c-Met/HDAC-IN-2

c-Met/HDAC-IN-2 is a highly potent c-Met and HDAC dual inhibitor with IC50s of 18.49 nM and 5.40 nM for HDAC1 and c-Met, respectively. c-Met/HDAC-IN-2 has antiproliferative activities against certain cancer cell lines. c-Met/HDAC-IN-2 can cause G2/M-phase arrest and induce apoptosis in HCT-116. c-Met/HDAC-IN-2 can be used for researching anti-cancer resistance[1].

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Signaling Pathways >> Cell Cycle/DNA Damage >> HDAC

Signaling Pathways >> Epigenetics >> HDAC

Signaling Pathways >> Protein Tyrosine Kinase/RTK >> c-Met/HGFR

HDAC1:18.49 nM (IC50)

c-Met:5.4 nM (IC50)

c-Met/HDAC-IN-2 (compound 14X) (0-20 μM; 72 hours) exhibits antiproliferative activities against HCT-116, MCF-7 and A549[1]. c-Met/HDAC-IN-2 (0.2-5 μM; 48 hours) induces of cancer cell apoptosis in a dose-dependent manner[1]. c-Met/HDAC-IN-2 (0.2-5 μM; 48 hours) significantly causes G2/M-phase arrest in HCT-116 cells in a dose dependent manner[1]. Cell Proliferation Assay Cell Line: HCT-116, MCF-7 and A549[1] Concentration: 0-20 μM Incubation Time: 72 hours Result: Exhibited antiproliferative activities against HCT-116, MCF-7 and A549 with IC50s of 0.22 ± 0.09 μM, 1.59 ± 0.06 μM and 0.22 ± 0.04 μM, respectively. Apoptosis Analysis Cell Line: HTC-116[1] Concentration: 0.2, 1 and 5 μM Incubation Time: 48 hours Result: The percentage of apoptotic cells was 4.19%, 11.53% and 21.48% at 0.2 μM, 1.0 μM and 5.0 μM, respectively. Cell Cycle Analysis Cell Line: HTC-116[1] Concentration: 0.2, 1 and 5 μM Incubation Time: 48 hours Result: Significantly caused G2/M-phase arrest in HCT-116 cells in a dose dependent manner.

[1]. Hu H, Chen F, Dong Y, et al. Discovery of Novel c-Mesenchymal-Epithelia transition factor and histone deacetylase dual inhibitors. Eur J Med Chem. 2020;204:112651.