c-met-in-2

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

EGFR/c-Met-IN-2 (Compound H-22) is a dual inhibitor of EGFR/c-Met that arrests the G2/M phase to inhibit cell proliferation and demonstrates antitumor activity [1].

c-Met-IN-23 (Compound 12g) functions as a c-Met inhibitor with an IC50 of 0.052 μM against c-Met. It also inhibits the MDR1 and MRP1/2 pumps in cancerous HepG2 and BxPC3 cells. As such, c-Met-IN-23 serves as an anticancer agent.

c-Met-IN-21 (compound 54) is a c-Met inhibitor with an IC50 value of 0.45 nM and exhibits antitumor activity in vivo.

c-Met-IN-22 (compound 51am) is an orally active c-Met inhibitor with an IC50 value of 2.54 nM. It exhibits both antiproliferative and antitumor activities and can induce apoptosis.

c-Met-IN-24 (compound 3g) serves as a dual-target inhibitor for STAT-3 (=4.7 μM) and c-MET (=12.67 μM), exhibiting anticancer properties. It arrests the G2/M cell cycle and induces apoptosis in SNB-75 cells, making it applicable in the research of central nervous system cancers.

c-Met-IN-26 (compound 1-170) is an effective inhibitor of c-Met, exhibiting an IC50 of 1.6 nM.

JNK-IN-8 (JNK Inhibitor XVI) is an irreversible JNK1/2/4 inhibitor (IC50: 4.7/18.7/1 nM) with over 10-fold selectivity compared to MNK2 and Fms, and no inhibition of Met, c-Kit, or PDGFRβ in the A375 cell line.

T-1840383 is an inhibitor of VEGF-induced VEGFR-2 phosphorylation and HGF-induced c-Met phosphorylation in vascular endothelial cells and cancer epithelial cells.

CSF1R-IN-2 is an oral-active SRC, MET and c-FMS inhibitor (IC50s: 0.12 nM, 0.14 nM and 0.76 nM for SRC, MET and c-FMS respectively).

Altiratinib (DCC-2701)(DCC-2701) is a novel c-MET/TIE-2/VEGFR inhibitor; effectively reduce tumor burden in vivo and block c-MET pTyr(1349)-mediated signaling, cell growth and migration as compared with an HGF antagonist in vitro.

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.

Merestinib (LY2801653) is an orally available, small molecule inhibitor of the proto-oncogene c-Met (Ki: 2 nM) with potential antineoplastic activity. Merestinib electively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing the constitutively activated c-Met protein.

1. Herbacetin induces apoptosis in HepG2 cells, by ROS and PI3K/Akt pathway. 2. Herbacetin suppresses the HGF-induced motility of human breast cancer MDA-MB-231 cells by inhibiting c-Met and Akt phosphorylation.

c-Met-IN-11 is a potent inhibitor of c-MET (IC50: 41.4 nM) and VEGFR-2 (IC50: 71.1 nM).

Golvatinib (E-7050) is an orally bioavailable dual kinase inhibitor of c-Met (hepatocyte growth factor receptor) and VEGFR-2 (vascular endothelial growth factor receptor-2) tyrosine kinases with potential antineoplastic activity. c-Met/VEGFR kinase inhibitor E7050 binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of tumor cell types and play important roles in tumor cell growth, migration and angiogenesis.

Foretinib phosphate is an orally bioavailable small molecule with potential antineoplastic activity. MET/VEGFR2 inhibitor GSK1363089 binds to and selectively inhibits hepatocyte growth factor (HGF) receptor c-MET and vascular endothelial growth factor receptor 2 (VEGFR2), which may result in the inhibition of tumor angiogenesis, tumor cell proliferation and metastasis. The proto-oncogene c-MET has been found to be over-expressed in a variety of cancers.

KRC-108 is a multiple kinase inhibitor. KRC-108 is a potent inhibitor of Ron, Flt3 and TrkA as well as c-Met. KRC-108 inhibited oncogenic c-Met M1250T and Y1230D more strongly than wild type c-Met. The anti-proliferative activity of KRC-108 was measured by performing a cytotoxicity assay on a panel of cancer cell lines. The GI(50) values (i.e., 50% inhibition of cell growth) for KRC-108 ranged from 0.01 to 4.22 μM for these cancer cell lines. KRC-108 was also effective for the inhibition of tumor growth in human HT29 colorectal cancer and NCI-H441 lung cancer xenograft models in athymic BALB/c nu/nu mice. This molecule should serve as a useful lead for inhibitors targeting kinases and may lead to new therapeutics for the treatment of cancer. (source: Invest New Drugs. 2012 Apr;30(2):518-23. doi: 10.1007/s10637-010-9584-2. Epub 2010 Nov 16. ).

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.

MAPK-IN-2 (compound 3h) is an efficacious MAPK inhibitor with antineoplastic properties that significantly hinders proliferation across various cancer cell lines. It demonstrates robust suppression of the MAPK pathway (EGFR WT IC50 = 281 nM, c-MET IC50 = 205 nM, B-RAF WT IC50 = 112 nM, CDK4/6 IC50 = 95 and 184 nM, respectively) and exhibits pronounced activity against mutated forms of EGFR and B-RAF (EGFR T790M IC50 = 69 nM and B-RAF V600E IC50 = 83 nM) [1].

VEGFR-2/c-Met-IN-1 is a dual inhibitor of VEGFR-2 and c-Met, with IC50 values of 138 nM and 74 nM, respectively, demonstrating antitumor activity [1].

H-Met-Val-OH is a dipeptide composed of an N-terminal methionine and a C-terminal valine residue that demonstrates inhibitory effects on recombinant flavin-containing monooxygenases FMO1 and FMO3. H-Met-Val-OH also shows potential in promoting neurite outgrowth, suggesting its relevance in neuroregenerative and enzymatic modulation studies involving FMO-catalyzed metabolic pathways.

Herbacetin (Standard) is a reference standard for research and analysis in studies involving Herbacetin. 1. Herbacetin induces apoptosis in HepG2 cells, by ROS and PI3K/Akt pathway. 2. Herbacetin suppresses the HGF-induced motility of human breast cancer MDA-MB-231 cells by inhibiting c-Met and Akt phosphorylation.