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DRUG CLASS:

c-MET inhibitor

Related drugs:
17h
SANOVO: Clinical Study on Savolitinib + Osimertinib in Treatment of EGFRm+/MET+ Locally Advanced or Metastatic NSCLC (clinicaltrials.gov)
P3, N=412, Active, not recruiting, Hutchison Medipharma Limited | Trial completion date: Aug 2026 --> May 2028 | Trial primary completion date: Aug 2026 --> May 2028
Trial completion date • Trial primary completion date
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MET (MET proto-oncogene, receptor tyrosine kinase)
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EGFR mutation • EGFR L858R • EGFR exon 19 deletion • MET overexpression
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Tagrisso (osimertinib) • Orpathys (savolitinib)
6d
A Study of PLB1001 in Non-small Cell Lung Cancer With c-Met Dysregulation(KUNPENG) (clinicaltrials.gov)
P2, N=145, Completed, Beijing Pearl Biotechnology Limited Liability Company | Trial completion date: Dec 2025 --> Jun 2025 | Active, not recruiting --> Completed
Trial completion • Trial completion date
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MET (MET proto-oncogene, receptor tyrosine kinase)
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vebreltinib (APL-101)
8d
Lung-MAP Sub-Study: Comparing Combinations of Targeted Drugs for Advanced Non-Small Cell Lung Cancer That Has EGFR and MET Gene Changes (A Lung-MAP Treatment Trial) (clinicaltrials.gov)
P2, N=66, Recruiting, SWOG Cancer Research Network | Trial completion date: May 2027 --> Jun 2028 | Trial primary completion date: May 2026 --> Jun 2027
Trial completion date • Trial primary completion date
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EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase)
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EGFR mutation • MET amplification
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Tagrisso (osimertinib) • Cyramza (ramucirumab) • Tabrecta (capmatinib)
8d
SKIPPirr: Premedication to Reduce Amivantamab Associated Infusion Related Reactions (clinicaltrials.gov)
P2, N=68, Active, not recruiting, Janssen Research & Development, LLC | Trial completion date: Jul 2026 --> Mar 2027
Trial completion date
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EGFR mutation • EGFR L858R • EGFR exon 19 deletion
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Tagrisso (osimertinib) • Rybrevant (amivantamab-vmjw) • dexamethasone • Lazcluze (lazertinib)
9d
New P1 trial
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK (Neurotrophic receptor tyrosine kinase)
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BRAF V600E • KRAS mutation • EGFR mutation • BRAF V600 • HER-2 mutation • EGFR T790M • MET exon 14 mutation • ALK fusion • ROS1 fusion • RET rearrangement
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Tepmetko (tepotinib) • Idafang (ivonescimab)
10d
A Post Approval Commitment Study on Tabrecta® (Capmatinib) in South Korea (clinicaltrials.gov)
P=N/A, N=44, Recruiting, Novartis Pharmaceuticals | N=250 --> 44
Enrollment change
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Tabrecta (capmatinib)
10d
Savolitinib in MET-amplified gastric or gastroesophageal junction adenocarcinoma: a phase 2 trial. (PubMed, Nat Med)
Savolitinib monotherapy showed encouraging antitumor activities and a tolerable safety profile in heavily treated, later-line METamp G/GEJ cancers, supporting further investigation in randomized controlled trials. ClinicalTrials.gov identifier: NCT04923932 .
P2 data • Journal
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MET (MET proto-oncogene, receptor tyrosine kinase)
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MET amplification
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Orpathys (savolitinib)
13d
An Effective and Systematic Strategy for Metabolic Profiling of Golvatinib In Vitro by Combining UHPLC-MS/MS and UHPLC-Q-Orbitrap-HRMS. (PubMed, J Sep Sci)
Detection was carried out by multiple reaction monitoring mode using the transitions m/z 634.3→184.2 for golvatinib and m/z 650.3→200.2 for golvatinib N-oxide. Further study demonstrated that CYP3A4 was the principal enzyme involved in metabolizing golvatinib. To the best of our knowledge, this is the first report combining ultra-high-performance liquid chromatography-tandem MS (UHPLC-MS/MS) with UHPLC-Quadrupole-Orbitrap-HRMS for profiling golvatinib metabolism in vitro, thereby laying a foundation for subsequent pharmacokinetic study.
Preclinical • Journal
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CYP3A4 (Cytochrome P450, family 3, subfamily A, polypeptide 4)
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larotinib (Z650) • golvatinib (E7050)
14d
Clinical response in advanced non-small cell lung cancer with high PD-L1 expression and MET exon 14 skipping mutation: a case analysis of overcoming immunotherapy resistance and literature review. (PubMed, Front Oncol)
Following discontinuation of Savolitinib due to drug-induced liver injury, Tislelizumab, previously associated with resistance, was reintroduced as a "rechallenge" successfully re-establishing disease control. Coupled with a systematic review of pertinent literature, this article explores the clinical features, therapeutic challenges, potential resistance mechanisms, and management approaches for such patients. It also outlines future research avenues for combination or sequential therapies, aiming to furnish a more holistic reference for clinical decision-making.
Review • Journal • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • MET (MET proto-oncogene, receptor tyrosine kinase)
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PD-L1 expression • PD-L1 overexpression • MET exon 14 mutation • MET expression
|
Tevimbra (tislelizumab-jsgr) • Orpathys (savolitinib)
15d
SACHI: Study on Savolitinib Combined With Osimertinib in Treatment of Advanced NSCLC With MET Amplification (clinicaltrials.gov)
P3, N=216, Completed, Hutchison Medipharma Limited | Active, not recruiting --> Completed | Trial completion date: Dec 2025 --> Aug 2025 | Trial primary completion date: Dec 2025 --> Aug 2025
Trial completion • Trial completion date • Trial primary completion date
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MET (MET proto-oncogene, receptor tyrosine kinase)
|
EGFR mutation • MET amplification
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cisplatin • Tagrisso (osimertinib) • carboplatin • pemetrexed • Orpathys (savolitinib)
15d
Trial suspension
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mTOR (Mechanistic target of rapamycin kinase)
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Erbitux (cetuximab) • Rybrevant (amivantamab-vmjw) • Rybrevant Faspro (amivantamab and hyaluronidase-lpuj)
19d
Comprehensive characterization of MET exon 14 skipping mutations in non-small cell lung cancer. (PubMed, Respir Res)
This study provides a comprehensive characterization of METΔex14 in NSCLC, revealing its dual role as a primary driver of oncogenesis and a potential resistance mechanism to EGFR/ALK inhibitors. The identification of concurrent genetic alterations and potential resistance mechanisms enhances our molecular understanding of treatment responses. These findings highlight the need for further investigation into targeted therapies that consider the genomic complexity of METΔex14 to improve treatment efficacy and patient outcomes.
Journal
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TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • FGFR3 (Fibroblast growth factor receptor 3) • TACC3 (Transforming acidic coiled-coil containing protein 3) • CDK4 (Cyclin-dependent kinase 4)
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KRAS mutation • MET amplification • MET exon 14 mutation
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GeneseeqPrime™ • GeneseeqPrime™HRD
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Xalkori (crizotinib) • Orpathys (savolitinib)