Samuraciclib

Samuraciclib (CT7001) is a potent, selective, ATP-competitive and orally active CDK7 inhibitor, with an IC₅₀ of 41 nM. Samuraciclib displays 45-, 15-, 230- and 30-fold selectivity over CDK1, CDK2 (IC₅₀ of 578 nM), CDK5 and CDK9, respectively. Samuraciclib inhibits the growth of breast cancer cell lines with GI₅₀ values between 0.2-0.3 µM. Samuraciclib has anti-tumor effects^[1][2]. IC50 & Target: IC50: 41 nM (CDK7/CycH/MAT1), 578 nM (CDK2/cycE1)^[1] In Vitro: Samuraciclib (ICEC0942; 0-10 µM; 24 hours; HCT116 cells) treatment promotes cell apoptosis^[1].
Samuraciclib (ICEC0942; 0-10 µM; 24 hours; HCT116 cells) treatment induces cell cycle arrest^[1].
Samuraciclib (ICEC0942; 0-10 µM; 0-24 hours; HCT116 cells) treatment inhibits the phosphorylation of PolII CTD in a dose and time dependent manner in HCT116 colon cancer cells. Samuraciclib also inhibits phosphorylation of CDK1, CDK2 and retinoblastoma^[1].
Samuraciclib (ICEC0942) inhibits the growth of MCF7, T47D, MDA-MB-231, HS578T, MDA-MB-468, MCF10A and HMEC cells with GI₅₀ values of 0.18 µM, 0.32 µM, 0. 33 µM, 0.21 µM, 0.22 µM, 0.67 µM and 1.25 µM, respectively^[1]. In Vivo: Samuraciclib (ICEC0942; 100 mg/kg; oral gavage; daily; for 14 days; female nu/nu-BALB/c athymic nude mice) treatment inhibits tumor growth by 60% at day 14, and is accompanied by highly significant reductions in PolII Ser2 and Ser5 phosphorylation in PBMCs and in tumors^[1].
The combination of Samuraciclib (ICEC0942) and ICI 47699 treatment shows complete growth arrest of estrogen receptor (ER)-positive tumor xenografts^[1].