MFDCH016 is a potent inhibitor of HDAC1/6 (IC50= 38/59 nM) and CDK4/6 (IC50= 680/720 nM). It induces apoptosis in MCF-7 cells and causes cell cycle arrest in the G2/M and G0/G1 phases. MFDCH016 modulates the HDAC-p21-CDK signaling pathway, increasing levels of acetylated H3 and p21, making it useful for breast cancer research.

MFDCH016 exhibits significant antiproliferative effects on MCF-7 cells, achieving inhibition rates of 55% and 86% at concentrations of 1 μM and 10 μM respectively over 72 hours. The compound demonstrates dose-dependent inhibition across several cancer cell lines, including MCF-7, T47D, A549, NCI-H460, NCI-H1299, FaDu, UDSCC-2, MC38, and CT26. MFDCH016 effectively suppresses MCF-7 breast cancer cells with a GI50 of 2.476 μM over a concentration range of 0.001-100 μM. It induces cell cycle arrest at the G0/G1 phase, reduces cell proportions in the S and G2/M phases, and culminates in apoptosis. MFDCH016 upregulates acetylated H3 and p21 protein levels while downregulating cyclin D1 expression, with these effects intensifying and peaking at 72 hours. The compound exhibits minimal cardiotoxicity in hERG-HEK stable cell lines with an average inhibition rate at 10 μM. It shows negligible activity against other CDKs, with IC50 values exceeding 5000 nM for most subtypes and over 10,000 nM for CDK1, CDK2, CDK7, and CDK10, demonstrating more than 700-fold selectivity for non-target CDKs. MFDCH016 moderately inhibits CYP1A2 (20.7%), CYP2C9 (29.2%), and CYP2C19 (26.5%), while showing weaker inhibition of CYP2D6 (14.8%).

MFDCH016 (40 mg/kg, administered intraperitoneally once daily for 14 days) is an effective in vivo antitumor agent, exhibiting significant antitumor activity in MCF-7 tumor-bearing mice without notable toxicity.