppl.3040

14 July, 2026 (Version: 20260714AU)

New Trametinib in Langerhans cell histiocytosis, Astrocytoma with BRAF R506_K507insLLR, R506_K507insVLR (V504_R506dup), Exon 13 insertion: 4

Preclinical study. BRAF mutants LLRins506/VLRins506 with stabilized R-spine resistant to all RAF inhibitors (vemurafenib, dabrafenib, PLX8394, LY3009120) but sensitive to MEK inhibitor trametinib in vitro and in vivo. This is a class 2 mutation. References: 34108213

New Vemurafenib, Dabrafenib, PLX8394, LY3009120 in Langerhans cell histiocytosis, Astrocytoma with BRAF R506_K507insLLR, R506_K507insVLR (V504_R506dup), Exon 13 insertion: R2

Preclinical study. BRAF mutants LLRins506/VLRins506 with stabilized R-spine resistant to all RAF inhibitors (vemurafenib, dabrafenib, PLX8394, LY3009120) but sensitive to MEK inhibitor trametinib in vitro and in vivo. This is a class 2 mutation. References: 34108213

Changed GQ1001 with ERBB2 Overexpression: 3

Cancer type(s) changed: Solid tumor, Breast cancer, Gastric cancer, Gastroesophageal junction adenocarcinoma, Salivary gland cancerSolid tumor, Breast cancer, Gastric cancer, Gastroesophageal junction cancer, Salivary gland cancer (First curated: 2026-07-13)

Changed Disitamab vedotin + Toripalimab with ERBB2 Overexpression, Protein expression, Low protein expression: 3

Cancer type(s) changed: Gastric cancer, Gastroesophageal junction adenocarcinomaGastric cancer, Gastroesophageal junction cancer (First curated: 2026-07-13)

13 July, 2026 (Version: 20260713AU)

New Anvatabart Opadotin in Breast cancer with ERBB2 Overexpression, Amplification: 3

Phase 2 ACE-Breast-06 trial. NCT05018702. N=32. ARX788 in HER2-positive breast cancer with active brain metastases. Primary endpoint CNS CBR 34.4% (95% CI 18.6-53.2). Key secondary endpoints: CNS ORR 25.0% (95% CI 11.5-43.4), median CNS PFS 5.6 months (95% CI 3.0-7.4), median PFS 5.5 months (95% CI 2.8-7.0), OS immature. References: 41245540

New Anvatabart Opadotin in Breast cancer with ERBB2 Overexpression, Amplification: 2

Phase 3 ACE-Breast-02. N=441. ARX788 improved PFS over lapatinib plus capecitabine (11.3 vs 8.2 months, HR 0.64, p=0.0006) by BICR. References: 39956849

New IKS014 in Solid tumours, Breast cancer, Esophageal cancer, Ovarian cancer, Gallbladder cancer with ERBB2 Overexpression, Low protein expression: 4

Phase 1 IKS014-01. NCT05872295. N=44. Partial responses observed in breast, esophageal, ovarian, gallbladder cancer across HER2+ and HER2 low tumors. References: 10.1016/j.annonc.2025.08.1505

New Disitamab vedotin + Toripalimab in Gastric cancer, Gastroesophageal junction cancer with ERBB2 Overexpression, Protein expression, Low protein expression: 3

Phase 1. NCT04280341. N=56. RP2D RC48 2.5 mg/kg + toripalimab 3 mg/kg q2w. In G/GEJ cancer (n=30), ORR 43%, median PFS 6.2 months, median OS 16.8 months. At RP2D (n=24), ORR 50%, median PFS 5.1 months, median OS 14.0 months. At RP2D, HER2-positive ORR 56%, median PFS 7.8 months; low HER2 ORR 46%, median PFS 5.1 months. References: 38235421

New GQ1001 in Solid tumor, Breast cancer, Gastric cancer, Gastroesophageal junction cancer, Salivary gland cancer with ERBB2 Overexpression: 3

Phase Ia GQ1001 trial. NCT04450732. N=32. ORR 40% (6/15) and DCR 60% (9/15) in 7.2 and 8.4 mg/kg dose cohorts in previously treated HER2 positive advanced solid tumors. References: 39789619

Changed Therapy in Breast cancer with ERBB2 Amplification, Overexpression, Protein expression, Low protein expression: 3

Therapy changed: Disitamab vedotinRC48-ADC. (First curated: 2021-06-07)

12 July, 2026 (Version: 20260712AU)

New Garsorasib, Garsorasib + Cetuximab in Colorectal adenocarcinoma with KRAS G12C: 3

Phase 2. NCT04585035. N=68. Garsorasib monotherapy ORR 19.2%, median PFS 5.5 months, median OS 13.1 months, median DOR 10.3 months. Garsorasib plus cetuximab ORR 45.2%, median PFS 7.5 months, median OS not reached, median DOR 8.2 months in KRAS G12C-mutated colorectal cancer. References: 40523897

New Elisrasib, Elisrasib + Pembrolizumab in Non-small cell lung cancer with KRAS G12C: 3

Phase 1/2 trial. NCT05410145. N=43 mono, 52 combo first-line KRAS G12C NSCLC. ORR 78% monotherapy (76.2% TPS<1%, 80% TPS≥1%). ORR 81% combination (71% TPS<1%, 72.7% in TPS 1-49%, 95% in TPS>=50%). Median PFS and DOR immature. 6m PFS rate 68.9% monotherapy, 74.6% combo. 6m DOR rate 77.2% monotherapy, 80.5% combination. ctDNA molecular response 83% mono, 100% combo. References: 10.1200/JCO.2026.44.16_suppl.8511

New Glecirasib in Non-small cell lung cancer with KRAS G12C: 3

Phase 2b. NCT05009329. N=119 (IRC FAS n=117). ORR 47.9% (56/117) (95% CI 38.5-57.3%). DCR 86.3%. Median TTR 1.4 months. Median DoR not reached (95% CI 7.2 months-NE). Median PFS 8.2 months (95% CI 5.5-13.1). Median OS 13.6 months (95% CI 10.9-NE). Primary endpoint met. References: 39762419

New Bi3706674 in Gastric cancer, Gastroesophageal cancer, Cholangiocarcinoma, Colorectal cancer, Ovarian cancer with KRAS Amplification: 4

Phase Ia/b NCT06056024. N=15 KRAS WT amp. BI3706674 monotherapy. DCR 58.3% (7/12). ORR 25% (3/12) with tumor shrinkage -60.3%, -34%, 34.3%. In upper GI cancers at dose level at 800-1200mg, ORR 43% (3/7), DCR 57% (4/7). References: 10.1200/JCO.2026.44.2_suppl.380

New BI-2865 in Gastroesophageal cancer, Solid tumours with KRAS Amplification: 4

Preclinical study. Pan-KRAS inhibitors BI-2493 and BI-2865. In KRAS wild-type amplified cancer cell lines (copy number >7), potent antitumor activity observed in vitro and in vivo. KRAS WT amplification common in gastroesophageal cancers. First study demonstrating direct pharmacologic KRAS inhibition antitumor activity in KRAS WT amplification preclinical models. References: 39711431

New FMC-376, FMC-376 + Cetuximab in Non-small cell lung cancer, Colorectal cancer, Pancreatic adenocarcinoma with KRAS G12C: 4

Preclinical study. FMC-376, dual ON+OFF KRAS G12C inhibitor, demonstrated tumour regression in sotorasib-resistant PDX models of NSCLC, CRC, PDAC, and synergistic anti-tumor activity with cetuximab. References: 10.1158/1535-7163.TARG-25-B119

New Elironrasib in Solid tumours with KRAS G12C: 4

Phase 1 trials NCT05462717, NCT06128551, NCT06162221: Elironrasib (RMC-6291) showed preliminary clinical activity in patients with KRAS G12C-addicted cancers who progressed on first-generation inactive state-selective KRAS G12C inhibitors. References: 39993169

New Olomorasib in Solid tumours, Non-small cell lung cancer, Colorectal adenocarcinoma with KRAS G12C: 4

Phase 1 NCT04956640. N=195. Olomorasib monotherapy. RP2D 150 mg BID. In 168 efficacy-evaluable patients, ORR and median PFS were higher in non-CRC solid tumors versus CRC, including in NSCLC patients with prior KRAS G12C inhibitor. Intracranial responses observed in untreated active brain metastases. References: 41820335

New HBW-012-E in Colon cancer, Pancreatic cancer with KRAS G12D: 4

Preclinical study. HBW-012-E, a novel KRAS G12D inhibitor, showed superior oral bioavailability and potency compared to MRTX1133, with complete tumor growth inhibition and ~40% tumor regression in a GP2D colon cancer model at 50 mg/kg BID PO. References: 10.1200/JCO.2024.42.16_suppl.3115

New Zoldonrasib in Non-small cell lung cancer with KRAS G12D: 4

Phase 1. NCT06040541. N=211. Zoldonrasib monotherapy in KRAS G12D solid tumors. In NSCLC evaluable patients (n=18) at RP2D 1200 mg QD, ORR 61% (95% CI 36-83), DCR 89% (95% CI 65-99), median time to response 1.4 months. Encouraging antitumor activity. References: 10.1158/1538-7445.AM2025-CT019

New ERAS-4001 in Non-small cell lung cancer, Pancreatic adenocarcinoma, Colorectal adenocarcinoma, Solid tumours with KRAS G12D, G12V, G12, Oncogenic mutations, Amplification: 4

Preclinical study. ERAS-4001 pan-KRAS inhibitor demonstrated tumor growth inhibition from 77% TGI to 83% tumor regression in KRAS G12D and G12V subcutaneous xenograft models. References: 10.1158/1538-7445.AM2025-4367

New RMC-5127 in Pancreatic adenocarcinoma, Colorectal cancer, Non-small cell lung cancer with KRAS G12V: 4

Preclinical study. RMC-5127, an oral RAS(ON) G12V-selective tri-complex inhibitor, induced tumor regressions in the majority of KRAS G12V mutant PDAC and NSCLC xenograft models, with brain penetrance and antitumor activity in intracranial models. References: 10.1158/1538-7445.AM2025-ND06

New LY4066434, LY4066434 + Cetuximab in Non-small cell lung cancer, Pancreatic adenocarcinoma, Colorectal adenocarcinoma, Gastric cancer, Endometrial cancer, Ovarian cancer with KRAS Oncogenic mutations: 4

Preclinical study. LY4066434, an oral pan-KRAS inhibitor, demonstrated robust anti-tumor activity in KRAS-mutant PDX models (NSCLC, pancreatic, colorectal, gastric) with tumor growth inhibition and regression. Combination with cetuximab or chemotherapies enhanced efficacy. In orthotopic brain tumor models of NSCLC, inhibited tumor growth and promoted survival. Clinical trial NCT06607185. References: 10.1158/1538-7445.AM2025-4375

New ERAS-0015 in Solid tumours with RAS G12, G13, Q61, Oncogenic mutations: 4

Preclinical study. ERAS-0015 demonstrated 3-7-fold more potent cellular proliferation inhibition versus RMC-6236 across RAS mutant cell lines. Comparable tumor growth inhibition achieved at 1/8th-1/10th the dose in multiple KRAS mutant CDX models. References: 10.1158/1538-7445.AM2025-390

08 July, 2026 (Version: 20260708AU)

New Adavosertib in Solid tumours with BRCA1 Oncogenic mutations: R2

Phase 2 NCI-MATCH subprotocol Z1I. NCT02465060. N=30. Adavosertib in BRCA1/2-mutated solid tumors. ORR 3.3% (90% CI, 0.2 to 14.9). PFS6 23.4% (90% CI, 10.7 to 36.2). OS6 57.3% (90% CI, 41.9 to 72.7). One PR (fallopian tube serous carcinoma) and six cases of SD >6 months. Primary endpoint not met. References: 42308463

New Adavosertib in Solid tumours with BRCA2 Oncogenic mutations: R2

Phase 2 NCI-MATCH subprotocol Z1I. NCT02465060. N=30. Adavosertib in BRCA1/2-mutated solid tumors. ORR 3.3% (90% CI, 0.2 to 14.9). PFS6 23.4% (90% CI, 10.7 to 36.2). OS6 57.3% (90% CI, 41.9 to 72.7). One PR (fallopian tube serous carcinoma) and six cases of SD >6 months. Primary endpoint not met. References: 42308463

29 June, 2026 (Version: 20260629AU)

Changed Entrectinib in Solid tumours with NTRK1 Fusions, CD74-NTRK1 fusion, CDC42BPA-NTRK1 fusion, CGN-NTRK1 fusion, EPS15L1-NTRK1 fusion, ERC1-NTRK1 fusion, LMNA-NTRK1 fusion, PDIA3-NTRK1 fusion, PEAR1- NTRK1 fusion, PLEKHA6-NTRK1 fusion, SQSTM1-NTRK1 fusion, TPM3-NTRK1 fusion, TPR-NTRK1 fusion, TRIM33-NTRK1 fusion: 2

Tier changed: 21B. Comments changed: FDA approved. Not PBS reimbursed. ALKA-372-001, STARTRK-1, and STARTRK-2 trials. NTRK fusion indication removed May 2026. Update 2026-06-29.TGA approved. Not PBS reimbursed. ALKA-372-001, STARTRK-1, and STARTRK-2 trials.. (First curated: 2020-11-10)

Changed Entrectinib in Solid tumours with NTRK2 Fusions, SQSTM1-NTRK2 fusion: 2

Tier changed: 21B. Comments changed: FDA approved. Not PBS reimbursed. ALKA-372-001, STARTRK-1, and STARTRK-2 trials. NTRK fusion indication removed May 2026. Update 2026-06-29.TGA approved. Not PBS reimbursed. ALKA-372-001, STARTRK-1, and STARTRK-2 trials.. (First curated: 2020-11-10)

Changed Entrectinib in Solid tumours with NTRK3 Fusions, AKAP13-NTRK3 fusion, EML4-NTRK3 fusion, ETV6-NTRK3 fusion, FAM19A2-NTRK3 fusion, KIF7-NTRK3 fusion, RBPMS-NTRK3 fusion: 2

Tier changed: 21B. Comments changed: FDA approved. Not PBS reimbursed. ALKA-372-001, STARTRK-1, and STARTRK-2 trials. NTRK fusion indication removed May 2026. Update 2026-06-29.TGA approved. Not PBS reimbursed. ALKA-372-001, STARTRK-1, and STARTRK-2 trials.. (First curated: 2020-11-10)

16 June, 2026 (Version: 20260616AU)

New Sacituzumab Tirumotecan + Pembrolizumab in Non-small cell lung cancer with CD274 Protein expression: 2

Phase 3 OptiTROP-Lung05. NCT06448312. N=413. Sac-TMT plus pembrolizumab significantly improved PFS over pembrolizumab (median not reached vs 5.7 months; HR 0.35). ORR was 70.2% vs 42.0%. In PD-L1 TPS 1-49% subgroup, PFS HR 0.28; in TPS ≥50% subgroup, PFS HR 0.47. In non-squamous histology, PFS HR 0.28; in squamous, PFS HR 0.44. OS trend favored sac-TMT plus pembrolizumab (HR 0.55). References: 10.1200/JCO.2026.44.16_suppl.8506

New BH-30643 in Non-small cell lung cancer with EGFR Exon 19 deletion, L858R, Exon 20 insertion, C797S, T790M: 2

Phase 1 SOLARA trial. NCT06706076. N=72. BH-30643 demonstrated ORR of 59% (10/17) in C797S-positive EGFRm NSCLC patients; ORR 50% with T790M, 66% without; C797S ctDNA reduction >99% in 7/9; responses across EGFRm subsets including CNS. References: 10.1200/JCO.2026.44.16_suppl.3014

New Tucatinib + Trastuzumab + Pertuzumab in Breast cancer with ERBB2 Amplification, Overexpression: 2

Phase 3 HER2CLIMB-05. NCT05132582. N=654. Tucatinib + trastuzumab + pertuzumab vs placebo + HP: median PFS 24.9 vs 16.3 months (HR 0.641, p<0.0001), cORR 22.6% vs 15.2%, median DOR 20.9 vs 16.9 months. Subgroup PFS improvements: de novo 28.9 vs 16.8, recurrent 21.3 vs 12.7, HR+ (with ET) 25.0 vs 18.1, HR- 24.9 vs 12.6, baseline BM 8.5 vs 4.2, no BM 27.2 vs 18.1 months; cORR and DOR also consistently improved across subgroups. References: 10.1200/JCO.2026.44.16_suppl.1005

New Trastuzumab rezetecan in Colorectal cancer with ERBB2 Overexpression, Amplification: 2

Phase 3 trial. NCT06199973. N=130. Trastuzumab rezetecan vs SOC for chemotherapy-refractory HER2-positive advanced CRC. IRC-assessed median PFS 5.5 vs 2.8 months, HR 0.33 (95% CI 0.21-0.53), 1-sided p<0.0001. ORR 40.7% vs 4.5%. DoR 4.4 vs 3.4 months. OS immature, HR 0.77 (95% CI 0.35-1.73). References: 10.1200/JCO.2026.44.16_suppl.3505

New Zanidatamab + Tislelizumab + Capecitabine + Oxaliplatin, Zanidatamab + Capecitabine + Oxaliplatin in Gastroesophageal adenocarcinoma with ERBB2 Overexpression, Amplification: 2

Phase 3 HERIZON-GEA-01. NCT05152147. N=914. Zanidatamab + tislelizumab + chemo improved PFS over trastuzumab + chemo (12.4 vs 8.1 months, HR 0.63). Zanidatamab + chemo improved PFS (12.4 vs 8.1 months, HR 0.65). OS was improved for zanidatamab + tislelizumab + chemo (26.4 vs 19.2 months, HR 0.72). OS for zanidatamab + chemo (24.4 months) did not meet significance (HR 0.80, p=0.06). ORR: 70.7%, 69.6%, and 65.7%. Median DOR: 20.7, 14.3, and 8.3 months. References: 42202319

New Izalontamab brengitecan in Triple-negative breast cancer with ESR1+ERBB2 NOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 2

Phase 3. NCT06382142. N=418. Iza-bren versus physician's choice in unresectable locally advanced or metastatic TNBC. Median PFS by BICR 8.5 vs 3.1 months (HR 0.29). Median OS 15.9 vs 12.5 months (HR 0.60). Confirmed ORR 51.7% vs 20.5% (OR 4.28). Dual-primary endpoints of PFS and OS met. References: 10.1200/JCO.2026.44.17_suppl.LBA1003

New Dostarlimab + Carboplatin + Paclitaxel in Endometrial cancer with Microsatellite Instability High: 2

Phase 3 RUBY trial. NCT03981796. dMMR/MSI-H primary advanced or recurrent endometrial cancer. Median PFS not reached for dostarlimab+CP vs 7.7 months for CP alone. 4-year PFS rate 57.9% vs 15.7%. Mixed cure model estimated 54% of patients considered cured. References: 10.1200/JCO.2026.44.16_suppl.5501

New Dostarlimab + Carboplatin + Paclitaxel in Endometrial cancer with Mismatch repair Deficient: 2

Phase 3 RUBY trial. NCT03981796. dMMR/MSI-H primary advanced or recurrent endometrial cancer. Median PFS not reached for dostarlimab+CP vs 7.7 months for CP alone. 4-year PFS rate 57.9% vs 15.7%. Mixed cure model estimated 54% of patients considered cured. References: 10.1200/JCO.2026.44.16_suppl.5501

New Neladalkib in Non-small cell lung cancer with ALK Fusion; G1202R: 3

Phase 1/2 ALKOVE-1. NCT05384626. N=656. Neladalkib in ALK+ NSCLC. TKI pre-treated (n=253): ORR 31%, DOR at 12m 64% and 18m 53%, IC-ORR 32%. Lorlatinib-naive subset: ORR 46%, DOR at 12m 80%, IC-ORR 63%. G1202R mutation: ORR 68%, DOR at 12m 80%. TKI-naive preliminary (n=44): ORR 86%, 12m DOR 91%, IC-ORR 78%. References: 10.1200/JCO.2026.44.16_suppl.8503

New ALK201 in Solid tumours with FGFR2 FGFR2b Overexpression, FGFR2-IIIb Overexpression: 3

Phase 1/2 NCT06656390. N=38. ALK201 showed ORR of 24% and DCR of 68% in evaluable patients (n=25); at ≥7.2 mg/kg, ORR was 35.7% and DCR was 100%. References: 10.1200/JCO.2026.44.16_suppl.3025

New MRG006A in Hepatocellular carcinoma with GPC3 Protein expression, Overexpression: 3

Phase 1/2 MRG006A-001 trial. NCT07093970. N=26. ORR 24% (intermediate/high GPC3), 33.3% high GPC3. DCR 68% and 75%. Median PFS 7.0 months (high GPC3). Median DOR 4.2 months. References: 10.1200/JCO.2026.44.16_suppl.3028

New Telisotuzumab Adizutecan in Colorectal cancer with MET Overexpression: 3

Phase 1. NCT05029882. N=122. ORR 15.6% (95% CI 9.6-23.2). DOR 5.9 months (95% CI 4.1-10.5). mPFS 4.6 months (95% CI 4.0-5.4). mOS 10.4 months (95% CI 8.9-13.1). In high c-Met expression (≥10%|3+) at ≥2.4 mg/kg, ORR 36%. References: 42066233

New Telisotuzumab adizutecan in Gastric cancer, Gastroesophageal junction adenocarcinoma with MET Protein expression, Overexpression, Amplification: 3

Phase 1 open-label multicenter study. N=42. Advanced gastric/gastroesophageal junction adenocarcinoma with 1-2 prior therapies. ORR 29%, clinical benefit rate 71%, median DOR 4.2 months, median PFS 4 months, median OS 5.8 months. Exploratory analysis showed ORR enrichment in patients with higher c-Met expression and MET focal amplification. References: 41910595

New Lunbotinib in Non-small cell lung cancer with RET Fusions: 3

Phase 2 pivotal trial. NCT05265091. N=71 pre-treated, N=92 treatment-naive. IRC-assessed ORR 87.1% (pre-treated) and 81.3% (treatment-naive). mPFS 27.5 months and NR. mDoR 25.7 months and NR. CNS ORR 82.6% and 75.0%. 24-month PFS rate 52.1% and 59.9%. 24-month OS rate 65.7% and 74.1%. References: 10.1200/JCO.2026.44.16_suppl.8505

New KIVU-305 in Colorectal cancer, Pancreatic adenocarcinoma, Gastric cancer, Non-small cell lung cancer with CEACAM5 Protein expression: 4

Preclinical study. KIVU-305, a CEACAM5-targeting ADC with exatecan payload, showed in vitro target-specific cytotoxicity at low nanomolar concentrations and robust bystander activity, and tumor regressions in multiple in vivo CEACAM5-positive CRC and PDAC xenograft models. References: 10.1158/1538-7445.AM2026-5648

New EBC-129 in Gastroesophageal adenocarcinoma with CEACAM5 Protein expression, Overexpression: 4

Phase 1. NCT05701527. N=21 (17 evaluable). Overall ORR 29.4%, DCR 82.4%, median PFS 17.86 weeks in IHC ≥20% cohort. In IHC ≥50% subgroup, ORR 50%, DCR 90%, median PFS 21.4 weeks. At 1.8 mg/kg with IHC ≥50%, ORR 50%, DCR 100%, median PFS 29.2 weeks. Protein expression at IHC 2+ and/or 3+. References: 10.1200/JCO.2026.44.16_suppl.3033

New MK-6070 in Prostate small cell carcinoma with DLL3 Protein expression: 4

Preclinical study. MK-6070 showed high specificity and anti-tumor activity in DLL3-expressing NEPC models in vitro and in vivo, with T cell activation and tumor infiltration. Anti-tumor activity in heterogeneous DLL3 tumors (PC7, 23-Lv-R4) wree observed with bystander effect killing surrounding DLL3-negative cells. References: 41041866

New TQB6411 in Non-small cell lung cancer, Oesophageal adenocarcinoma, Gastroesophageal adenocarcinoma, Colorectal cancer with EGFR Protein expression, Overexpression: 4

Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%. Median PFS and duration of response not reported. Not biomarker pre-selected. References: 10.1200/JCO.2026.44.16_suppl.3032

New CS5007 in Colorectal cancer, Lung cancer, Head and neck squamous cell carcinoma, Solid tumors with EGFR+ERBB3 Protein expression: 4

Preclinical study. CS5007 demonstrated high-affinity binding and potent tumor growth inhibition comparable or superior to control ADCs in CDX models with EGFR/HER3 expression. Antigen-dependent tumor growth inhibition with antitumor activity was observed across EGFR/HER3 expression levels. References: 10.1158/1538-7445.AM2025-2954

New VVD-159642 in Solid tumours with ERBB2 Overexpression: 4

Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors. References: 41066541

New Trastuzumab deruxtecan in Solid tumours with ERBB2 Protein expression, Amplification, Oncogenic mutations: 4

Pilot study NCT04294628. N=61. T-DXd demonstrated ORR 25% (1 CR, 14 PR) with responses also in bHER2 null patients. TOP1 target modulation and DDR induction in 14 of 15 paired biopsies showing PD response. References: 10.1200/JCO.2026.44.16_suppl.3031

New VVD-159642 in Solid tumours with HRAS G12C, G12V: 4

Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors. References: 41066541

New Vorasidenib in Intrahepatic cholangiocarcinoma with IDH2 R172K: 4

Case report. IDH2 p.R172K intrahepatic cholangiocarcinoma. Post-transplant. Off-label vorasidenib. Partial response by RECIST 1.1 at 9 months (30% reduction from baseline). Confirmed at 11 months (32% reduction). Durable response ongoing at approximately one year. ctDNA reduction from 2.30 MTM/mL to 1.52 MTM/mL at one month and continued decline. References: 42286810

New D3S-003 in Pancreatic cancer, Non-small cell lung cancer with KRAS G12D: 4

Preclinical study. D3S-003, a dual-state KRAS G12D inhibitor. In HPAC pancreatic xenografts, 30% tumor regression (PR) and 100% complete remission (CR). Across KRAS G12D NSCLC and pancreatic PDX/CDX models, overall response rate (ORR) was 70%. References: 10.1158/1538-7445.AM2026-4569

New BBO-11818 in Colorectal cancer, Pancreatic cancer, Lung cancer with KRAS G12D, G12V, G12C, Oncogenic mutations: 4

Preclinical study. BBO-11818, a noncovalent pan-KRAS inhibitor, showed inhibition of MAPK signaling and cellular viability in KRAS-driven lines and tumor regressions in KRAS-mutant xenograft models. Combination with anti-PD-1, anti-EGFR antibodies, and a RAS:PI3Kα breaker showed enhanced efficacy. References: 41790032

New VVD-159642 in Solid tumours with KRAS G12R, G12C, G12E, G12A, G12V, Q61H, Q61K, G13C, Q61R, Q61L, Amplification, Oncogenic mutations: 4

Preclinical study. In mice, VVD-699 and analogs targeting PI3Kα Cys242 showed tumor growth inhibition in multiple cell lines, including KRASamp, HER2OE PDX, and PDX (EGFR mutant, KRAS G12D, and KRAS G12C/PIK3CA H1047R). Combination with binimetinib showed tumor stasis in xenografts. Combination with G12C inhibitors achieved 100% complete and durable responses in orthotopic lung tumors. References: 41066541

New Telisotuzumab Adizutecan in Colorectal cancer with MET Protein expression: 4

Phase 1. NCT05029882. N=122. ORR 15.6% (95% CI 9.6-23.2). DOR 5.9 months (95% CI 4.1-10.5). mPFS 4.6 months (95% CI 4.0-5.4). mOS 10.4 months (95% CI 8.9-13.1). In high c-Met expression (≥10%|3+) at ≥2.4 mg/kg, ORR 36%. References: 42066233

New TQB6411 in Non-small cell lung cancer, Oesophageal adenocarcinoma, Gastroesophageal adenocarcinoma, Colorectal cancer with MET Protein expression, Overexpression: 4

Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%. Median PFS and duration of response not reported. Not biomarker pre-selected. References: 10.1200/JCO.2026.44.16_suppl.3032

New Pembrolizumab in Intrahepatic cholangiocarcinoma with Microsatellite Instability High: 4

Case report. MSI-H intrahepatic cholangiocarcinoma. Pembrolizumab resulted in rapid tumor shrinkage sustained for 30 months. References: 40032770

New CRB-701 in Cervical cancer with NECTIN4 Protein expression: 4

Phase 1/2 CRB-701 (SYS6002) trial. NCT06265727. N=54. Unconfirmed ORR 22.2% at 2.7 mg/kg and 37.5% at 3.6 mg/kg. Confirmed partial responses: 1/18 at 2.7 mg/kg, 3/16 at 3.6 mg/kg. One confirmed complete response at 2.7 mg/kg. References: 10.1200/JCO.2026.44.16_suppl.5508

New BAT8008 in Cervical cancer with TACSTD2 Protein expression: 4

Phase 1 BAT8008-001-CR. NCT05620017. N=68. BAT8008 in advanced cervical cancer: cORR 29.3% (2.4 mg/kg), DCR 78.0%, mPFS 6.7 months, mDoR 9.0 months. Efficacy independent of TROP-2 expression. References: 10.1200/JCO.2026.44.16_suppl.5507

Changed Sacituzumab govitecan in Triple-negative breast cancer with ESR1+ERBB2 NOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 2

Comments changed: Phase 3 ASCENT-03 trial, NCT05382299, N=558, Sacituzumab govitecan significantly improved PFS (9.7 months vs 6.9 months) over chemotherapy in patients with untreated advanced triple-negative breast cancer not eligible for PD-1/PD-L1 inhibitors, with similar ORR (48% vs 46%) and higher median duration of response (12.2 vs 7.2 months). PFS2 was 18.2 vs 14.0 months (HR 0.70).. References changed: 41124233, 10.1200/JCO.2026.44.16_suppl.1001. (First curated: 2026-03-03)

15 June, 2026 (Version: 20260615AU)

New Belzutifan in Pheochromocytoma, Paraganglioma with SDHB Oncogenic mutations (germline): 3

Phase 2 LITESPARK-015 trial. NCT04924075. N=72. Belzutifan ORR 26% (95% CI 17-38), all partial responses. Disease control 85%. Median DOR 20.4 months (12-month DOR estimate 64%). Median PFS 22.3 months. OS at 24 months 76%. SDHB-related tumour predisposition syndrome in 33% of participants. References: 41124218

New STX-478 in Solid tumours with PIK3CA H1047R, H1047L, H1047Y, H1047A, M1043I, M1043L, M1043Y, M1043A, G1049R: 4

Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated activities in PI3Kalpha-mutant xenografts. References: 37623743

New STX-478 in Solid tumours with PIK3CA E542K, E545K, Helical domain mutation, Wildtype: R2

Preclinical study. STX-478, mutant-selective allosteric PI3Kα inhibitor, demonstrated activities in PI3Kalpha-mutant xenografts. References: 37623743

Changed STX-478 in Solid tumours with PIK3CA : 3

Alterations changed: H1047R, H1047L, M1043, G1049R, Kinase domain mutation E545K, Helical domain mutationH1047R, H1047L, M1043, E545K, G1049R, Kinase domain mutation, Helical domain mutation. (First curated: 2024-09-15)

10 June, 2026 (Version: 20260610AU)

New Zanidatamab + Tislelizumab + Capecitabine + Oxaliplatin, Zanidatamab + Capecitabine + Oxaliplatin in Gastric cancer, Gastroesophageal adenocarcinoma with ERBB2 Overexpression, Amplification: 2

Phase 3 HERIZON-GEA-01. NCT05152147. N=914. Zanidatamab + tislelizumab + chemo improved PFS over trastuzumab + chemo (12.4 vs 8.1 months, HR 0.63). Zanidatamab + chemo improved PFS (12.4 vs 8.1 months, HR 0.65). OS was improved for zanidatamab + tislelizumab + chemo (26.4 vs 19.2 months, HR 0.72). OS for zanidatamab + chemo (24.4 months) did not meet significance (HR 0.80, p=0.06). ORR: 70.7%, 69.6%, and 65.7%. Median DOR: 20.7, 14.3, and 8.3 months. References: 42202319

08 June, 2026 (Version: 20260608AU)

New Pembrolizumab in Intrahepatic cholangiocarcinoma with Microsatellite Instability High: 4

Case report. MSI-H intrahepatic cholangiocarcinoma. Pembrolizumab resulted in rapid tumor shrinkage sustained for 30 months. References: 40032770

New Sacituzumab Tirumotecan + Pembrolizumab in Non-small cell lung cancer with CD274 Protein expression: 4

Phase 3 OptiTROP-Lung05. NCT06448312. N=413. Sac-TMT plus pembrolizumab significantly improved PFS over pembrolizumab (median not reached vs 5.7 months; HR 0.35). ORR was 70.2% vs 42.0%. In PD-L1 TPS 1-49% subgroup, PFS HR 0.28; in TPS ≥50% subgroup, PFS HR 0.47. In non-squamous histology, PFS HR 0.28; in squamous, PFS HR 0.44. OS trend favored sac-TMT plus pembrolizumab (HR 0.55). References: 42214392, 10.1200/JCO.2026.44.16_suppl.8506

New Neladalkib in Non-small cell lung cancer with ALK Fusion, G1202R: 3

Phase 1/2 ALKOVE-1. NCT05384626. N=656. Neladalkib in ALK+ NSCLC. TKI pre-treated (n=253): ORR 31%, DOR at 12m 64% and 18m 53%, Intracranial (IC)-ORR 32%. Lorlatinib-naive subset: ORR 46%, DOR at 12m 80%, IC-ORR 63%. G1202R mutation: ORR 68%, DOR at 12m 80%. TKI-naive preliminary (n=44): ORR 86%, 12m DOR 91%, IC-ORR 78%. References: 10.1200/JCO.2026.44.16_suppl.8503

Changed Pembrolizumab in Solid tumours with Microsatellite Instability High: 1B

Comments changed: TGA provisional approval for MSI-H/dMMR. FDA approved. In phase 2 KEYNOTE-158. NCT02628067. N=233. Noncolorectal MSI-H/dMMR advanced cancer. ORR 34.3%. Median PFS 4.1 months. Median OS 23.5 months. In phase . NCT01876511, N=41. Immune-related ORR was 40% in dMMR colorectal vs 0% in pMMR colorectal. Immune-related 20-week PFS rate was 78% in dMMR vs 11% in pMMR colorectal. Median PFS and OS not reached in dMMR colorectal vs 2.2 and 5.0 months in pMMR colorectal. dMMR non-colorectal had ORR 71% and PFS rate 67%.. (First curated: 2020-12-10)

Changed Setidegrasib in Non-small cell lung cancer, Pancreatic adenocarcinoma with KRAS G12D: 3

References changed: 41879829, 10.1016/j.annonc.2024.08.675. (First curated: 2026-04-12)

Changed Therapy in Solid tumours with KRAS G12D: 3

Therapy changed: SetidegrasibASP3082. (First curated: 2024-09-15)

Changed Therapy in Non-small cell lung cancer, Pancreatic adenocarcinoma, Colorectal adenocarcinoma with KRAS G12, G12D, G12V, G12C, G12A, G12S: 4

Therapy changed: DaraxonrasibRMC-6236. (First curated: 2025-05-24)

Changed Therapy in Pancreatic adenocarcinoma, Non-small cell lung cancer with KRAS G12, G12D, G12V, G12R, G12D, G12V, G12A: 4

Therapy changed: DaraxonrasibRMC-6236. (First curated: 2023-10-30)

Changed Therapy in Non-small cell lung cancer with RRAS Q87L: 4

Therapy changed: DaraxonrasibRMC-6236. (First curated: 2026-05-07)

Changed Therapy in Non-small cell lung cancer with RRAS2 Q72L: 4

Therapy changed: DaraxonrasibRMC-6236. (First curated: 2026-05-07)

07 June, 2026 (Version: 20260607AU)

New ALK201 in Solid tumours with FGFR2 FGFR2b Overexpression, FGFR2-IIIb Overexpression: 4

Phase 1/2. NCT06656390. N=38. ALK201 showed ORR of 24% and DCR of 68% in evaluable patients (n=25); at ≥7.2 mg/kg, ORR was 35.7% and DCR was 100%. In IHC2+/3+ in >=5% of cells, ORR was 27%.(n=11). References: 10.1200/JCO.2026.44.16_suppl.3025

New MRG006A in Hepatocellular carcinoma with GPC3 Protein expression, Overexpression: 4

Phase 1/2 MRG006A-001. NCT07093970. N=26. ORR 23.1% (33.3% in high GPC3 expression). DCR 68.0% (75.0% in high GPC3). CBR 32.0% (50.0% in high GPC3). Median PFS 7.0 months. Median DOR 4.2 months. References: 10.1200/JCO.2026.44.16_suppl.3028

New BL-M05D1 in Pancreatic cancer, Gastric cancer, Gastroesophageal adenocarcinoma, Biliary tract cancer with CLDN18 Protein expression: 4

Phase 1. NCT06349811. BL-M05D1 in CLDN18.2+ solid tumors. At 4.0 mg/kg: Pancreatic cancer ORR 35.7%, mPFS 5.6 months; Gastric cancer ORR 39.2%, mPFS 5.4 months; Biliary tract cancer ORR 37.9%, mPFS 5.9 months. Second-line Pancreatic cancer ORR 50.0%, mPFS 5.7 months; Gastric cancer ORR 44.8%, mPFS 7.7 months; Biliary tract cancer ORR 45.0%, mPFS 5.9 months. DCR 89-93%. References: 10.1200/JCO.2026.44.16_suppl.3030

New TQB6411 in Non-small cell lung cancer with EGFR Exon 19 deletion, L858R: 4

Phase 1. NCT07043751. N=26. TQB6411 in advanced solid tumors. ORR 50.0% (4/8) in ≥4mg/kg dose group (PR: 3 NSCLC, 1 EC). DCR 100%. References: 10.1200/JCO.2026.44.16_suppl.3032

New EBC-129 in Gastric cancer, Gastroesophageal adenocarcinoma with CEACAM5 Protein expression, Overexpression: 4

Phase 1. NCT05701527. N=21 (17 evaluable). Overall ORR 29.4%, DCR 82.4%, median PFS 17.86 weeks in IHC ≥20% at IHC 2+/3+. In IHC ≥50% subgroup, ORR 50%, DCR 90%, median PFS 21.4 weeks. At 1.8 mg/kg with IHC ≥50%, ORR 50%, DCR 100%, median PFS 29.2 weeks. References: 10.1200/JCO.2026.44.16_suppl.3033

06 June, 2026 (Version: 20260606AU)

New QLS31905 + Gemcitabine + Nab-paclitaxel, QLS31905 + Oxaliplatin + Capecitabine in Pancreatic cancer, Gastric cancer with CLDN18 Protein expression: 3

Phase 1b/2 trial. NCT06041035. N=131 (88 PC, 43 GC). RP2D 800 mg/kg Q3W. In PC: ORR 59.8%, DCR 89.0%, median PFS 8.7 months, median DoR 8.9 months, median OS 15.9 months. In GC: ORR 74.4%, DCR 93.0%, median PFS 10.1 months, DoR not reached. Claudin 18.2 positivity defined as >=1% tumor cells with >=1+ staining intensity. References: 10.1200/JCO.2026.44.16_suppl.4003

New BGB-B2033 in Hepatocellular carcinoma with GPC3 Protein expression: 3

Phase 1. NCT06427941. N=61 (59 efficacy-evaluable HCC). Confirmed ORR 20.3% (95% CI 11.0-32.8); at doses above predicted target efficacious dose, ORR 28.9% (11/38); 10 of 12 responders had ongoing response at data cutoff. References: 10.1200/JCO.2026.44.16_suppl.3016

New Luvometinib in Type 1 neurofibromatosis with NF1 Oncogenic mutations (germline): 3

Phase 3. NCT05913037. N=167. Luvometinib vs placebo. Confirmed ORR 43.8% vs 10.9%. Median DOR 15.1 months, 85.2% rate of DOR ≥12 months. Median TTR 3.9 months. References: 10.1200/JCO.2026.44.16_suppl.3017

New SKB500 in Small cell lung cancer, Oesophageal squamous cell carcinoma with CD276 Overexpression: 4

Phase 1 FIH study of SKB500 (B7-H3 ADC). NCT06736327. N=150. RP2D established 12 mg/kg. ORR 54.5% (30/55) DCR 92.7% (51/55) at 12mg/kg at ≥6 weeks follow-up. SCLC cohort ORR 71.4% (15/21) DCR 100%. ESCC cohort ORR 55.6% (10/18) DCR 88.9%. Response seen across B7-H3 expression level. Relationship between B7-H3 expression level and ORR not established. References: 10.1200/JCO.2026.44.16_suppl.3011

New BG-C9074 in Ovarian cancer, Breast cancer, Cholangiocarcinoma, Endometrial cancer, Lung squamous cell carcinoma with VTCN1 Protein expression: 4

Phase 1 trial. NCT06233942. N=114 efficacy-evaluable. cORR 28.1% (OC 34.5%, TNBC 31.3%, HR+/HER2- BC 17.9%). 2 CRs (1 OC, 1 TNBC). Note responses across doses and B7-H4 expression levels. References: 10.1200/JCO.2026.44.16_suppl.3013

Changed Lorlatinib in Non-small cell lung cancer with ALK EML4-ALK Fusion, Fusions: 1

Comments changed: PBS reimbursed after progression on ALK inhibitor other than Crizotinib. Phase 3 CROWN trial. NCT03052608. N=296. Lorlatinib vs crizotinib in first-line ALK-positive NSCLC. Median PFS not reached vs 9.1 months (HR 0.19). 7-year PFS 55% vs 3%. Median intracranial TTP not reached vs 16.4 months (HR 0.06). No new intracranial progression after 30 months on lorlatinib. Median DOR not reached; 53% remaining in response. In patients with baseline brain metastases, median PFS 86.3 vs 6.0 months. For patients progression-free at 24 months on lorlatinib, 79% probability of progression-free at 7 years. OS immature. Requires fluorescence in situ hybridisation (FISH) testing for ALK gene rearrangement, defined as 15% (or greater) positive cells. Last updated 2026-06-06.PBS reimbursed after progression on ALK inhibitor other than Crizotinib. Requires fluorescence in situ hybridisation (FISH) testing for ALK gene rearrangement, defined as 15% (or greater) positive cells. In Phase 3 trial vs crizotinib (CROWN): OS was superior at12 months 78% vs 39%. References changed: 30413378, 33207094, 42217582, 10.1016/j.annonc.2020.08.228230413378, 33207094, 10.1016/j.annonc.2020.08.2282. (First curated: 2020-04-16)

05 June, 2026 (Version: 20260605AU)

New Sacituzumab Govitecan + Pembrolizumab in Triple-negative breast cancer with CD274+ESR1+ERBB2 NOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression and CD274:protein expression: 2

Phase 3 ASCENT-04 trial. NCT05382286. N=443. SG + pembro improved PFS vs chemo + pembro (11.2 vs 7.8 months; HR 0.65). Median PFS2 was improved in the SG + pembro group vs chemo + pembro group despite crossover therapy (not reported; HR 0.49). Median time to first subsequent therapy was 17.3 vs 9.8 months. Median time to second subsequent therapy was NR vs 21.0 months. References: 10.1200/JCO.2026.44.17_suppl.LBA1000

New Tucatinib + Trastuzumab + Pertuzumab in Breast cancer with ERBB2 Amplification, Overexpression: 2

Phase 3 HER2CLIMB-05. NCT05132582. N=654. Tucatinib+HP improved PFS over placebo+HP (HR 0.641, p<0.0001). cORR improved across all stratified subgroups (de novo/recurrent, HR status, brain metastases). References: 10.1200/JCO.2026.44.16_suppl.1005

Changed Sacituzumab Govitecan + Pembrolizumab in Triple-negative breast cancer with CD274+ESR1+ERBB2 : 2

Alterations changed: NOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression and CD274:protein expressionNOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression and NOT CD274:protein expression. (First curated: 2026-03-03)

03 June, 2026 (Version: 20260603AU)

New Encorafenib + Cetuximab + FOLFIRI in Colorectal adenocarcinoma with BRAF V600E: 2

Phase 3. BREAKWATER Cohort 3. NCT04607421. N=147. ORR 64.4% vs 39.2% (Odds ratio 2.76). PFS significant by BICR (key secondary endpoint met). Median treatment duration 67.9 vs 32.1 weeks. References: 10.1200/JCO.2026.44.17_suppl.LBA3503

New Trastuzumab rezetecan in Colorectal adenocarcinoma with ERBB2 Overexpression, Amplification: 2

Phase 3 trial. NCT06199973. N=130. Trastuzumab rezetecan improved PFS vs standard of care (5.5 vs 2.8 months, HR 0.33) and ORR (40.7% vs 4.5%). OS immature (HR 0.77). DoR 4.4 vs 3.4 months. References: 10.1200/JCO.2026.44.16_suppl.3505

New Tunlametinib + Vemurafenib in Colorectal adenocarcinoma with BRAF V600E: 3

Phase 3. NCT06008119. N=157. Tunlametinib+vemurafenib significantly improved PFS (4.2 vs 1.5 months; HR 0.374; P<0.001) and ORR (37.1% vs 7.7%; P<0.0001) over investigator's choice in previously treated BRAF V600E-mutant mCRC, with DCR 81.9% vs 38.5%. References: 10.1200/JCO.2026.44.17_suppl.LBA3509

New SSGJ-707 in Non-small cell lung cancer with CD274 Protein expression: 3

Phase 2. NCT06361927. N=83. SSGJ-707 monotherapy in first-line advanced NSCLC with PD-L1 TPS>=1%. FDA-aligned dose 10 mg/kg Q3W (n=34): ORR 67.6%, median DOR NR, median PFS 12.4 months, median OS NR. Subgroup analysis: SQ histology ORR 75.0%, median PFS 8.9 months; NSQ histology ORR 63.6%, median PFS 12.4 months; TPS≥50% ORR 76.9%, median PFS 12.4 months. In patients with detectable ctDNA at baseline: median PFS NR for those with nondetectable ctDNA at C3D1 versus 7.6 months for those with detectable ctDNA at C3D1. References: 10.1200/JCO.2026.44.16_suppl.8514

New SYS6043 in Ovarian cancer, Small cell lung cancer, Breast cancer, Cervical cancer, Nasopharyngeal carcinoma, Non-squamous non-small cell lung cancer, Endometrial cancer with CD276 Overexpression: 3

Phase 1/2 trial. ChiCTR2400094683. N=502. SYS6043, a novel B7-H3-targeting ADC. Primary endpoint ORR in Phase 2. Efficacy analyses focused on Q3W cohorts. SCLC (n=50) ORR 64.0%, DCR 92.0%; at 6 mg/kg Q3W ORR 75.0% including one CR. OC: ORR 46.2%, DCR 87.2%, median PFS 5.6 months at 6 mg/kg Q3W. BC: ORR 83.8%, DCR 100%. nsq-NSCLC: ORR 57.1%. CC: ORR 38.5%. NPC: ORR 37.9%. EC: ORR 30.0%. References: 10.1200/JCO.2026.44.16_suppl.3002

New BL-M14D1 in Small-cell lung cancer, Neuroendocrine carcinoma with DLL3 Protein expression: 3

Phase 1 trial. NCT06505824. N=127. BL-M14D1 in heavily pre-treated SCLC and NEC. SCLC (N=83): ORR 71.1%, cORR 57.8%, DCR 94.0%, mPFS 7.2 months. NEC (N=22): ORR 40.9%, cORR 27.3%, DCR 90.9%, mPFS 5.3 months. Doses 4.0 and 4.5 mg/kg. References: 10.1200/JCO.2026.44.16_suppl.3001

New BL-M07D1 in Ovarian cancer with ERBB2 Protein expression: 3

Phase 2 studies. NCT06031584; NCT06131450. N=65. T-Bren at 3.8mg/kg D1Q3W: cORR 88.9% platinum-sensitive OC, 47.5% platinum-resistant OC; median PFS not reached; 9-mo PFS rate 85.7% and 61.2% respectively; median prior lines 2. References: 10.1200/JCO.2026.44.16_suppl.3003

New Ori-C101 in Hepatocellular carcinoma with GPC3 Protein expression: 3

Phase 1b BEACON study. NCT05652920. N=19. GPC3-directed CAR-T Ori-C101 in heavily pretreated advanced HCC. Confirmed ORR 50.0% (9/18), DCR 77.8% (14/18). At RP2D (Dose Level 3), confirmed ORR was 66.7% (6/9), DCR was 88.9% (8/9). Median OS was 14.4 months. References: 10.1200/JCO.2026.44.16_suppl.2508

New GFH375 in Cholangiocarcinoma with KRAS G12D: 3

Phase 1/2 NCT06500676. N=20 cholangiocarcinoma (CCA) and 41 colorectal cancer (CRC). CCA: ORR 35.0% (7/20), DCR 95.0%, median PFS 6.3 months. CRC: ORR 11.4% (4/35), DCR 77.1%, median PFS 4.1 months. References: 10.1200/JCO.2026.44.16_suppl.3008

New RNK08954 in Non-small cell lung cancer with KRAS G12D: 3

Phase 1 NCT06667544. N=47 NSCLC KRAS G12D. ORR 38.5% (15/39). DCR 94.9%. Median DoR not reached. Median PFS pending. References: 10.1200/JCO.2026.44.16_suppl.3006

New TSN1611 in Non-small cell lung cancer with KRAS G12D: 3

Phase 1/2. NCT06385925. N=117 total (26 NSCLC). In evaluable NSCLC patients at 600-1200 mg BID: ORR 50% (10 PR, 8 SD), DCR 90%. Median PFS not mature, 9-month PFS rate 54.5%. Intracranial responses observed. References: 10.1200/JCO.2026.44.16_suppl.8516

New DN022150 in Solid tumors, Pancreatic cancer with KRAS G12D: 3

Phase 1/2a. CTR20242749. N=31 evaluable. DN022150 in KRAS G12D advanced solid tumors. ORR 37.5% at 450mg, 31.3% at 650mg. DCR 87.5% and 93.8% respectively. 96.8% target lesion reduction. References: 10.1200/JCO.2026.44.16_suppl.3007

New Onvansertib + FOLFIRI + Bevacizumab in Colorectal adenocarcinoma with KRAS Oncogenic mutations: 3

Phase 2 CRDF-004 trial. NCT06106308. N=110. Onvansertib plus FOLFIRI and bevacizumab in first-line RAS-mutated mCRC: ORR 72.2% vs 43.2% SoC (p=0.051); 6-month ORR 55.6% vs 21.1% FOLFIRI+Bev (p=0.045); median PFS not reached vs 10.97 months SoC; PFS HR 0.37 vs SoC (p=0.048); 12-month PFS rate 61.9% vs 30.1%. References: 10.1200/JCO.2026.44.16_suppl.3510

New Onvansertib + FOLFIRI + Bevacizumab in Colorectal adenocarcinoma with NRAS Oncogenic mutations: 3

Phase 2 CRDF-004 trial. NCT06106308. N=110. Onvansertib plus FOLFIRI and bevacizumab in first-line RAS-mutated mCRC: ORR 72.2% vs 43.2% SoC (p=0.051); 6-month ORR 55.6% vs 21.1% FOLFIRI+Bev (p=0.045); median PFS not reached vs 10.97 months SoC; PFS HR 0.37 vs SoC (p=0.048); 12-month PFS rate 61.9% vs 30.1%. References: 10.1200/JCO.2026.44.16_suppl.3510

New NT-175 in Colorectal adenocarcinoma, Pancreatic adenocarcinoma, Breast cancer, Solid tumours with TP53 R175H: 3

Phase 1. NCT05877599. N=21 infused. NT-175 in TP53 R175H-mutated advanced solid tumors. ORR 47.6% overall, 53.8% in DL3. PR in 10 pts (5/6 PDAC, 2/10 CRC, 2/2 BC, 1 other). DCR 66.7%. 5 of 7 evaluable PR pts with ≥6 months follow-up remain in PR. References: 10.1200/JCO.2026.44.16_suppl.2506

New GFH375 in Colorectal cancer with KRAS G12D: 4

Phase 1/2 NCT06500676. N=20 cholangiocarcinoma (CCA) and 41 colorectal cancer (CRC). CCA: ORR 35.0% (7/20), DCR 95.0%, median PFS 6.3 months. CRC: ORR 11.4% (4/35), DCR 77.1%, median PFS 4.1 months. References: 10.1200/JCO.2026.44.16_suppl.3008

New Tremelimumab + Durvalumab + Pemetrexed + Carboplatin in Non-small cell lung cancer with KRAS Oncogenic mutations: 4

Phase 2b TRITON. NCT06008093. N=84 (41 vs 43). ORR 39.0% vs 34.9% for T+D+CT vs P+CT. Median DoR NR vs 6.4 months. 6-month response rate 100% vs 58.3%. In KRAS mut-only ORR 48.0% vs 33.3%. Interim analysis. Primary endpoint PFS not yet reported. References: 10.1200/JCO.2026.44.16_suppl.8515

New Encorafenib + Cetuximab + Nivolumab, Nivolumab in Colorectal adenocarcinoma with BRAF+Microsatellite Instability BRAF:V600E and NOT Microsatellite instability:high: R2

Phase 2 trial. SWOG S2107. NCT05308446. N=85. Randomized 2:1. In previously treated MSS BRAFV600E mCRC, adding nivolumab to encorafenib + cetuximab did not improve PFS (5.8 vs 6.3 months, HR 1.10) or OS (13.5 vs 11.6 months, HR 0.85). ORR 35% vs 32%. Primary endpoint not met. Ongoing correlative studies for biomarkers. References: 10.1200/JCO.2026.44.16_suppl.3504

01 June, 2026 (Version: 20260601AU)

New Daraxonrasib in Pancreatic ductal adenocarcinoma with KRAS G12, G12D, G12V, G13, Q61, Oncogenic mutations: 2

Phase 3 RASolute 302 trial. NCT06625320. N=500. Daraxonrasib improved OS vs chemotherapy in RAS G12 population (13.2 vs 6.6 months; HR 0.40) and overall population (13.2 vs 6.7 months; HR 0.40). PFS improved in RAS G12 population (7.3 vs 3.5 months; HR 0.45) and overall population (7.2 vs 3.6 months; HR 0.49). References: 10.1200/JCO.2026.44.17_suppl.LBA5, 10.1056/NEJMoa2605555

New Daraxonrasib in Pancreatic adenocarcinoma with KRAS G12, G12D, G12V, G12R, G12A, G12L, G12S, G13, Q61, Oncogenic mutations: 3

Phase 1-2. NCT05379985. Daraxonrasib in previously treated RAS-mutated PDAC. In RAS G12 mutations (second-line, 300 mg, n=26): ORR 35% (95% CI 17-56), median DOR 8.2 months, median PFS 8.5 months, median OS 13.1 months. In RAS G12/G13/Q61 mutations (n=38): ORR 29% (95% CI 15-46), median DOR 8.2 months, median PFS 8.1 months, median OS 15.6 months. References: 42090791

New Rogaratinib in Gastrointestinal stromal tumour with SDHA Loss of protein expression, Oncogenic mutations, Loss-of-function mutations: 3

Phase 2 trial. NCT04595747. N=24. Rogaratinib achieved ORR of 41.7% (10 PR). Median PFS was 31.0 months. 1-year PFS was 77.4%. Objective responses seen across all SDH molecular subsets. References: 42191879

New Rogaratinib in Gastrointestinal stromal tumour with SDHB Loss of protein expression, Oncogenic mutations, Loss-of-function mutations: 3

Phase 2 trial. NCT04595747. N=24. Rogaratinib achieved ORR of 41.7% (10 PR). Median PFS was 31.0 months. 1-year PFS was 77.4%. Objective responses seen across all SDH molecular subsets. References: 42191879

New Rogaratinib in Gastrointestinal stromal tumour with SDHC Loss of protein expression, Oncogenic mutations, Loss-of-function mutations, Promoter hypermethylation: 3

Phase 2 trial. NCT04595747. N=24. Rogaratinib achieved ORR of 41.7% (10 PR). Median PFS was 31.0 months. 1-year PFS was 77.4%. Objective responses seen across all SDH molecular subsets. References: 42191879

31 May, 2026 (Version: 20260531AU)

New Silevertinib in Non-small cell lung cancer with EGFR Oncogenic mutations AND NOT L858R AND NOT Exon 19 deletion, P-loop mutations, Alpha-c-helix mutations: 3

Phase 2. NCT05256290. N=43. Treatment-naive nonclassical EGFR mutant NSCLC. ORR 60% (ITT), PACC 56%, compound 69%. DCR 91%. CNS ORR 86%. 6-month PFS rate 86% overall, 80% in CNS metastasis patients. ctDNA clearance 81%. References: 10.1200/JCO.2026.44.16_suppl.8519

New DZD6008 in Non-small cell lung cancer with EGFR C797S: 3

Phase 1/2 TIAN-SHAN1 and TIAN-SHAN2. NCT06905197, NCT06813365. N=24. DZD6008 in pretreated EGFR C797X+ NSCLC. ORR 41.7% overall, 23.1% at 40 mg, 60.0% at 60 mg. Median DoR and PFS not reached. 9-month PFS rates 54.5% and 64.8% at recommended phase 2 doses. References: 10.1200/JCO.2026.44.16_suppl.8520

New TSN1611 in Non-small cell lung cancer with KRAS G12D: 3

Phase 1/2. NCT06385925. N=117 total (26 NSCLC). In evaluable NSCLC patients at 600-1200 mg BID: ORR 50% (10 PR) with DCR 90%. Median PFS not mature, 9-month PFS rate 54.5%. Intracranial responses seen. References: 10.1200/JCO.2026.44.16_suppl.8516

30 May, 2026 (Version: 20260530AU)

New Sunvozertinib in Non-small cell lung cancer with EGFR Exon 20 insertion, A767_S768insASV (A767_V769dupASV), D770_N771insSVD (S768_D770dupSVD), A763_Y764insFQEA, A763_Y764insLQEA, S768_V769insTLA, V769_D770insGLV, V769_D770insGSV, V769_D770insGVQ, V769_D770insSSV, D770_N771insESH, D770_N771insG, D770_N771insGF, D770_N771insGL, D770_N771insSTD, D770_N771insTAW, D770_N771insCGN, D770_N771insGY, N771_P772insG, N771_P772insH, N771_P772insHN, N771_P772insN, N771_P772insT, N771_P772insV, N771_P772insFH, N771_P772insGF, N771_P772insGT, N771_P772insGY, N771_P772insTH, P772_H773insDNP, P772_H773insGHP, P772_H773insLNP, P772_H773insPHP, P772_H773insPNP, P772_H773insQ, P772_H773insRNP, P772_H773insTNP, P772_H773insTQPNP, P772_H773insYNP, H773_V774insLM, H773_V774insAH, H773_V774insGHPH, H773_V774insGNPH, H773_V774insH, H773_V774insNPH, H773_V774insPH, H773_V774insPHPH, H773_V774insTH, H773_V774insY, H773_V774insNPNPY, H773_V774insNPY, H773_V774insPNPY, H773_V774insYNPY, V774_C775insHV, C775_S776insPHVC: 2

Phase 3. WU-KONG28. NCT05668988. N=324. Sunvozertinib demonstrated significantly longer median PFS versus carboplatin + pemetrexed (10.3 vs 7.5 months; HR 0.65) in first-line advanced nonsquamous NSCLC with EGFR exon 20 insertions. 12-month PFS rates were 46.1% versus 26.7%. ORR was 58.9% versus 31.1%. Median duration of response 11.2 versus 7.1 months. Median best percentage change in tumor size 42.1% versus 24.7%. OS data immature. References: 42212913, 10.1200/JCO.2026.44.17_suppl.LBA8500

Changed Asciminib in Chronic myelogenous leukaemia with ABL1 BCR-ABL1 Fusion, T315I, E255K, E255V, Y253H, F359V, Q252H, G250H, E459K: 3

Comments changed: Phase 1 NCT02081378. Asciminib in chronic-phase CML after TKI failure. N=150 heavily pretreated (70% ≥3 TKIs). Among those with hematologic relapse, 92% achieved complete hematologic response; 54% without CCyR at baseline achieved CCyR. Major molecular response (MMR) achieved or maintained by 12 months in 48% of evaluable patients, including 57% with ponatinib resistance/intolerance and 28% with T315I mutation at baseline. MMR maintained in 40 of 44 patients.. (First curated: 2020-05-21)

25 May, 2026 (Version: 20260525AU)

New Enasidenib + Cisplatin + Gemcitabine + Durvalumab in Cholangiocarcinoma with IDH2 R172, R172W, R172K, R172M: 4

Case series. Retrospective analysis. N=6. IDH2-mutated intrahepatic cholangiocarcinoma. One patient treated with enasidenib plus chemoimmunotherapy with time on treatment 18.1 months. References: 10.1016/j.annonc.2025.05.365

New Enasidenib in Cholangiocarcinoma with IDH2 R172: 4

Multi-institutional retrospective study. IDH2-mutated cholangiocarcinoma. N=40. Off-label enasidenib subsequent line (N=8) median PFS 3.9 months (1.1-5.1). Survival similar to IDH1 mutated, further investigation warranted. References: 10.1200/JCO.2026.44.2_suppl.567

New LY3410738, LY3410738 + Cisplatin + Gemcitabine, LY3410738 + Durvalumab in Cholangiocarcinoma, Glioma with IDH1 R132C, R132G, R132L, R132S: 4

Phase 1. NCT04521686. N=119. LY3410738 monotherapy ORR 5.2% in relapsed/refractory cholangiocarcinoma and 11.1% in glioma with DCR 56.9% and 63.0% respectively. LY3410738 plus CISGEM in newly diagnosed cholangiocarcinoma showed ORR 42.1%, median DOR 8.1 months, median PFS 10.2 months. Responses were seen in IDH1 (2/30) mutant treated with monotherapy. References: 41026608

New LY3410738, LY3410738 + Cisplatin + Gemcitabine, LY3410738 + Durvalumab in Cholangiocarcinoma, Glioma with IDH2 R172G, R172K, R172M, R172W: 4

Phase 1. NCT04521686. N=119. LY3410738 monotherapy ORR 5.2% in relapsed/refractory cholangiocarcinoma and 11.1% in glioma with DCR 56.9% and 63.0% respectively. LY3410738 plus CISGEM in newly diagnosed cholangiocarcinoma showed ORR 42.1%, median DOR 8.1 months, median PFS 10.2 months. Responses were seen in IDH2 (1/16) mutant treated with monotherapy. References: 41026608

New Venetoclax + Decitabine in Cholangiocarcinoma with IDH2 R172W: 4

Case report. Metastatic refractory IDH2 R172W-mutant cholangiocarcinoma. Venetoclax plus decitabine resulted in ongoing near-complete response for 15 months. Regression in multiple lesions observed. First report demonstrating benefit from V + D in solid tumor. References: 39913887

New Ivosidenib in Cholangiocarcinoma with IDH2 R172K: R2

Case series and preclinical study. NCT02073994. Two IDH1-mutated cholangiocarcinoma patients treated with ivosidenib achieved 17 and 23.5 months stable disease before progression via acquired IDH2 or IDH1 D279N mutation. In vitro IDH1 R132H/D279N cells resistant to ivosidenib but sensitive to LY3410738 which blocked (R)-2HG production and cellular transformation. References: 36056177

New Ivosidenib in Cholangiocarcinoma with IDH1 D279N: R2

Case series and preclinical study. NCT02073994. Two IDH1-mutated cholangiocarcinoma patients treated with ivosidenib achieved 17 and 23.5 months stable disease before progression via acquired IDH2 or IDH1 D279N mutation. In vitro IDH1 R132H/D279N cells resistant to ivosidenib but sensitive to LY3410738 which blocked (R)-2HG production and cellular transformation. References: 36056177

New LY3410738 in Cholangiocarcinoma with IDH1 R132C and D279N: 4

Case series and preclinical study. NCT02073994. Two IDH1-mutated cholangiocarcinoma patients treated with ivosidenib achieved 17 and 23.5 months stable disease before progression via acquired IDH2 or IDH1 D279N mutation. In vitro IDH1 R132H/D279N cells resistant to ivosidenib but sensitive to LY3410738 which blocked (R)-2HG production and cellular transformation. References: 36056177

Changed Pembrolizumab in Head and neck squamous cell carcinoma with CD274 Protein expression: 1

Comments changed: TGA approved. Not PBS reimbursed. Approved for CPS >= 1; PBS-subsidised if the PD-L1 CPS >= 20 in the tumour sample.. (First curated: 2020-04-16)

Changed Atezolizumab in Non-small cell lung cancer with CD274+EGFR+ALK CD274:Protein expression and NOT EGFR:Oncogenic mutations and NOT ALK:fusion: 1

Comments changed: TGA approved. PBS reimbused. Phase 3 IMpower110 trial (NCT02409342, N=572) evaluated first-line atezolizumab in EGFR and ALK negative NSCLC patients with PD-L1 expression ≥1% on tumor cells or tumor-infiltrating immune cells covering ≥1% of tumor area. Atezolizumab significantly improved median OS compared to chemotherapy (20.2 vs 13.1 months, improvement of 7.1 months).. (First curated: 2020-12-11)

Changed Amivantamab in Non-small cell lung cancer with EGFR Exon 20 insertion: 1

Comments changed: TGA approved. Not PBS Listed. FDA accelerated approval 2021-05-21. Median PFS 8.3 months. "Phase 1 CHRYSALIS trial. N=81. Amivantamab, an EGFR-MET bispecific antibody, showed an ORR of 40% (3 complete responses) and median DOR of 11.1 months in patients with EGFR Exon20ins NSCLC progressing on platinum chemotherapy, with a median PFS of 8.3 months.. (First curated: 2021-05-22)

Changed Amivantamab + Carboplatin + Pemetrexed in Non-small cell lung cancer with EGFR Exon 20 insertion: 1

Comments changed: PBS listed. Phase 3 trial. PAPILLON. NCT04538664. N=308. Amivantamab-chemotherapy (carboplatin-pemetrexed) was associated with superior progression-free survival (11.4 months versus 6.7 months) and a higher overall response rate (73% vs 47%) compared to chemotherapy alone in patients with advanced NSCLC with EGFR exon 20 insertions as first line treatment.TGA approved. Not PBS Listed. Not FDA approved. Phase 3 trial. PAPILLON. NCT04538664. N=308. Amivantamab-chemotherapy (carboplatin-pemetrexed) was associated with superior progression-free survival (11.4 months versus 6.7 months) and a higher overall response rate (73% vs 47%) compared to chemotherapy alone in patients with advanced NSCLC with EGFR exon 20 insertions as first line treatment.. (First curated: 2023-10-29)

Changed Sacituzumab Govitecan in Triple-negative breast cancer with ESR1+ERBB2 NOT ESR1:protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 1

Comments changed: TGA approved; Not PBS reimbursed. FDA approved. Phase 3 ASCENT trial (NCT02574455, N=468): Sacituzumab govitecan significantly improved PFS (5.6 vs 1.7 months) and OS (12.1 vs 6.7 months) over single-agent chemotherapy in metastatic triple-negative breast cancer, with an ORR of 35%.. (First curated: 2020-05-01)

Changed Selpercatinib in Non-small cell lung cancer with RET Fusion, KIF5B-RET fusion, CCDC6-RET fusion, NCOA4-RET fusion, KIF13A-RET fusion, KIAA1549L-RET fusion, KIAA1468-RET fusion, PRKAR1A-RET fusion: 1

Comments changed: TGA approved. Not PBS reimbursed. Phase 3 trial. LIBRETTO-431. NCT04194944. N=261. Selpercatinib (1st line) improved PFS over chemoimmunotherapy (24.8 vs 11.2 months). ORR was similar between the two arms at 84% and 65%. The cause-specific hazard ratio for the time to CNS progression was 0.28.. (First curated: 2023-10-29)

Changed Bosutinib in Chronic myelogenous leukaemia with ABL1 BCR-ABL1 Fusion: 1B

Comments changed: TGA approved. Not PBS reimbursed. Third or later line treatment. BFORE trial.. (First curated: 2020-05-21)

21 May, 2026 (Version: 20260521AU)

New Temsirolimus in Endometrial cancer, Solid tumours except Breast Cancer, Colorectal cancer with PIK3CA Oncogenic mutations, H1047R: 3

Phase 2. TAPUR basket trial. N=83. Temsirolimus in PIK3CA-mutated solid tumors. Primary endpoint disease control (DC) defined as OR or SD ≥16 weeks. BC cohort DC rate 9%, Median PFS 8 weeks, Median OS 36 weeks. CRC cohort DC rate 9%, Median PFS 8 weeks, Median OS 37 weeks. UC cohort DC rate 37%, Median PFS 16 weeks, Median OS 37 weeks, Median DOSD 31 weeks. HP cohort DC rate 31%, Median PFS 9 weeks, Median OS 27 weeks, Median DOSD 28 weeks. Overall OR rate 8%. Null hypothesis of 15% DC rate rejected for UC and HP cohorts. H1047R mutation subgroup OR rate 18%. DOR for PR in UC up to 84 weeks. DOR for PR in HP up to 229 weeks ongoing. Antitumor activity demonstrated in UC and HP cohorts but not BC or CRC. References: 42018965

New Temsirolimus in Breast cancer, Colorectal cancer with PIK3CA Oncogenic mutations: R2

Phase 2. TAPUR basket trial. N=83. Temsirolimus in PIK3CA-mutated solid tumors. Primary endpoint disease control (DC) defined as OR or SD ≥16 weeks. BC cohort DC rate 9%, Median PFS 8 weeks, Median OS 36 weeks. CRC cohort DC rate 9%, Median PFS 8 weeks, Median OS 37 weeks. UC cohort DC rate 37%, Median PFS 16 weeks, Median OS 37 weeks, Median DOSD 31 weeks. HP cohort DC rate 31%, Median PFS 9 weeks, Median OS 27 weeks, Median DOSD 28 weeks. Overall OR rate 8%. Null hypothesis of 15% DC rate rejected for UC and HP cohorts. H1047R mutation subgroup OR rate 18%. DOR for PR in UC up to 84 weeks. DOR for PR in HP up to 229 weeks ongoing. Antitumor activity demonstrated in UC and HP cohorts but not BC or CRC. References: 42018965

18 May, 2026 (Version: 20260518AU)

New Osimertinib in Colorectal adenocarcinoma with EGFR T790M: 4

Case report and preclinical study. Single patient with EGFR T790M mutated colorectal cancer. Patient-derived xenograft and cell line models generated from colon specimen. In vitro IC50 values showed sensitivity to irinotecan and osimertinib versus resistance to oxaliplatin, erlotinib, and cetuximab, validated PDX model validated irinotecan and fluorouracil sensitivity and oxaliplatin resistance. Sensitivity to osimertinib maintained despite BRAF V600E mutation. References: 35135168

New Osimertinib in Colorectal adenocarcinoma with EGFR T790M: 4

Case report. Metastatic colorectal cancer. EGFR T790M mutation detected on cell-free DNA. RAS/RAF wild-type. Fourth-line off-label osimertinib. Clinical response with decrease in hepatic metastases size. Variant allele frequency reduced from 13.3% to 2.1%. DOR 7 months. References: 37969405

New Erlotinib in Colorectal adenocarcinoma with EGFR T790M: R2

Case report and preclinical study. Single patient with EGFR T790M mutated colorectal cancer. Patient-derived xenograft and cell line models generated from colon specimen. In vitro IC50 values showed sensitivity to irinotecan and osimertinib versus resistance to oxaliplatin, erlotinib, and cetuximab, validated PDX model validated irinotecan and fluorouracil sensitivity and oxaliplatin resistance. Sensitivity to osimertinib maintained despite BRAF V600E mutation. References: 35135168

New Precemtabart tocentecan in Colorectal cancer with CEACAM5 Protein expression: 4

Phase 1. PROCEADE-CRC-01. NCT05464030. N=40. Heavily pretreated irinotecan-refractory metastatic colorectal cancer. Precemtabart tocentecan. Confirmed ORR 7.5% (3/40), unconfirmed 15.0% (6/40), all at dose levels ≥2.4 mg/kg. Median PFS 5.9 months (95% CI: 4.6–7.2); at dose levels ≥2.4 mg/kg (n=34), median PFS 6.7 months (95% CI: 4.6–8.8). References: 40739424

Changed Durvalumab + Savolitinib in Papillary renal cell carcinoma with HGF Amplification: 3

Comments changed: Phase 2. CALYPSO. N=41. Savolitinib plus durvalumab in metastatic papillary renal cancer. ORR 34% in ITT population versus 53% in MET-driven patients (n=17). Median PFS 6.5 months versus 13.9 months and OS 18.3 months versus 27.4 months i n ITT and MET-driven populations respectively. ctDNA clearance correlated with improved OS (31.3 v 7.2 months). Updated 2026-05-18Phase 2 CALYPSO: MET-driven PRCC. ORR 57% (8/14). References changed: 41861260, 10.1200/JCO.2021.39.15_suppl.4511. (First curated: 2021-06-15)

Changed Durvalumab + Savolitinib in Papillary renal cell carcinoma with MET Alteration, Amplification, Oncogenic mutations: 3

Comments changed: Phase 2. CALYPSO. N=41. Savolitinib plus durvalumab in metastatic papillary renal cancer. ORR 34% in ITT population versus 53% in MET-driven patients (n=17). Median PFS 6.5 months versus 13.9 months and OS 18.3 months versus 27.4 months i n ITT and MET-driven populations respectively. ctDNA clearance correlated with improved OS (31.3 v 7.2 months). Updated 2026-05-18Phase 2 CALYPSO: MET-driven PRCC. ORR 57% (8/14). References changed: 41861260, 10.1200/JCO.2021.39.15_suppl.4511. (First curated: 2021-06-15)

17 May, 2026 (Version: 20260517AU)

New Neladalkib in Solid tumours with ALK Fusion: 3

Phase 1/2 ALKOVE-1. NCT05384626. N=21. Neladalkib in ALK+ solid tumors other than NSCLC. ORR 48% (10/21) across 11 tumor types. DOR range 1.3+ - 8.6+ months (9/10 ongoing). ALK TKI-naive ORR 83% (5/6) all ongoing. CNS activity included complete resolution of CNS mets in alectinib- and lorlatinib-pretreated pts. References: 10.1016/j.annonc.2025.08.1541

New Alectinib in Solid tumours, Non-small cell lung cancer, Pancreatic adenocarcinoma, Neuroendocrine carcinoma, Neuroendocrine tumour, Sarcoma with ALK Fusion, EML4-ALK fusion, TNS1-ALK fusion, TPR-ALK fusion, KIF5B-ALK fusion, CAD-ALK fusion: 3

Phase 2. MoST substudy 14. ACTRN12621000312842. N=16. Alectinib in ALK-altered solid tumours and NSCLC with negative standard care testing. ORR 50% (n=8, 95% CI 28-72%) plus one unconfirmed PR. Median PFS 16.0 months (95% CI 5.7-17.5); median OS not reached. 6-month PFS rate 73%. 1L NSCLC discordant testing: 3 of 4 responded (1 CR, 2 PR). Solid tumours (n=12): 5 responses across diverse histologies. No response in nasopharyngeal carcinoma with R1275Q/HRAS G13R. References: 10.1016/j.annonc.2025.08.1565

New FOG-001 in Solid tumors, Desmoid tumors, Ameloblastoma, Adamantinomatous craniopharyngioma, Salivary gland carcinoma with CTNNB1 Oncogenic mutation: 4

Phase 1/2. NCT05919264. N=83. FOG-001 monotherapy in patients with solid tumors bearing Wnt pathway-activating mutations (WPAM+). In Wnt-β-catenin driven solid tumors (N=14), ORR was 43% and DCR 79%. In desmoid tumors (N=5), ORR and DCR were 60% and 100%, respectively. In MSS CRC, DCR was 50% at higher dose levels (240–480 mg/m2) with molecular responses (≥50% ctDNA reduction) in 60% of pts. References: 10.1158/1535-7163.TARG-25-B031

Changed Tepotinib in Non-small cell lung cancer with MET Exon 14 Deletion, Exon 14 splicing mutation, Exon 14 skipping mutation: 1

Tier changed: 1B. Comments changed: TGA approved. PBS listed. FDA approved. VISION trial. NCT02864992. N=152. Detection of MET exon14 skipping mutation was performed on either liquid biopsy or biospy of the archival tumour tissue. Across all lines of therapy in the efficacy population (N=99), ORR was 48% in the liquid-biopsy group and 50% in the tissue-biopsy group. Molecular cfDNA response to tepotinib was defined as complete response at least 75% of depletion of cfDNA.TGA approved. FDA approved. VISION trial. NCT02864992. N=152. Detection of MET exon14 skipping mutation was performed on either liquid biopsy or biospy of the archival tumour tissue. Across all lines of therapy in the efficacy population (N=99), ORR was 48% in the liquid-biopsy group and 50% in the tissue-biopsy group. Molecular cfDNA response to tepotinib was defined as complete response at least 75% of depletion of cfDNA.. (First curated: 2020-05-20)

13 May, 2026 (Version: 20260513AU)

Changed Abemaciclib + Letrozole, Abemaciclib + Anastrazole in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 1

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2020-04-16)

Changed Palbociclib + Letrozole in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 1

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2020-04-16)

Changed Ribociclib + Letrozole in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 1

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2020-04-16)

Changed Elacestrant in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 2

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2022-05-24)

Changed Giredestrant + Everolimus in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 2

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2025-10-19)

Changed Camizestrant + Palbociclib, Camizestrant + Ribociclib, Camizestrant + Abemaciclib in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression and ESR1:Oncogenic mutations, ESR1:D538G, ESR1:Y537S, ESR1:Y537N: 2

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2026-03-03)

Changed Vepdegestrant in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression; ESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression and ESR1:Oncogenic mutations: 2

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2026-03-03)

Changed Gedatolisib + Fulvestrant + Palbociclib, Gedatolisib + Fulvestrant, in Breast cancerPIK3CA:oncogenic mutations + ESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 2

Biomarker changed: ESR1+ERBB2+PIK3CAERBB2+ESR1+PIK3CA. (First curated: 2025-10-19)

Changed Zanidatamab + Palbociclib + Fulvestrant in Breast cancerESR1:Protein expression AND ERBB2:Amplification, ESR1:Protein expression AND ERBB2:Overexpression: 3

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2026-03-03)

Changed Gedatolisib + Palbociclib + Letrozole, Gedatolisib + Palbociclib + Fulvestrant in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 3

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2025-07-30)

Changed PF-07104091 in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 3

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2024-01-31)

Changed PF-07220060 in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 3

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2024-01-31)

Changed PF-07248144 in Breast cancerESR1:Protein expression and NOT ERBB2:amplification and NOT ERBB2:overexpression: 4

Biomarker changed: ESR1+ERBB2ERBB2+ESR1. (First curated: 2024-06-09)

Changed Therapy in Breast cancer with FGFR1 Amplification: R2

Therapy changed: Fulvestrant + Palbociclib, Fulvestrant + Ribociclib, Fulvestrant + Abemaciclib, Letrozole + Palbociclib, Letrozole + Ribociclib, Letrozole + Abemaciclib, Fulvestrant, Letrozole, Anastrozole, Exemestane, Tamoxifen, Goserelin, Medroxyprogesterone Acetate. (First curated: 2020-04-15)

11 May, 2026 (Version: 20260511AU)

New Palbociclib + Avelumab in Solid tumours with CDK4 Amplification: R2

Phase 2. ACTRN12620000568910. N=64. Palbociclib priming followed by avelumab in advanced solid tumours with CDK4/6 pathway alterations, including sarcomas and pancreatic cancer yielded no confirmed objective responses. PFS6 was 40% in the gain-of-function cohort and 16% in the loss-of-function cohort. Median OS was 12.7 months (gain-of-function) and 5.6 months (loss-of-function). Updated 2026-05-11. References: 10.1016/j.annonc.2025.08.2175

New Palbociclib + Avelumab in Solid tumours with CDKN2A Oncogenic mutations, Deletions, Truncating mutations, Loss-of-function mutations: R2

Phase 2. ACTRN12620000568910. N=64. Palbociclib priming followed by avelumab in advanced solid tumours with CDK4/6 pathway alterations, including sarcomas and pancreatic cancer yielded no confirmed objective responses. PFS6 was 40% in the gain-of-function cohort and 16% in the loss-of-function cohort. Median OS was 12.7 months (gain-of-function) and 5.6 months (loss-of-function). Updated 2026-05-11. References: 10.1016/j.annonc.2025.08.2175

New VT3989 in Mesothelioma, Solid tumours with NF2 Oncogenic mutations: 4

Phase 1/2. NCT04665206. N=172 (135 mesothelioma). VT3989 ORR 26% in 47 mesothelioma patients at clinically optimized doses. ORR 32% (DCR 86%; median PFS 10 months) in 22 mesothelioma patients with optimized doses and UACR thresholds. References: 41111090

New RMC-6236 in Non-small cell lung cancer with RRAS Q87L: 4

Preclinical and retrospective study. N=8,488 NSCLC sequenced. RRASQ87L or RRAS2Q72L mutations identified in 0.45% (38/8,488). RMC-6236 suppressed proliferation in vitro. In vivo, RMC-6236 significantly inhibited growth of RRASQ87L/RRAS2Q72L-mutant HBEC-derived xenografts. Supports inclusion of RRAS/RRAS2 in diagnostic panels and clinical investigation of pan-RAS inhibitors. References: 41543339

New RMC-6236 in Non-small cell lung cancer with RRAS2 Q72L: 4

Preclinical and retrospective study. N=8,488 NSCLC sequenced. RRASQ87L or RRAS2Q72L mutations identified in 0.45% (38/8,488). RMC-6236 suppressed proliferation in vitro. In vivo, RMC-6236 significantly inhibited growth of RRASQ87L/RRAS2Q72L-mutant HBEC-derived xenografts. Supports inclusion of RRAS/RRAS2 in diagnostic panels and clinical investigation of pan-RAS inhibitors. References: 41543339

New Cetuximab in Colorectal adenocarcinoma with KRAS+NRAS+BRAF+EGFR+PIK3CA+MAP2K1+AKT1+MET+PTEN+ERBB2 NOT KRAS:Oncogenic mutation and NOT NRAS:Oncogenic mutation and NOT BRAF:Oncogenic mutation and NOT EGFR:Oncogenic mutation and NOT PIK3CA:Exon 20 mutation and NOT MAP2K1:Oncogenic mutation and NOT AKT1:Oncogenic mutation and NOT MET:Oncogenic mutation and NOT PTEN:Oncogenic mutation and NOT ERBB2:amplification: 4

Phase 2. CAVE-2 GOIM. NCT05291156. N=156. Cetuximab plus avelumab did not improve OS over cetuximab monotherapy (14.8 vs 12.9 months) or PFS (5.3 vs 4.3 months) in RAS/BRAF WT refractory mCRC. In negative hyperselection subgroup (no resistance PVs), mPFS was significantly prolonged (5.35 vs 3.65 months) and mOS improved (15.0 vs 11.1 months) compared to positive hyperselection. ORR 12% vs 3% in negative vs positive hyperselection. References: 41443411

New Cetuximab, Panitumumab in Colorectal adenocarcinoma with KRAS Oncogenic mutations, Amplification: R2

Translational study. N=10 progression biopsies. Acquired KRAS mutations in 60% (6/10) and amplification in 1/10 of colorectal cancer cases resistant to anti-EGFR therapy. KRAS mutant alleles detectable in plasma 10 months prior to radiographic progression. In vitro resistant cell lines (DiFi-R, Lim1215-R) regained sensitivity with combinatorial EGFR and MEK inhibition. Ectopic KRAS expression conferred cetuximab resistance in parental lines. Suggests blood-based monitoring and early MEK inhibitor initiation. References: 22722830

New LY3410738 in Cholangiocarcinoma, Glioma with IDH1 R132: 4

Phase I. NCT04521686. N=119. LY3410738 dual IDH1/2 inhibitor in IDH-mutant solid tumors. Monotherapy relapsed/refractory cholangiocarcinoma ORR 5.2% (N=58), median PFS 3.5 months, median OS 13.9 months. Monotherapy glioma ORR 11.1% (N=27), median PFS 7.9 months. Responses were seen in both IDH1 and IDH2 groups across dose levels. References: 41026608

New LY3410738 in Cholangiocarcinoma, Glioma with IDH2 R172, R140: 4

Phase I. NCT04521686. N=119. LY3410738 dual IDH1/2 inhibitor in IDH-mutant solid tumors. Monotherapy relapsed/refractory cholangiocarcinoma ORR 5.2% (N=58), median PFS 3.5 months, median OS 13.9 months. Monotherapy glioma ORR 11.1% (N=27), median PFS 7.9 months. Responses were seen in both IDH1 and IDH2 groups across dose levels. References: 41026608

New TNG908, TNG908 + AG-270, TNG908 + Abemaciclib, TNG908 + Palbociclib in Solid tumours, Glioblastoma, Non-small cell lung cancer, Mesothelioma, Pancreatic adenocarcinoma, Cholangiocarcinoma, Bladder cancer with MTAP Deletion: 4

Phase I/II trial. NCT05275478. TNG908 is a brain-penetrant, MTA-cooperative PRMT5 inhibitor for MTAP-deleted advanced or metastatic solid tumors including glioblastoma. Preclinical efficacy in MTAP-null xenografts demonstrated sustained tumor regressions in ~30% of models across histologies. Orthotopic GBM model showed antitumor activity. Combination with MAT2A or CDK4/6 inhibitors drove synergistic benefit in vitro and in vivo. References: 39756156

New Savolitinib + Osimertinib in Non-small cell lung cancer with EGFR+MET EGFR:Oncogenic mutations and MET:amplification: 3

Phase 2. Savolitinib Plus Osimertinib. N=30. EGFR-mutated, MET-amplified advanced NSCLC. ORR was 57% (Savolitinib + Osimertinib) versus 13% (Savolitinib + Placebo). Median PFS was 7.4 months versus 1.6 months. In higher MET cutoffs subgroup, ORR 63% versus 29%, Median PFS 8.2 months versus 4.0 months. References: 41308232

Removed AZD1390 + Radiotherapy in Non-small cell lung cancer with ATM alterations Protein expression: Tier 4   (First curated: 2020-04-16)

Changed AZD1390 + Radiotherapy with ATM Protein expression: 4

Cancer type(s) changed: Glioblastoma, Non-small cell lung cancer Comments changed: Preclinical study. Brain-penetrant ATM inhibitor AZD1390 combined with radiation induced tumor regressions and increased survival versus IR alone in syngeneic and patient-derived glioma and orthotopic lung-brain metastatic models.. (First curated: 2020-04-16)

Changed KIN-2787 in Solid tumours with BRAF Class II mutations, Class III mutations: 4

Comments changed: Preclinical study. KIN-2787 pan-RAF inhibitor. In vitro biochemical assays IC50 0.06-3.46 nM against RAF1, BRAF, and ARAF. Class II and III BRAF mutant cell lines IC50 < 50 nM; 19- and 7-fold more sensitive versus wild-type. In vivo xenografts (A-375, BxPC-3, WM3629) showed dose-dependent tumor growth inhibition (TGI up to 101-118%; p <=0.0001).. (First curated: 2022-11-29)

Changed Seribantumab in Solid tumours with NRG1 Fusion; CD74-NRG1 fusion; VAMP2-NRG1 fusion; SLC3A2-NRG1 fusion: 4

Comments changed: Preclinical study. Seribantumab effectively inhibits growth of patient-derived and isogenic cell line and xenograft models with NRG1 rearrangements in vitro and in vivo.. (First curated: 2021-03-31)

07 May, 2026 (Version: 20260507AU)

New Daraxonrasib in Pancreatic ductal adenocarcinoma with HRAS G12D: 3

Phase 1-2 study. NCT05379985. N=168. Daraxonrasib 300 mg in previously treated RAS-mutated PDAC. RAS G12 second-line subgroup ORR 35% (95% CI, 17 to 56). Median duration of response 8.2 months. Median PFS 8.5 months. Median OS 13.1 months. All RAS G12, G13, or Q61 mutations subgroup ORR 29%. Median PFS 8.1 months. Median OS 15.6 months. Supports ongoing Phase 3 RASolute 302 trial (NCT06625320). References: 42090791

New Daraxonrasib in Pancreatic ductal adenocarcinoma with KRAS G12, G12D, G12V, G12R, G12A, G12L, G12S, G13, Q61, Q61H, Oncogenic mutations: 3

Phase 1-2 study. NCT05379985. N=168. Daraxonrasib 300 mg in previously treated RAS-mutated PDAC. RAS G12 second-line subgroup ORR 35% (95% CI, 17 to 56). Median duration of response 8.2 months. Median PFS 8.5 months. Median OS 13.1 months. All RAS G12, G13, or Q61 mutations subgroup ORR 29%. Median PFS 8.1 months. Median OS 15.6 months. Supports ongoing Phase 3 RASolute 302 trial (NCT06625320). References: 42090791

New Panitumumab in Colorectal adenocarcinoma with KRAS+NRAS+BRAF+EGFR NOT KRAS:Oncogenic mutations AND NOT NRAS:Oncogenic mutations AND NOT BRAF:Oncogenic mutations AND NOT EGFR:Oncogenic mutations: R2

Phase 2 CHRONOS trial. NCT03227926. N=27 (52 screened). ctDNA-guided panitumumab rechallenge in tissue-RAS WT mCRC after prior anti-EGFR therapy. Primary endpoint ORR met (30% partial response). Disease control 63%. Results favorably compare with standard third-line treatments. Further larger randomized trials warranted. References: 35915157

Changed Trastuzumab deruxtecan in Non-small cell lung cancer with ERBB2 Oncogenic mutation: 1B

Tier changed: 1B2. Comments changed: TGA approved. Not PBS listed. Phase 2 trial. DESTINY-Lung02. NCT04961073. N=152. Dose optimization study. Confirmed ORR was 49% (Median DOR 16.8 months) and 56% (NE) in T-DXd 5.4mg/kg and 6.4 mg/kg respectively. Grade ≥3 treatment related adverse events occurred in 38.6% and 58% of patients receiving 5.4 and 6.4 mg/kg, respectively.. (First curated: 2023-11-05)

04 May, 2026 (Version: 20260504AU)

New Binimetinib + Encorafenib + Cetuximab in Colorectal adenocarcinoma with BRAF D594G: R2

Phase 2. BIG BANG. UMIN000031857. N=32. Binimetinib, encorafenib, and cetuximab in BRAF non-V600E mutated mCRC. Primary cohort (N=12) confirmed ORR 16.7%, Median PFS 3.3 months, Median OS 9.7 months. Anti-EGFR refractory cohort (N=20) confirmed ORR 10.0%, Median PFS 3.0 months, Median OS 7.6 months. Comparatively, class 1/2 tumors (N=7) ORR 28.6%. References: 10.1200/JCO.2024.42.16_suppl.3585

02 May, 2026 (Version: 20260502AU)

New Datopotamab deruxtecan in Non-small cell lung cancer with TACSTD2 Protein expression, Overexpression: 4

Exploratory biomarker analysis of ICARUS-LUNG01. N=100. Pretreated advanced NSCLC. Overall ORR 26.0% with Median PFS 3.6 months (NSQ 4.8 vs Sq 2.9 months). Median DoR 7.0 months. Median OS 11.9 months (Non-squamous 12.6 vs Sq 6.3 months). Standard IHC did not find association with ORR, but H score >= 100 higher (vs H-score < 100) was associated with higher PFS, requiring further validation. References: 41999747

30 April, 2026 (Version: 20260430AU)

Changed Futibatinib with FGFR2 Amplification: R2

Cancer type(s) changed: Gastric cancer, Gastroesophageal adenocarcinomaGastric cancer, Gastroesophageal junction cancer (First curated: 2026-04-23)

24 April, 2026 (Version: 20260424AU)

New Futibatinib in Gastric cancer, Gastroesophageal junction cancer with FGFR2 Amplification: R2

Phase 2 study. N=28. In patients with FGFR2 amplified gastric or GEJ cancer, futibatinib ORR was 17.9% (5 partial responses). Median DOR 3.9 months. DCR 50.0%. Median PFS 2.9 months. Median OS 5.9 months. Note, the lower bound of the 95% confidence interval (6.1%) falls below the 10% threshold. References: 39919334

23 April, 2026 (Version: 20260423AU)

New AMG 410 in Colorectal adenocarcinoma, Pancreatic adenocarcinoma, Non-small cell lung cancer, Solid Tumours with KRAS G12D, G12V, G12C, G13D, Amplification: 4

Preclinical study. Abstract ND01. AMG 410. Pan-KRAS inhibitor. Median IC50 12 nM in KRAS-mutant cells. Tumor stasis or regression observed in colorectal, pancreatic, and lung cancer CDX and PDX models harboring KRAS G12D, G12V, G12C, & G13D. Enhanced in vivo efficacy in combination with targeted therapies or immunotherapy. First-in-human study in solid tumor indications planned.'. References: 10.1158/1538-7445.AM2025-ND01

12 April, 2026 (Version: 20260412AU)

New Setidegrasib in Non-small cell lung cancer, Pancreatic adenocarcinoma with KRAS G12D: 3

Phase 1. NCT05382559. N=203. Setidegrasib 600 mg weekly in KRAS p.G12D-mutated advanced NSCLC and pancreatic ductal adenocarcinoma. NSCLC (n=45): ORR 36%, median PFS 8.3 months, 12-month OS 59%. Pancreatic (n=21): ORR 24%, median PFS 3.0 months, median OS 10.3 months, median DoR 4.2 months. Second- or third-line NSCLC subgroup (n=32): ORR 38%, median PFS 11.2 months. References: 41879829

10 April, 2026 (Version: 20260410AU)

New BH-30643 in Non-small cell lung cancer with EGFR Exon 19 deletion, Exon 19 deletion and T790M, Exon 19 deletion and T790M and C797S, L858R and T790M, L858R and T790M and C797S, G719A and S768I, G719A and L861Q, Exon 20 insertion: 4

Preclinical study. BH-30643. EGFR-mutant NSCLC CDX, PDX, and cell line models. In PC-9 (exon 19 del) CDX, BH-30643 led to deep tumor regressions similar to osimertinib at 25 mg/kg. Deep responses in double mutant CDX (cis L858R/T790M and exon 19 del/T790M). In triple-mutant PDX and CDX (cis exon 19 del/T790M/C797S and cis L858R/T790M/C797S), deep responses observed with BH-30643 while osimertinib showed no effect. Intracranial xenograft showed 90% tumor reduction. Atypical mutations (cis G719A/S768I and cis G719A/L861Q) maintained strong activity. EGFR ex20ins in 34 Ba/F3 cell lines showed median IC50 of 6.06 nM. First-in-human study NCT06706076 (SOLARA) ongoing.'. References: 10.1200/JCO.2025.43.16_suppl.3110

08 April, 2026 (Version: 20260408AU)

Changed Abemaciclib in Meningioma with CDKN2A Oncogenic mutation: 3

References changed: 41545592, 10.1200/JCO.2024.42.16_suppl.2001. (First curated: 2024-06-02)

07 April, 2026 (Version: 20260407AU)

New Everolimus + Bevacizumab in Malignant peripheral nerve sheath tumor with NF1 Oncogenic mutations; Loss-of-function mutations; Deletion: R2

Phase 2. SARC016. N=25 (17 NF1, 8 sporadic). Chemotherapy refractory MPNST. Everolimus plus bevacizumab. Clinical benefit rate (CR, PR, or SD >= 4 months) was 12% (3/25) failing activity threshold of 25%. Stage 1 1/15, Stage 2 2/10 additional. Median cycles 3. Combination not considered active. References: 31427883

New Everolimus in Non-small cell lung cancer with NF1 Oncogenic mutations; Loss-of-function mutations; Deletion: R2

Phase 2 basket study. N=12. Everolimus failed to meet prespecified ORR threshold of 30% (12.5% ORR including 1 CR with STK11) in patients with advanced solid malignancies harboring TSC1, TSC2, NF1, NF2 or STK11 mutations. 8 patients evaluable (4 STK11 and 4 NF1) for response with one response noted in STK11. No response seen in NSCLC NF1 mutants. References: 34422335

Changed Everolimus in Non-small cell lung cancer with STK11 Oncogenic mutations: 4

Comments changed: Phase 2 basket study. N=12. Everolimus failed to meet prespecified ORR threshold of 30% (12.5% ORR including 1 CR with STK11) in patients with advanced solid malignancies harboring TSC1, TSC2, NF1, NF2 or STK11 mutations. 8 patients evaluable (4 STK11 and 4 NF1) for response with one response noted in STK11.. (First curated: 2024-08-21)

03 April, 2026 (Version: 20260403AU)

New Bemarituzumab + mFOLFOX6 in Gastric cancer, Gastroesophageal junction adenocarcinoma with FGFR2 FGFR2b Overexpression, FGFR2-IIIb Overexpression: 3

Phase 2. FIGHT. NCT03694522. N=155. Bemarituzumab plus mFOLFOX6 median PFS 9.5 months versus placebo 7.4 months (HR 0.68; p=0.073) in FGFR2b-selected gastric or gastro-oesophageal junction adenocarcinoma. Primary endpoint not statistically significant but promising clinical efficacy observed. Confirmatory phase 3 trials planned. References: 36244398

New Bemarituzumab + mFOLFOX6 in Gastric cancer, Gastroesophageal junction adenocarcinoma with FGFR2 FGFR2b Overexpression, FGFR2-IIIb Overexpression: 3

Phase 3. FORTITUDE-101. NCT05052801. N=547. In FGFR2b ≥10% advanced Gastric and gastroesophageal cancer (Bemarituzumab n=159, Placebo n=165), bemarituzumab + mFOLFOX6 improved median OS vs placebo + mFOLFOX6 (17.9 vs 12.5 months; HR 0.61, P=0.005) at primary analysis. Median PFS 8.6 vs 6.7 months (HR 0.71, P=0.019). Follow-up analysis median OS 14.5 vs 13.2 months (HR 0.82). References: 10.1016/j.annonc.2025.09.092

New BG-C137 in Solid tumours, Gastric Cancer with FGFR2 FGFR2b Protein expression, FGFR2-IIIb Protein expression, FGFR2b Overexpression, FGFR2-IIIb Overexpression, FGFR2b Amplification, FGFR2-IIIb Amplification: 4

Preclinical study. BG-C137. FGFR2b-targeting ADC with topoisomerase inhibitor payload. In vitro and in vivo FGFR2b-expressing tumor models. Single dose showed strong anti-tumor efficacy in FGFR2b-amplified and non-amplified PDX models with strong bystander killing effect in vitro in heterogeneous FGFR2b expression models. References: 10.1158/1538-7445.AM2025-3778

Changed Bemarituzumab + FOLFOX in Gastric cancer, Gastroesophageal junction adenocarcinoma, Oesophageal adenocarcinoma with FGFR2 : 4

Alterations changed: Overexpression, FGFR2b Overexpression, FGFR2-IIIb OverexpressionOverexpression, FGFR2b:Overexpression, FGFR2-IIIb:Overexpression. (First curated: 2022-11-01)

Changed Bemarituzumab in Gastroesophageal junction adenocarcinoma, Gastric Cancer with FGFR2 : 4

Alterations changed: Overexpression, FGFR2b Overexpression, FGFR2-IIIb Overexpression, AmplificationOverexpression, FGFR2b:Overexpression, FGFR2-IIIb:Overexpression, amplification. (First curated: 2020-06-26)

Changed Olaparib with BRCA2 Oncogenic mutations: 3

Cancer type(s) changed: Breast cancer, Endometrial cancer, Other solid tumors (First curated: 2026-04-02)

Changed Olaparib with BRCA2 Oncogenic mutations: 4

Cancer type(s) changed: Biliary tract cancer, Non-small cell lung cancer, Small cell lung cancer, Gastric cancer, Ureteric carcinoma, Sarcoma, Oesophageal carcinoma, Duodenal adenocarcinoma, Neuroendocrine carcinoma, Solid tumoursBiliary tract cancer, Non-small cell lung cancer, Small cell lung cancer, Gastric cancer, Ureteric carcinoma, Sarcoma, Oesophageal carcinoma, Duodenal carcinoma, Neuroendocrine carcinoma, Solid tumours (First curated: 2026-04-02)

02 April, 2026 (Version: 20260402AU)

New MCB-294, MCB-36 in Solid tumours with KRAS G12D, G12C, G12V, G12S, G12A, G13D, V14I, L19F, Q22K, D33E, Q61H, K117N, A146V: 4

Preclinical study. MCB-294 dual-state pan-KRAS inhibitor and MCB-36 VHL-recruiting degrader demonstrated superior activity versus Bl-2865 and MRTX1133. Inhibited growth of KRAS-dependent cancer cells and patient-derived organoids. Reduced tumor progression in multiple preclinical models. Suppressed KRAS(G12C) inhibitor-resistant cancer cells. References: 40780213

New MCB-294, MCB-36 in Solid tumours with KRAS G10L, T58A, R68S: R2

Preclinical study. MCB-294 dual-state pan-KRAS inhibitor and MCB-36 VHL-recruiting degrader demonstrated superior activity versus Bl-2865 and MRTX1133. Inhibited growth of KRAS-dependent cancer cells and patient-derived organoids. Reduced tumor progression in multiple preclinical models. Suppressed KRAS(G12C) inhibitor-resistant cancer cells. References: 40780213

New Olaparib in Breast cancer, Endometrial cancer with BRCA1 Oncogenic mutations: 3

Phase 2 basket trial. TAPUR. NCT02693535. N=119. Olaparib evaluated in BRCA1/2-altered solid tumors across breast (n=28), biliary tract (n=19), lung (n=25), uterine (n=15), and histology-pooled (n=32) cohorts. Primary endpoint disease control (CR/PR/SD >= 16 weeks) rates were 69%, 50%, 41%, 47%, and 41% respectively, rejecting the null 15% DC rate hypothesis for all cohorts. Signal of activity declared for all cohorts. ORR of the Breast cancer cohort was 43% (12/28). ORR of the Endometrial cancer cohort was 20% (3/15). References: 41100773

New Olaparib in Breast cancer, Endometrial cancer, Other solid tumors with BRCA2 Oncogenic mutations: 3

Phase 2 basket trial. TAPUR. NCT02693535. N=119. Olaparib evaluated in BRCA1/2-altered solid tumors across breast (n=28), biliary tract (n=19), lung (n=25), uterine (n=15), and histology-pooled (n=32) cohorts. Primary endpoint disease control (CR/PR/SD >= 16 weeks) rates were 69%, 50%, 41%, 47%, and 41% respectively, rejecting the null 15% DC rate hypothesis for all cohorts. Signal of activity declared for all cohorts. ORR of the Breast cancer cohort was 43% (12/28). ORR of the Endometrial cancer cohort was 20% (3/15). References: 41100773

New Olaparib in Biliary tract cancer, Non-small cell lung cancer, Small cell lung cancer, Sweat gland carcinoma, Gastric cancer with BRCA1 Oncogenic mutations: 4

Phase 2 basket trial. TAPUR. NCT02693535. N=119. Olaparib evaluated in BRCA1/2-altered solid tumors across breast (n=28), biliary tract (n=19), lung (n=25), uterine (n=15), and histology-pooled (n=32) cohorts. Primary endpoint disease control (CR/PR/SD >= 16 weeks) rates were 69%, 50%, 41%, 47%, and 41% respectively, rejecting the null 15% DC rate hypothesis for all cohorts. Signal of activity declared for all cohorts. ORR of Biliary tract cancer was (2/19) 10% (0/6 gallbladder carcinoma). ORR for NSCLC is 2/17 (12%) and one (of 2) responder in SCLC. Responders seen in solid tumour cohort: sweat gland carcinoma, and gastric cancer. References: 41100773

New Olaparib in Biliary tract cancer, Non-small cell lung cancer, Small cell lung cancer, Gastric cancer, Ureteric carcinoma, Sarcoma, Oesophageal carcinoma, Duodenal carcinoma, Neuroendocrine carcinoma, Solid tumours with BRCA2 Oncogenic mutations: 4

Phase 2 basket trial. TAPUR. NCT02693535. N=119. Olaparib evaluated in BRCA1/2-altered solid tumors across breast (n=28), biliary tract (n=19), lung (n=25), uterine (n=15), and histology-pooled (n=32) cohorts. Primary endpoint disease control (CR/PR/SD >= 16 weeks) rates were 69%, 50%, 41%, 47%, and 41% respectively, rejecting the null 15% DC rate hypothesis for all cohorts. Signal of activity declared for all cohorts. ORR of Biliary tract cancer was (2/19) 10%. (0/6 gallbladder carcinoma). ORR for NSCLC is 2/17 (12%) and one (of 2) responder in SCLC. Responders seen in solid tumour cohort: gastric cancer, ureteric carcinoma, Sarcoma, Oesophageal carcinoma, Duodenal carcinoma, Neuroendocrine carcinoma. References: 41100773

New Capivasertib + Abiraterone in Prostate cancer with PTEN Loss of protein expression: 2

Phase 3 CAPItello-281 trial. NCT04493853. N=1012. In PTEN-deficient metastatic hormone-sensitive prostate cancer, capivasertib plus abiraterone improved rPFS versus placebo plus abiraterone (median 33.2 versus 25.7 months; HR 0.81, 95% CI 0.66-0.98, P = 0.034). OS HR was 0.90 (95% CI 0.71-1.15, P = 0.401) at 26.4% maturity. Post hoc rPFS analyses for PTEN loss cut-offs ≥95%, ≥99%, and 100% showed consistent treatment arm performance with numerically improved treatment effect as cut-off increased. References: 41120017

Changed Puxitatug samrotecan in Solid tumoursProtein expression: 3

Biomarker changed: VTCN1VCTN1. (First curated: 2024-09-14)

Changed BBO-11818 + Cetuximab in Colorectal adenocarcinoma with KRAS G12D: 4

References changed: 4179003210.1158/2159-8290.CD-25-1280. (First curated: 2026-03-11)

Changed BBO-11818 in Solid tumours with KRAS G12D, G12V, G12C, G12A, G12S, G13D, Amplification and NOT Oncogenic mutation: 4

References changed: 4179003210.1158/2159-8290.CD-25-1280. (First curated: 2026-03-11)

Changed BBO-11818 in Solid tumours with BRAF V600E: R2

References changed: 4179003210.1158/2159-8290.CD-25-1280. (First curated: 2026-03-11)

Changed BBO-11818 in Solid tumours with KRAS G12R, Q61R, Q61: R2

References changed: 4179003210.1158/2159-8290.CD-25-1280. (First curated: 2026-03-11)

Changed BBO-11818 in Solid tumours with NRAS Oncogenic mutations: R2

References changed: 4179003210.1158/2159-8290.CD-25-1280. (First curated: 2026-03-11)

16 March, 2026 (Version: 20260316AU)

Changed Niraparib with BAP1 Oncogenic mutations: R2

Cancer type(s) changed: Solid tumours except Mesothelioma (First curated: 2022-06-04)

12 March, 2026 (Version: 20260312AU)

Changed Amivantamab in Non-small cell lung cancer with EGFR Exon 20 insertion: 1

Tier changed: 1B. (First curated: 2021-05-22)

Changed Amivantamab + Carboplatin + Pemetrexed in Non-small cell lung cancer with EGFR Exon 20 insertion: 1

Tier changed: 1B. (First curated: 2023-10-29)