Domatinostat tosylate (4SC-202) is a selective class I HDAC inhibitor with IC 50 of 1.20 μM, 1.12 μM, and 0.57 μM for HDAC1 , HDAC2 , and HDAC3 , respectively. It also displays inhibitory activity against Lysine specific demethylase 1 (LSD1) . In Vitro Domatinostat tosylate significantly reduces proliferation of all epithelial and mesenchymal UC cell lines (IC 50 0.15-0.51 μM), inhibits clonogenic growth and induces caspase activity. Domatinostat tosylate provokes apoptosis activation in CRC cells, while caspase inhibitors (z-VAD-CHO and z-DVED-CHO) significantly alleviate Domatinostat tosylate-exerted cytotoxicity in CRC cells. Meanwhile, Domatinostat tosylate induces dramatic G2-M arrest in CRC cells. Further studies show that AKT activation might be an important resistance factor of Domatinostat tosylate. Domatinostat tosylate-induced cytotoxicity is dramatically potentiated with serum starvation, AKT inhibition (by perifosine or MK-2206), or AKT1-shRNA knockdown in CRC cells. On the other hand, exogenous expression of constitutively active AKT1 (CA-AKT1) decreases the sensitivity by Domatinostat tosylate in HT-29 cells. Notably, Domatinostat tosylate, at a low concentration, enhances oxaliplatin-induced in vitro anti-CRC activity. Domatinostat tosylate treatment induces potent cytotoxic and proliferation-inhibitory activities against established HCC cell lines (HepG2, HepB3, SMMC-7721) and patient-derived primary HCC cells. Domatinostat tosylate induces apoptosis signal-regulating kinase 1 (ASK1) activation, causing it translocation to mitochondria and physical association with Cyp-D. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Oral gavage of Domatinostat tosylate inhibits HT-29 xenograft growth in nude mice, and when combined with oxaliplatin, its activity is further strengthened. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid