c met IN 1

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

EGFR/c-Met-IN-1 (compound TS-41) is a dual inhibitor targeting EGFR and c-Met, with IC50 values of 68.1 nM for EGFRL858R and 0.26 nM for c-Met. EGFR/c-Met-IN-1 induces apoptosis and cell cycle arrest in A549-P cells, and reduces phosphorylation of EGFR, c-Met, and downstream AKT. This compound effectively inhibits tumor growth both in vitro and in vivo.

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].

PARP1/c-Met-IN-1 (Compound 16) serves as a selective dual inhibitor targeting both 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 at the G2/M phase in MDA-MB-231 cells. Furthermore, PARP1/c-Met-IN-1 displays notable antitumor activity in mouse models [1].

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.

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.

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

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.

c-Met-IN-15 exhibits antibacterial activity.

c-Met-IN-12 is a selective, orally active type II c-Met kinase inhibitor (IC50: 10.6 nM). c-Met-IN-12 is a high inhibitor of AXL, Mer and TYRO3 kinases (>80% inhibition at 1 μM). c-Met-IN-12 can be used as a scaffold to further enhance kinase selectivity. c-Met-IN-12 exhibits anti-tumour activity.

c-Met-IN-16, a c-Met inhibitor, is utilized in cancer research.

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-IN-10 is a potent c-Met kinase inhibitor (IC50: 16 nM). c-Met-IN-10 inhibits the activity of cancer cells A549, H460 and HT-29, and inhibits A549 cell movement by inhibiting HT-29 cell colony formation, which in turn induces apoptosis in HT-29 and A549 cells. c-Met-IN-10 can be used in anticancer studies. -Met-IN-10 is capable of being used in anticancer studies.

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

c-Met-IN-13 is a potent inhibitor of c-Met (IC50: 2.43 nM) that exhibits significant cytotoxicity and anti-proliferative effects against cancer cells in a concentration-dependent and time-dependent manner, demonstrating therapeutic potential against cancer.

c-Met-IN-14, a N-sulfonylamidine-based derivative, is a selective c-Met kinase inhibitor with an IC50 value of 2.89 nM. It exhibits anticancer properties by inhibiting c-Met phosphorylation and arresting the cell cycle at the G2/M phase. Additionally, c-Met-IN-14 promotes dose-dependent apoptosis in A549 cells.

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.

ABBV-969 Payload (Br-Val-Ala-NH2-bicyclo[1.1.1]pentane-7-MAD-MDCPT) is a drug-linker conjugate employed in the synthesis of antibody-drug conjugates (ADCs). The ABBV-969 Payload contains a Topoisomerase I inhibitor molecule and a chemical linker, enabling coupling with anti-c-Met antibodies to generate ABBV-969 ADCs with targeted anticancer activity.

EGFR-IN-8, a dual inhibitor targeting both EGFR and c-Met, shows potential as a promising candidate for further development in treating EGFR TKI-resistant NSCLC.

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).