c-met

c-Met inhibitor 1 is a c-Met receptor signaling pathway inhibitor, used for the treatment of cancer including glioblastoma, gastric, and pancreatic cancer.

C-Met inhibitor D9 is a c-Met kinase inhibitor.

c-met-IN-1 is a potent and selective c-Met inhibitor (IC50: 1.1 nM) with antitumor activity.

c-Met-IN-2 is a selective and orally available c-Met inhibitor (IC50: 0.6 nM) exhibiting antitumor activity.

C-Met-IN-18, an ATP-competitive type-III inhibitor, targets both wild-type (WT) and D1228V mutant c-MET with IC50 values of 0.013 µM and 0.20 µM, respectively. It is utilized in research pertaining to c-MET-driven cancers [1].

c-Met-IN-17 is a potent inhibitor of c-Met kinase with an IC50 of 0.031 μM, making it relevant for anticancer research. [1]

c-Met-IN-19 (Compound 21j) is a potent c-Met inhibitor with an IC50 of 1.99 nM, demonstrating cytotoxic effects on various cancer cell lines, including A549, HT-29, SGC-7901, and MDA-MB-231, with IC50 values of 0.25, 0.36, 0.98, and 0.76 μM, respectively [1].

c-Met/HDAC-IN-4, a dual inhibitor of c-Met/HDAC, exhibits an IC 50 value of 28.92 nM for c-Met. This compound effectively induces G 0 /G 1 phase cell cycle arrest and apoptosis in MDA-MB-231 breast cancer cells. Additionally, c-Met/HDAC-IN-4 suppresses both the proliferation and invasion of breast cancer cell lines.

PROTACc-Met degrader-1 (Compound Met-DD4) is an orally effective PROTAC degrader targeting c-Met with a DC50 of 6.21 nM. It inhibits the proliferation of c-Met-addicted MKN-45 cells with an IC50 of 4.37 nM and causes cell cycle arrest in the G0/G1 phase. In a xenograft mouse model using MKN-45 cells, PROTACc-Met degrader-1 demonstrates antitumor activity.

PROTACc-Met degrader-2 (PROTAC2) is a c-Met degrader developed using PROTAC technology, with a DC50 value of 50 nM.

C-Met/Axl-IN-1 (Compound 22a) is an oral, selective type II c-Met/Axl inhibitor with IC50 values of 1 nM and 10 nM, respectively. It effectively suppresses tumor cell proliferation, induces cell cycle arrest, and apoptosis (apoptosis), showcasing potent anti-tumor activity.

PROTACc-Met degrader-3 (Compound 22b) is a c-Met PROTAC degrader. It facilitates the ubiquitination and degradation of c-Met, with a DC50 of 0.59 nM in EBC-1 cells. PROTACc-Met degrader-3 is applicable in lung cancer research.

c-Met degrader-1 (Compound H11) is an orally active c-Met degrader that operates via the ubiquitin-proteasome system. It exhibits anti-hepatocellular carcinoma (HCC) activity and hampers tumor growth in MHCC97H xenografts. Additionally, c-Met degrader-1 suppresses the proliferation of HCC cells, disrupts the cell cycle, and induces apoptosis. It may also potentially overcome resistance to Type I c-Met inhibitors.

c-Met ligand-Linker Conjugate 1 is a Target Protein Ligand-Linker Conjugate that consists of a c-Met ligand and a PROTAC linker, capable of recruiting E3 ligase. This compound is used in the synthesis of PROTACc-Met degrader-5.

c-Met ligand-Linker Conjugate 2 is a synthetic target protein ligand-linker complex used in the synthesis of PROTACs, such as PROTACc-Met degrader-6. PROTACc-Met degrader-6 is a c-Met PROTAC degrader that exhibits antitumor activity.

PROTACc-Met degrader-5 (Compound D19) is an orally active c-Met PROTAC degrader, with a DC50 of 0.42 nM in EBC-1 cells and 0.32 nM in Hs746T cells. It effectively induces apoptosis, causes G1 cell cycle arrest, and inhibits cell migration and invasion. This compound shows strong antiproliferative and degradative effects on c-Met-dependent cancer cells and those resistant to Tepotinib.

PROTACc-Met degrader-6 is a potent and orally active c-Met PROTAC degrader. It effectively promotes the degradation of c-Met protein, with DC50 values of 0.52 nM in EBC-1 cells and 0.45 nM in Hs746T cells. This compound almost completely abolishes the migration and invasion capabilities of tumor cells, significantly induces apoptosis (apoptosis), and arrests the cell cycle at the G0/G1 phase. PROTACc-Met degrader-6 is useful for studying various cancers, including non-small cell lung cancer and gastric cancer.

c-Met/HDAC-IN-2 is a potent dual inhibitor of c-Met and HDAC, exhibiting IC50 values of 5.40 nM for c-Met and 18.49 nM for HDAC1, respectively. It demonstrates antiproliferative effects on various cancer cell lines, induces G2/M-phase arrest, and triggers apoptosis in HCT-116 cells, making it a promising candidate for anti-cancer resistance research.

c-Met/HDAC-IN-3, a dual inhibitor targeting both c-Met and HDAC, exhibits potent inhibitory activity with IC50 values of 12.50 nM for c-Met and 26.97 nM for HDAC1. It induces apoptosis and causes cell cycle arrest in the G2/M phase.

Anti-HGFR/c-Met Antibody is a human-derived antibody expressed in CHO cells, targeting HGFR/c-Met. It possesses a huIgG1 heavy chain and a huλ light chain, with an estimated molecular weight (MW) of 150 kDa. For isotype control, refer to Human IgG1 kappa, Isotype Control.

Anti-c-Met/HGFR Antibody is a humanized IgG1 monoclonal antibody that targets c-Met.

Antiproliferative Against-3 (comp 33) demonstrates significant activity against Hela (IC 50 = 0.21 µM), A549 (IC 50 = 0.39 µM), and MCF-7 (IC 50 = 0.33 µM) cell lines. Additionally, it induces apoptosis in a dose-dependent manner by arresting A549 cells in the G1 phase.

Telisotuzumab(ABT-700) is a humanized recombinant antibody targeting the therapeutic hepatocyte growth factor receptor (MET) with high affinity for c-Met.Telisotuzumab has inhibitory effects on c-Met signaling and antitumor activity.

MK-2461 is a novel inhibitor that targets multiple proteins and competitively binds to ATP sites, specifically inhibiting the activated c-Met protein with an average inhibitory concentration (IC50) of 2.5 nM.