Catalog No.
Product Name
Application
Product Information
Citations
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TRKA Inhibitor
ONO-7579 is an orally bioavailable inhibitor targeting TRKA, primarily inhibiting its phosphorylation to reduce tumor growth. In studies with colorectal cancer cell line KM12, it exhibits an EC50 of 17.6 ng/g, indicating that this concentration effectively reduces phosphorylated TRKA activity by 50%. ONO-7579 is useful in cancer research, particularly in exploring therapeutic strategies against tumors reliant on TRKA signaling. -
TrkA Inhibitor
TrkA-IN-8 is a potent TrkA inhibitor with a Kd value of 3.3 µM. This compound demonstrates concentration-dependent inhibition of cell proliferation in lung cancer cell lines, particularly in non-small cell lung cancer. TrkA-IN-8 is valuable for research applications aimed at understanding the role of TrkA signaling in oncogenesis and therapeutic resistance. -
Ligands for Target Protein for PROTAC
GNF-8625 is a potent TRK inhibitor that functions by targeting TRK receptor tyrosine kinases, specifically TRKA, TRKB, and TRKC, with IC50 values of 0.8 nM, 22 nM, and 5.4 nM, respectively. This compound can be utilized in conjunction with Thalidomide to create a PROTAC degrader, enabling targeted protein degradation. GNF-8625 is valuable in research applications investigating TRK-mediated pathways and offers potential in therapeutic strategies for cancers involving aberrant TRK signaling. -
TrkA Inhibitor
VMD-928 is an orally active, allosteric, and irreversible inhibitor targeting tropomyosin receptor kinase A (TrkA). By blocking the downstream signaling pathways initiated by nerve growth factor (NGF) binding, VMD-928 inhibits cell proliferation and invasion while promoting cancer cell apoptosis. This compound is of significant interest in research related to various cancers, including prostate cancer, thymic carcinoma, mesothelioma, squamous cell carcinoma of the head and neck, lung squamous cell carcinoma, ovarian cancer, and hepatocellular carcinoma. -
Src-FAK-Paxillin Inhibitor
JP-153 is a Src-FAK-Paxillin signaling inhibitor that specifically targets the Src-dependent phosphorylation of paxillin at tyrosine 118, leading to downstream inhibition of Akt activation at serine 473. This compound effectively reduces VEGF-induced migration and proliferation in retinal endothelial cells, making it a valuable tool for studying neovascular eye diseases. Researchers can utilize JP-153 to explore the molecular mechanisms underlying angiogenesis and potential therapeutic interventions. -
VEGFR2/FAK Inhibitor
ZINC09875266 is a dual inhibitor that specifically targets Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) and Focal Adhesion Kinase (FAK). This compound demonstrates potent inhibitory activity that can suppress angiogenesis and cancer cell proliferation. Research applications include studying tumor growth and metastasis in various cancer models. -
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). -
Tyrosine Kinase Inhibitor
Zurletrectinib is a potent tyrosine kinase inhibitor that selectively targets TRK kinases (TRKA IC50 = 0.81 nM; TRKB IC50 = 0.145 nM; TRKC IC50 = 0.184 nM). Its enhanced binding affinity results in superior efficacy, especially against various resistance mutations (effectively targeting 13 out of 18 known mutations). This compound is particularly useful for research applications related to glioma and exploring TRK signaling pathways in tumor biology. -
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. -
ALK Inhibitor
SMU-B is a potent orally active inhibitor of anaplastic lymphoma kinase (ALK) with an IC50 of less than 0.5 nM, along with c-ros oncogene 1 (ROS1) and c-MET, exhibiting IC50 values of 1.87 nM and 28.9 nM for AXL. This compound demonstrates significant antiproliferative activity against MKN45, H1993, and H441 cell lines, with IC50s of 0.02 μM, 1.58 μM, and 2.82 μM, respectively. Additionally, SMU-B has shown promising antitumor efficacy in various mouse models, highlighting its potential for cancer research applications. -
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. -
c-Met Inhibitor
c-Met-IN-17 is a potent inhibitor of c-Met kinase, exhibiting an IC50 of 0.031 μM. This compound demonstrates significant biological activity and serves as a valuable tool in anticancer research. Additionally, c-Met-IN-17 features an alkyne group, facilitating its use as a click chemistry reagent through copper-catalyzed azide-alkyne cycloaddition (CuAAc) with azide-containing molecules. -
c-Met Inhibitor
AC-386 is a potent c-Met inhibitor with an IC50 value of 7.42 nM. It demonstrates significant antiproliferative effects against specific cancer cell lines, making it a valuable tool for investigating mechanisms of anti-cancer resistance. This compound is particularly useful for research in cancer biology and therapeutic development targeting c-Met pathways. -
EGFR/c-Met Inhibitor
EGFR/c-Met-IN-2 is a dual inhibitor targeting the epidermal growth factor receptor (EGFR) and c-Met. This compound effectively inhibits cell proliferation by inducing a G2/M cell cycle arrest, demonstrating significant antitumor activity. It is suitable for research applications investigating cancer biology and therapeutic responses in tumors driven by EGFR and c-Met signaling pathways. -
PROTAC c-Met Degrader
PROTAC c-Met degrader-2 is a PROTAC-based degrader that selectively targets c-Met for degradation through the ubiquitin-proteasome pathway, exhibiting a DC50 of 50 nM. This compound employs a unique linkage incorporating a CRBN ligand derived from Thalidomide, facilitating targeted protein degradation. It serves as a valuable tool for researching c-Met-related pathways and their implications in various cancers, enhancing the understanding of therapeutic strategies involving c-Met modulation. -
c-Met Inhibitor
c-Met-IN-13 is a potent inhibitor of the c-Met receptor with an IC50 value of 2.43 nM. This compound exhibits significant cytotoxic effects against cancer cells, demonstrating antiproliferative activity that is both concentration- and time-dependent. c-Met-IN-13 is valuable for research applications focused on cancer biology and therapeutic development targeting c-Met signaling pathways. -
c-MET Inhibitor
c-Met-IN-11 is a selective inhibitor of c-MET and VEGFR-2. It demonstrates potent biological activity with IC50 values of 41.4 nM for c-MET and 71.1 nM for VEGFR-2, making it a valuable tool for studying signaling pathways in cancer. This compound is suitable for applications in cancer research, particularly in exploring the role of c-MET in tumor growth and metastasis. -
VEGFR-2/c-Met Inhibitor
VEGFR-2/c-Met-IN-2 is a selective inhibitor targeting VEGFR-2 and c-Met, demonstrating IC50 values of 83 nM and 48 nM, respectively. This compound exhibits significant cytotoxicity against the HCT-116 cell line, with an IC50 of 3.403 µM. Its potent inhibitory effects make it a valuable tool for research into angiogenesis and cancer metastasis. -
Type-III c-MET Inhibitor
c-Met-IN-18 is an ATP-competitive type-III c-MET inhibitor that effectively targets both wild-type and D1228V mutant forms of c-MET, with IC50 values of 0.013 µM and 0.20 µM, respectively. This compound is primarily utilized in research focused on c-MET-driven cancers. Additionally, c-Met-IN-18 features an alkyne moiety, enabling it to participate in copper-catalyzed azide-alkyne cycloaddition (CuAAc) reactions, allowing for diverse applications in chemical biology. -
c-Met Inhibitor
PF 04254644 is an orally active inhibitor of the c-Met receptor, also known as mesenchymal-epithelial transition factor (MET). It selectively targets the hepatocyte growth factor receptor, leading to significant biological effects, including myocardial degeneration in animal models. This compound serves as a valuable tool for research into cardiovascular diseases and cancer, facilitating the exploration of c-Met signaling pathways and therapeutic interventions. -
c-MET Inhibitor
Zgwatinib (SOMG-833) is a highly selective and ATP-competitive inhibitor of c-MET, exhibiting an IC50 of 0.93 nM. It demonstrates over 10,000-fold selectivity against 19 related tyrosine kinases, including c-MET family members. Zgwatinib effectively inhibits c-MET-mediated cell proliferation, making it a promising candidate for research focused on c-MET-driven human cancers. -
c-Met Inhibitor
KRC-00715 is a potent oral inhibitor of c-Met with an IC50 of 9.0 nM, exhibiting high selectivity for gastric cancer cells. This compound effectively induces G1/S phase arrest in c-Met-overexpressing cell lines, resulting in diminished downstream signaling through Akt and Erk pathways as well as reduced c-Met activity. In the gastric cancer cell line Hs746, KRC-00715 demonstrates an IC50 of 39 nM and shows significant efficacy in reducing tumor size in Hs746T xenograft mouse models, highlighting its potential application in cancer research and therapeutics. -
c-Met Inhibitor
SOMCL-863 is a selective and orally bioavailable c-Met inhibitor, demonstrating significant antitumor activity in both in vitro and in vivo models. This compound serves as a valuable tool in cancer research, aiding in the exploration of pathways involving c-Met and its role in tumor progression. -
c-Met Inhibitor
EMD 1204831 is a potent and selective inhibitor of the c-Met receptor tyrosine kinase, exhibiting an IC50 of 9 nM. This compound effectively suppresses c-Met activity, making it a valuable tool for investigating the role of c-Met in cancer biology. Its application can lead to insights into tumor growth, metastasis, and potential therapeutic strategies targeting c-Met dysregulation. -
c-Met/VEGFR-2 Inhibitor
T-1840383 is a highly potent ATP-competitive inhibitor targeting c-Met and VEGFR-2, demonstrating IC50 values of 1.9 nM for c-Met, 7.7 nM for VEGFR1, 2.2 nM for VEGFR2, and 5.5 nM for VEGFR3. This compound effectively inhibits key signaling pathways associated with cancer progression and angiogenesis. It is suitable for research applications focused on tumor growth and vascular development, making it a valuable tool in oncology and vascular biology studies. -
Stable Isotope
Crizotinib-d8 is a deuterated analog of Crizotinib, functioning as an ATP-competitive inhibitor of ALK and c-Met. This compound exhibits potent biological activity, with IC50 values of 20 nM and 8 nM, respectively, and effectively inhibits tyrosine phosphorylation of NPM-ALK and c-Met in cellular assays. Additionally, Crizotinib-d8 serves as an inhibitor of ROS1. This stable isotope is primarily utilized in pharmacokinetic studies and metabolic research involving Crizotinib to enhance understanding of its therapeutic mechanisms. -
RON Kinase/c-Met Inhibitor
LCRF-0004 is a potent inhibitor of RON kinase, exhibiting an IC50 value of 10 nM. Additionally, LCRF-0004 also demonstrates significant inhibitory activity against c-Met, with an IC50 of 12 nM. This compound is valuable for research in cancer biology, particularly in studies focusing on RON kinase and c-Met signaling pathways.
