Met
Met, the hepatocyte growth factor receptor, is a receptor tyrosine kinase that integrates growth, survival, migration, and tissue-remodelling cues during morphogenesis, wound repair, organ homeostasis, and cancer metastasis[1]. Mechanistically, HGF binding activates c-Met and downstream signaling programs linked to proliferation, motility, invasion, and survival[2]. In disease models, aberrant MET activation supports tumor growth and metastatic progression, making HGF/MET signaling a practical axis for cancer biology and drug-response studies[3]. Compared with the related HGF isoform NK1, full-length HGF activates c-Met through an asymmetric complex, whereas NK1 forms a symmetric c-Met signaling complex[4]. For experimental applications, MET inhibitors and HGF/MET-blocking agents provide tools to test kinase-dependent signaling, invasion, and therapeutic vulnerability in MET-driven models[5].
References:
- [1]. Trusolino L, et al. MET signalling: principles and functions in development, organ regeneration and cancer. Nat Rev Mol Cell Biol. 2010 Dec;11(12):834-48. [Content Brief]
- [2]. Birchmeier C, et al. Met, metastasis, motility and more. Nat Rev Mol Cell Biol. 2003 Dec;4(12):915-25. [Content Brief]
- [3]. Gherardi E, et al. Targeting MET in cancer: rationale and progress. Nat Rev Cancer. 2012 Jan 24;12(2):89-103. [Content Brief]
- [4]. Uchikawa E, et al. Structural basis of the activation of c-MET receptor. Nat Commun. 2021 Jul 1;12(1):4074. [Content Brief]
- [5]. Comoglio PM, et al. Drug development of MET inhibitors: targeting oncogene addiction and expedience. Nat Rev Drug Discov. 2008 Jun;7(6):504-16. [Content Brief]
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Met Related Products (36)
Related Products (36)
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Antibodies (3)
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Cabozantinib
0 ImagesSynonyms: XL184; BMS-907351Cabozantinib is a potent and orally active inhibitor of VEGFR2 and MET, with IC50 values of 0.035, and 1.3 nM, respectively. Cabozantinib displays strong inhibition of KIT, RET, AXL, TIE2, and FLT3 (IC50=4.6, 5.2, 7, 14.3, and 11.3 nM, respectively). Cabozantinib shows antiangiogenic activity. Cabozantinib disrupts tumor vasculature and promotes tumor and endothelial cell apoptosis.
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Capmatinib
0 ImagesSynonyms: INC280; INCB28060Capmatinib (INC280; INCB28060) is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib is largely metabolized by CYP3A4 and aldehyde oxidase.
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JNJ-38877605
0 ImagesJNJ-38877605 is an orally active ATP-competitive inhibitor of c-Met with an IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases. JNJ-38877605 inhibits c-Met phosphorylation and regulates lipid accumulation. JNJ-38877605 can be used for tumor and metabolic disease reseach.
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PARP1/c-Met-IN-3
0 ImagesCat. No.: HY-181928CAS No.: 3123529-62-1PARP1/c-Met-IN-3 (Compound L19) is a selective c-Met and PARP1 inhibitor, with an IC50 of 5.4 nM against c-Met and an IC50 of 3.7 nM against PARP1. PARP1/c-Met-IN-3 inhibits PARP2 enzymatic activity with an IC50 of 4.52 nM, and shows no specificity for PARP1 and PARP2. PARP1/c-Met-IN-3 induces cell cycle arrest and apoptosis. PARP1/c-Met-IN-3 exhibits anti-tumor activity against triple-negative breast cancer.
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c-Met-IN-31
0 ImagesCat. No.: HY-181776c-Met-IN-31 is a c-Met inhibitor with an IC50 value of 0.021 μM. c-Met-IN-31 also inhibits VEGFR-2 and EGFR activities, with IC50 values of 0.32 μM and 9.3 μM, respectively. c-Met-IN-31 inhibits cancer cell proliferation. c-Met-IN-31 suppresses neovascularization in the chick chorioallantoic membrane (CAM) assay, exhibiting in vivo anti-angiogenic activity. c-Met-IN-31 can be used in research related to breast cancer and lung cancer.
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PROTAC c-Met degrader-1
0 ImagesPROTAC c-Met degrader-1 is a selective and orally active c-Met PROTAC degrader with a DC50 of 6.21 nM against c-Met. PROTAC c-Met degrader-1 induces CRBN-dependent ubiquitination and proteasomal degradation of c-Met. PROTAC c-Met degrader-1 induces G0/G1 phase arrest in c-Met-dependent cancer cells. PROTAC c-Met degrader-1 kills c-Met-dependent cancer cells. PROTAC c-Met degrader-1 inhibits tumor growth in animal models. PROTAC c-Met degrader-1 can be used for the research of gastric cancer.
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c-Met-IN-24
0 ImagesCat. No.: HY-162803c-Met-IN-24 (compound 3g) is a dual-target inhibitor of STAT-3 (=4.7 μM) and c-MET (=12.67 μM) with anticancer activity. c-Met-IN-24 arrests the G2/M cell cycle and induces apoptosis in SNB-75 cells. c-Met-IN-24 can be used in the study of central nervous system cancers.
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c-Met-IN-16
0 ImagesCat. No.: HY-120908CAS No.: 1208248-23-0c-Met-IN-16 is a c-Met inhibitor that can be used for cancer research.
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KRC-108
0 ImagesCat. No.: HY-123237CAS No.: 1146944-35-5KRC-108, an aminopyridine, is an orally active multiple kinase inhibitor with IC50s of 80 nM, 23 nM, 3 nM, 70 nM, 30 nM, 39 nM for c-Met, c-Met M1250T, c-Met Y1230D, Ron, Flt3 and TrkA, respectively. KRC-108 induces cell cycle arrest, apoptotic cell death, and autophagy. KRC-108 exhibits anti-tumor activity in vivo in HT29 colorectal cancer, NCI-H441 lung cancer xenograft models in athymic BALB/c nu/nu mice.
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Taligantinib
0 ImagesCat. No.: HY-177134CAS No.: 2243235-80-3Taligantinib (Compound Example 70) is an orally active and selective dual inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2) and hepatocyte growth factor receptor (c-Met). Taligantinib suppresses tumor angiogenesis and cell proliferation. Taligantinib is promising for research of solid tumors such as non-small cell lung cancer and hepatocellular carcinoma.
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