Catalog No.
Product Name
Application
Product Information
Citations
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dual c-Met/Ron inhibitor
MK8033 Hcl is a novel and specific dual ATP competitive c-Met/Ron inhibitor (IC50=1 nM Wt c-Met) under investigation as a treatment for cancer. -
dual inhibitor for c-Met and EGFR
Norcantharidin (Endothall anhydride) is a synthetic anticancer compound which is a dual inhibitor for c-Met and EGFR in human colon cancers. -
PROTAC degrader
SJF-8240 (PROTAC 7) is a proteolysis-targeting chimera (PROTAC) designed to selectively degrade the receptor tyrosine kinase c-Met. It induces polyubiquitination and subsequent proteasomal degradation of c-Met, leading to effective inhibition of downstream signaling. SJF-8240 exhibits potent antiproliferative activity in GTL16 gastric cancer cells, with an IC₅₀ of 66.7 nM, making it a promising tool for targeted cancer therapy and c-Met–driven tumor research. -
MET Degrader
PRO-6E is a PROTAC that targets Cereblon to induce degradation of the MET protein. It achieves up to 81.9% degradation of MET at 1 μM in MKN-45 cells, effectively inhibiting tumor growth both in vitro and in vivo. Additionally, PRO-6E promotes apoptosis and cell cycle arrest, making it a valuable tool for research on MET-related oncogenic processes. -
PI3Kα/c-Met Inhibitor
DFX117 is a selective, orally active inhibitor targeting PI3Kα and c-Met tyrosine kinase. This compound effectively inhibits the PI3K/Akt/mTOR pathway, demonstrating significant antiproliferative activity against cancer cell lines such as NCI-H1975, NCI-H1993, and HCC827, with IC50 values ranging from 0.02 to 0.08 µM. DFX117 induces cell cycle arrest at the G0/G1 phase and promotes apoptosis in A549 and NCI-H1975 cells. Additionally, DFX117 exhibits notable antitumor efficacy in murine models, making it a valuable tool for cancer research. -
EGFR/c-Met Inhibitor
EGFR/c-Met-IN-1 is a dual inhibitor targeting both EGFR and c-Met, with IC50 values of 68.1 nM for EGFRL858R and 0.26 nM for c-Met. This compound induces apoptosis and causes cell cycle arrest in A549-P cells by downregulating the phosphorylation of EGFR, c-Met, and downstream AKT pathways. EGFR/c-Met-IN-1 demonstrates significant tumor growth inhibition in vitro and in vivo, making it a valuable reagent for cancer research focused on targeting these pathways. -
EGFR/c-Met Inhibitor
EGFR-IN-8 is a dual inhibitor of the epidermal growth factor receptor (EGFR) and c-Met, demonstrating potential efficacy against EGFR TKI-resistant non-small cell lung cancer (NSCLC). This compound offers a novel approach for effectively targeting resistance mechanisms in NSCLC, providing a valuable tool for oncological research and drug development. Its unique pharmacological profile positions it as a promising candidate for further investigation in cancer therapy. -
c-MET Kinase Inhibitor
Capmatinib hydrochloride is a selective c-MET kinase inhibitor that competitively targets ATP (IC50 = 0.13 nM). It effectively inhibits the phosphorylation of c-MET and its downstream signaling pathways, including ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib hydrochloride demonstrates potent antitumor activity by inhibiting c-MET-dependent tumor cell proliferation and migration, as well as inducing apoptosis. This compound is primarily metabolized by CYP3A4 and aldehyde oxidase, making it relevant for studies in cancer research and therapeutic development. -
c-MET Inhibitor
ABN401 is a selective ATP-competitive inhibitor of c-MET, exhibiting an IC50 of 10 nM. This compound demonstrates cytotoxic effects on MET-addicted cancer cells, with IC50 values ranging from 2 to 43 nM. ABN401 has shown oral bioavailability in preclinical models, with 42.1% to 56.2% in rats and 27.4% to 37.7% in dogs, and possesses significant antitumor activity, making it a valuable tool for cancer research and therapeutic development. -
c-MET Kinase Inhibitor
Capmatinib dihydrochloride hydrate is a potent, orally bioavailable inhibitor of c-Met kinase, exhibiting an IC50 value of 0.13 nM. This selective and ATP-competitive inhibitor disrupts the phosphorylation of c-MET and its downstream signaling pathways, including ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride hydrate demonstrates substantial antitumor activity by effectively inhibiting c-MET-dependent tumor cell proliferation, migration, and promoting apoptosis. Primarily metabolized by CYP3A4 and aldehyde oxidase, this compound is instrumental in cancer research focused on targeting c-Met-associated pathways. -
c-MET Kinase Inhibitor
Capmatinib dihydrochloride is a selective, ATP-competitive inhibitor of the c-MET kinase, exhibiting an IC50 of 0.13 nM. This compound effectively inhibits the phosphorylation of c-MET and its downstream effector pathways, including ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride demonstrates potent antitumor activity by suppressing c-MET-dependent tumor cell proliferation and migration, while also inducing apoptosis. The drug undergoes significant metabolism via CYP3A4 and aldehyde oxidase, making it relevant for studies involving c-MET-driven malignancies. -
c-Met/HDAC Inhibitor
c-Met/HDAC-IN-3 is a dual inhibitor targeting c-Met and histone deacetylase 1 (HDAC1), exhibiting IC50 values of 12.50 nM and 26.97 nM, respectively. This compound demonstrates significant biological activity by inducing apoptosis and causing cell cycle arrest at the G2/M phase. c-Met/HDAC-IN-3 serves as a valuable tool for research in cancer biology and therapeutic development, particularly in studies focused on synergistic inhibition of oncogenic pathways. -
Mer/c-met Inhibitor
Mer/c-Met-IN-1 is a potent dual inhibitor targeting Mer and c-Met with IC50 values of 1 nM and 19 nM, respectively. This compound effectively inhibits cancer cell proliferation and migration while inducing apoptosis. Mer/c-Met-IN-1 is valuable for research into various cancers, including colon cancer, providing insights into therapeutic strategies and mechanisms of action. -
c-Met/HDAC Inhibitor
c-Met/HDAC-IN-2 is a highly potent dual inhibitor targeting c-Met and histone deacetylases (HDACs), exhibiting IC50 values of 18.49 nM for HDAC1 and 5.40 nM for c-Met. This compound demonstrates significant antiproliferative effects against various cancer cell lines, notably inducing G2/M-phase cell cycle arrest and apoptosis in HCT-116 cells. c-Met/HDAC-IN-2 is a valuable tool for investigating mechanisms of anti-cancer resistance and exploring therapeutic strategies in oncology research. -
c-Met Inhibitor
c-Met-IN-9 is a potent c-Met kinase inhibitor with an IC50 value of 12 nM. This 4-phenoxypyridine derivative effectively induces apoptosis in cancer cells and exhibits significant antitumor activity. It is suitable for research applications focused on cancer biology and therapeutic development targeting the c-Met signaling pathway. -
c-Met Inhibitor
LAH-1 is a potent inhibitor of c-Met, demonstrating oral bioavailability and favorable membrane permeability with an IC50 of 49 nM. It exhibits significant anticancer activity by inducing apoptosis and inhibiting cellular migration and invasion. This compound is useful in research applications focused on cancer therapeutics and the modulation of c-Met signaling pathways. -
c-Met Kinase Inhibitor
c-Met-IN-10 is a highly potent inhibitor of the c-Met kinase, exhibiting an IC50 value of 16 nM. This compound demonstrates significant inhibitory activity against various cancer cell lines, including A549, H460, and HT-29, with IC50 values ranging from 0.56 to 1.59 μM. c-Met-IN-10 effectively suppresses colony formation in HT-29 cells, induces apoptosis in HT-29 and A549 cells, and inhibits A549 cell motility. This reagent is valuable for research applications focused on cancer biology and therapeutic interventions targeting c-Met pathways. -
c-Met Inhibitor
c-Met-IN-14 is a selective inhibitor of the c-Met kinase, classified as an N-sulfonylamidine derivative, with an IC50 value of 2.89 nM. This compound effectively inhibits c-Met phosphorylation, leading to the arrest of the cell cycle at the G2/M phase and demonstrating significant anticancer activity. Additionally, c-Met-IN-14 induces apoptosis in A549 lung cancer cells in a dose-dependent manner, making it a valuable tool for cancer research and therapeutic studies targeting c-Met signaling pathways. -
PROTAC c-Met Degrader
PROTAC c-Met Degrader-4 is a potent orally active PROTAC designed to target c-MET for degradation. It exhibits remarkable intracellular degradation potency with a DC50 value of less than 0.5 nM and effectively induces cell cycle arrest and apoptosis while inhibiting cell invasion and migration. This compound is particularly useful in cancer research, demonstrating the ability to suppress proliferation and inhibit the growth of various cancers, including non-small cell lung cancer and gastric cancer. In vivo studies also highlight its effectiveness in reducing tumor growth in Hs746T xenograft models. -
PARP1/c-Met Inhibitor
PARP1/c-Met-IN-1 is a selective dual inhibitor targeting PARP1 and c-Met, demonstrating IC50 values of 3.3 nM and 32.2 nM, respectively. This compound effectively induces apoptosis and causes cell cycle arrest in the G2/M phase in MDA-MB-231 cells. Additionally, PARP1/c-Met-IN-1 has shown significant antitumor activity in murine models, making it a valuable tool for cancer research and therapeutic development. -
VEGFR-2/c-Met Inhibitor
VEGFR-2/c-Met-IN-1 is a potent dual inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2) and c-Met, with IC50 values of 138 nM and 74 nM, respectively. This compound demonstrates significant antitumor activity, making it a valuable tool for cancer research. Its dual mechanism of action allows for the exploration of therapeutic strategies aimed at inhibiting tumor growth and angiogenesis. -
Anti-c-MET ADC
Telisotuzumab vedotin is an antibody-drug conjugate targeting c-MET, comprised of the anti-c-MET monoclonal antibody Telisotuzumab and the cytotoxic agent Monomethyl Auristatin E. This compound demonstrates antitumor efficacy in vivo while maintaining acceptable toxicity levels. It is primarily utilized in research focusing on non-small cell lung cancer (NSCLC), making it a valuable tool for investigating therapeutic approaches in this area. -
c-Met Agonist
Fosgonimeton is a c-Met agonist known to activate the hepatocyte growth factor receptor. This compound exhibits neuroprotective properties, demonstrating efficacy in models of neuroinflammation induced by LPS as well as in Alzheimer's disease models characterized by amyloid-beta pathology. Its potential applications extend to research aimed at understanding neurodegenerative diseases and therapeutic interventions. -
c-Met Receptor Activator
Terevalefim is a mimetic of hepatocyte growth factor (HGF) that selectively activates the c-Met receptor. This compound demonstrates significant biological activity in modulating cell proliferation, survival, and migration, making it a crucial tool in cancer research. Terevalefim is particularly relevant for studies focused on tumor microenvironment interactions and therapeutic targets in various malignancies. -
TAM/c-Met Inhibitor
PF-07265807 is a potent inhibitor of TAM receptors and the c-Met kinase, exhibiting IC50 values of 6.1 nM for AXL, 13.2 nM for MER, and 21.6 nM for TYRO3. This compound is primarily utilized in research focused on cancer biology, particularly in understanding tumor progression and metastasis. Its selective inhibition of specific tyrosine kinases offers valuable insights into therapeutic strategies targeting these pathways in oncology. -
C-Met Inhibitor
Dalmelitinib is a selective c-Met kinase inhibitor with an IC50 of 2.9 nM, targeting the ATP-binding region of the c-Met receptor. This compound effectively induces phosphorylation of MET while partially or completely inhibiting the phosphorylation of downstream signaling proteins AKT and ERK. Dalmelitinib demonstrates potent anti-proliferative effects on cancer cells with c-Met oncogene amplification, making it a valuable reagent for research applications in cancers such as human non-small cell lung cancer (NSCLC). -
c-Met/AXL Inhibitor
BPI-9016M is a potent, orally active dual inhibitor of c-Met and AXL tyrosine kinases. It demonstrates significant biological activity by suppressing tumor cell growth, migration, and invasion in lung adenocarcinoma. This compound is valuable for research applications targeting cancer signaling pathways and metastasis. -
c-MET Inhibitor
(rel)-Tivantinib is a potent and selective inhibitor of the receptor tyrosine kinase c-MET. This compound also targets GSK3α and GSK3β, which are involved in the cellular mechanisms associated with non-small cell lung cancer (NSCLC). Its inhibition of c-MET signaling pathways and modulation of GSK3 activity position (rel)-Tivantinib as a valuable tool for researching therapeutic strategies in cancer biology. -
c-Met PROTAC Degrader
PROTAC c-Met degrader-1 is a selective and orally active degrader targeting c-Met, exhibiting a DC50 of 6.21 nM. This compound promotes CRBN-dependent ubiquitination and subsequent proteasomal degradation of c-Met, effectively inducing G0/G1 phase arrest in c-Met-dependent cancer cells. Furthermore, PROTAC c-Met degrader-1 demonstrates significant anticancer activity by killing c-Met-dependent cells and inhibiting tumor growth in animal models, making it a valuable tool for research in gastric cancer. -
JNK/c-Met Inhibitor
JNK-IN-16 is a potent inhibitor of both JNK and c-Met, exhibiting IC50 values of 72 nM and 120 nM, respectively. This compound demonstrates significant anti-cancer activity, making it valuable for research in cancer biology and therapeutic development. Its dual inhibition profile allows for exploration in signaling pathways associated with tumor progression and metastasis. -
c-Met/HGFR Inhibitor
Meleagrin is a potent c-Met/HGFR inhibitor derived from the alkaloid roquefortine C, produced by fungi of the genus Penicillium. This compound exhibits significant antimicrobial and anti-proliferative activities, making it valuable in research focused on cancer biology. Meleagrin serves as a promising lead compound for targeting c-Met-dependent metastatic and invasive breast cancers, contributing to the development of novel therapeutic strategies. -
c-Met/TRK Inhibitor
1D228 is a potent c-Met/TRK inhibitor that exhibits significant antitumor activity. By inhibiting cyclin D1, 1D228 induces G0/G1 cell cycle arrest and effectively reduces cancer cell proliferation and migration. This compound is relevant for research applications focused on gastric, liver, and vascular tumors. -
ALK/c-Met/ROS1 Inhibitor
Crizotinib acetate is an orally bioavailable inhibitor targeting ALK, c-Met, and ROS1 through ATP competition. It demonstrates potent inhibition of tyrosine phosphorylation in cell-based assays, with IC50 values of 20 nM for ALK, 8 nM for c-Met, 24 nM for NPM-ALK, and 11 nM for c-Met. The compound has shown significant efficacy in inhibiting tumor growth, making it a valuable tool in cancer research and therapeutic applications targeting these pathways. -
c-Met inhibitor
PF-04217903 phenolsulfonate is a potent ATP-competitive inhibitor of the c-Met kinase with a Ki value of 4.8 nM for human c-Met. It demonstrates over 1,000-fold selectivity against a profile of 208 kinases, highlighting its specificity. This compound possesses antiangiogenic properties and is useful in research applications related to cancer therapy and the modulation of tumor microenvironments. -
c-Met Inhibitor
Tepotinib hydrochloride is a highly selective, reversible, ATP-competitive inhibitor of c-Met, exhibiting an IC50 of 3 nM and over 200-fold selectivity for c-Met compared to other kinases such as IRAK4, TrkA, Axl, IRAK1, and Mer. This compound effectively inhibits c-Met phosphorylation and promotes autophagy. Tepotinib hydrochloride demonstrates significant antitumor activity and is applicable in cancer research targeting c-Met-driven pathways. -
c-Met Inhibitor
c-Met-IN-16 is a potent inhibitor of the c-Met receptor tyrosine kinase, known to play a crucial role in tumor growth and metastasis. This compound demonstrates significant biological activity in targeting aberrant c-Met signaling pathways associated with various cancers. c-Met-IN-16 is primarily used in cancer research to explore therapeutic strategies and mechanisms of resistance in c-Met-driven malignancies. -
c-Met Kinase Inhibitor
c-Met-IN-15 is a selective inhibitor of c-Met kinase, a critical regulator of cell proliferation and survival. At a concentration of 10 μM, c-Met-IN-15 demonstrates 21.1% inhibition of c-Met kinase activity, making it a valuable tool for studying c-Met signaling pathways. This compound is suitable for research applications related to cancer biology, particularly in contexts involving c-Met dysregulation. -
c-Met Inhibitor
c-Met-IN-26 is a potent c-Met inhibitor, exhibiting an IC50 of 1.6 nM. This compound plays a crucial role in cancer research, targeting the c-Met signaling pathway to disrupt tumor proliferation and metastasis. Its high specificity makes it a valuable tool for studying the molecular mechanisms underlying c-Met-related oncogenesis and for evaluating potential therapeutic interventions. -
VEGFR-2/c-Met Inhibitor
Taligantinib is a selective dual inhibitor of vascular endothelial growth factor receptor 2 (VEGFR-2) and hepatocyte growth factor receptor (c-Met). This orally active compound effectively suppresses tumor angiogenesis and cell proliferation. Taligantinib is of particular interest in the research of solid tumors, including non-small cell lung cancer and hepatocellular carcinoma, making it a valuable tool for cancer biology studies. -
Type IIb c-Met Inhibitor
KIN-8741 is a highly selective Type IIb c-Met inhibitor that targets the c-Met kinase, effectively addressing various mutations associated with this oncogenic pathway. Demonstrating significant antitumor activity, KIN-8741 is particularly effective in models of non-small cell lung cancer characterized by MET gene amplification and exon 14 deletions. This reagent is suitable for research applications focusing on c-Met-driven cancers, especially in advanced tumors with MET exon 14 jump mutations and acquired drug resistance. -
c-Met Inhibitor
c-Met-IN-19 is a potent c-Met inhibitor with an IC50 of 1.99 nM. This compound exhibits significant cytotoxic effects on various cancer cell lines, including A549, HT-29, SGC-7901, and MDA-MB-231, demonstrating IC50 values of 0.25, 0.36, 0.98, and 0.76 μM, respectively. c-Met-IN-19 is valuable for research applications focused on cancer therapies targeting the c-Met pathway. -
c-Met/ALK Inhibitor
CM-118 is a selective inhibitor of c-Met and ALK, targeting the HGF-induced c-Met phosphorylation and impairing ALK phosphorylation in key variants including EML4-ALKv1, ALK F1174L, and EML4-ALKv1 L1196M. With IC50 values of 0.92, 1.25, 1.9, and 3.5 μM respectively, CM-118 demonstrates significant anticancer activity against tumors reliant on c-Met or ALK oncogenic pathways. This compound is useful for investigating therapeutic strategies in cancers driven by these targets. -
c-Met Inhibitor
c-Met-IN-21 is a highly potent c-Met inhibitor, exhibiting an IC50 value of 0.45 nM. This compound demonstrates significant anti-tumor efficacy in vivo, making it a valuable tool for research in cancer biology and therapeutic applications targeting c-Met signaling pathways. Its potent inhibitory activity offers the potential for studying tumor proliferation and metastasis mechanisms. -
c-MET Inhibitor
(3S,4S)-Tivantinib is a selective inhibitor of the receptor tyrosine kinase c-MET. In addition to its primary target, (3S,4S)-Tivantinib also inhibits glycogen synthase kinase 3 alpha (GSK3α) and glycogen synthase kinase 3 beta (GSK3β), which are critical in the pathogenesis of non-small cell lung cancer (NSCLC). This compound is utilized in research focused on understanding c-MET-related signaling pathways and evaluating therapeutic strategies for NSCLC. -
MET/VEGFR2/KDR Inhibitor
Foretinib phosphate is a potent inhibitor of the c-MET and VEGFR2 receptors, which play crucial roles in tumor growth and angiogenesis. By selectively targeting hepatocyte growth factor receptor c-MET and vascular endothelial growth factor receptor 2, Foretinib phosphate exhibits significant anti-tumor activity, potentially reducing tumor cell proliferation and metastasis. Its unique mechanism offers distinct advantages over other treatments, making it a valuable tool for research in oncology, particularly in studies related to lung cancer and the pathways involving MEK1/2, FER, and AURKB. -
HGF/c-Met Inhibitor
Norleual is a hepatocyte growth factor (HGF) and c-Met inhibitor with an IC50 of 3 pM. As an angiotensin IV analog and AT4 receptor antagonist, Norleual demonstrates significant antiangiogenic properties. This compound is utilized in research focused on cancer biology, vascular biology, and angiogenesis-related studies. -
c-Met Inhibitor
c-Met-IN-12 is a potent and selective type II c-Met kinase inhibitor, exhibiting an IC50 of 10.6 nM. This compound effectively inhibits c-Met as well as AXL, Mer, and TYRO3 kinases, demonstrating an inhibition rate exceeding 80% at 1 μM concentration. c-Met-IN-12 shows promising antitumor efficacy and serves as a valuable scaffold for the development of further kinase selectivity enhancements in cancer research applications.
