c met IN 1

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

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].

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.

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.

Sitravatinib (MGCD516) is an inhibitor targeting multiple RTKs involved in driving sarcoma cell growth, including c-Met, c-Kit, PDGFRα β, PDGFR, and Axl.

Lmtk3-in-1 is a potent ATP-competitive lemur tyrosine kinase 3 (LMTK3) (Kd=2.5 μM) inhibitor that degrades LMTK3 through the ubiquitin proteasome pathway. LMTK3-IN-1 has shown anticancer activity in a variety of cancer cell lines and in vivo BC mouse models. LMTK3-IN-1 (10-20 μM) can induce the apoptosis of BC cell line.

SYN1143 (AMG-1) is a potent inhibitor of human RON and c-Met.In vitro kinase assays showed that compound I is a potent inhibitor of human RON and c-Met with IC50s of 9 and 4 nmol L, respectively.

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).

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.

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

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-Kit-IN-1 (DCC-2618) is an effective inhibitor of c-Met and c-Kit (IC50s<200 nM).

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.

RIPK3-IN-1 is a selective and potent RIPK3 inhibitor (IC50: 9.1 nM) that inhibits the activities of c-Met kinase, RIPK1 and RIPK2.RIPK3-IN-1 has potential tumorigenic activity and can be used to study apoptosis.

Axl-IN-8 (NO.1) is a potent AXL inhibitor (IC50 < 1 nM) and also inhibits c-MET (IC50: 1-10 nM).

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.

TAM&Met-IN-1 is a potent inhibitor of TAM and c-Met, acting on AXL (IC50: 6.1 nM), MER (IC50: 13.2 nM) and TYRO3 (IC50: 21.6 nM). TAM&Met-IN-1 can be used in anticancer studies.

WZ8040 is a novel mutant-selective irreversible EGFRT790M inhibitor, does not inhibit ERBB2 phosphorylation (T798I).

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].