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.

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].

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.

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).

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-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.

MET Transcription-IN-1 (Compound C3) is an orally active inhibitor of MET transcription that efficiently binds to and stabilizes the G-quadruplex in the MET promoter region, thereby inhibiting c-Met expression. It can overcome resistance caused by specific c-Met mutations and effectively inhibits tumor cell proliferation, migration, and invasion, inducing cell cycle arrest and apoptosis. This compound exhibits antitumor activity and is applicable in the study of tumors such as non-small cell lung cancer.

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.

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

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

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).