Samuraciclib (CT7001) 是一种有效的，具有选择性，ATP 竞争性和口服活性的CDK7抑制剂，IC50为 41 nM。Samuraciclib 对CDK7的选择性分别是 CDK1，CDK2 (IC50为 578 nM)，CDK5 和 CDK9 的 45 倍，15 倍，230 倍和 30 倍。Samuraciclib 以 GI50值为 0.2-0.3 μM 来抑制乳腺癌细胞系的生长，具有有效的抗肿瘤作用。
| 生物活性 | Samuraciclib (CT7001) is a potent, selective, ATP-competitive and orally activeCDK7inhibitor, with anIC50of 41 nM. Samuraciclib displays 45-, 15-, 230- and 30-fold selectivity overCDK1,CDK2(IC50of 578 nM),CDK5andCDK9, respectively. Samuraciclib inhibits the growth of breastcancercell lines with GI50values between 0.2-0.3 μM. Samuraciclib has anti-tumor effects[1][2]. |
| IC50& Target[1][2] | CDK7/CycH/MAT1 41 nM (IC50) | CDK2/cycE1 578 nM (IC50) | CDK1 1.8 μM (IC50) | CDK4 49 μM (IC50) | CDK5 9.4 μM (IC50) | CDK6 34 μM (IC50) | CDK9 1.2 μM (IC50) |
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体外研究
(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 GI50values 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].
Apoptosis Analysis[1] | Cell Line: | HCT116 cells | | Concentration: | 0 μM, 0.1 μM, 1 μM and 10 μM | | Incubation Time: | 24 hours | | Result: | Induced caspase 3/7 and demonstrated PARP cleavage. |
Cell Cycle Analysis[1] | Cell Line: | HCT116 cells | | Concentration: | 0 μM, 0.01 μM, 0.1 μM, 1 μM and 10 μM | | Incubation Time: | 24 hours | | Result: | Showed accumulation of cells in G2/M. |
Western Blot Analysis[1] | Cell Line: | HCT116 cells | | Concentration: | 0 μM, 0.1 μM, 1 μM and 10 μM | | Incubation Time: | 0 hour, 4 hours, 8 hours, 16 hours or 24 hours | | Result: | PolII CTD phosphorylation was inhibited in a dose and time dependent manner in HCT116 colon cancer cells. |
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体内研究
(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].
| Animal Model: | Female nu/nu-BALB/c athymic nude mice (7-week old) with MCF7 cells[1]. | | Dosage: | 100 mg/kg | | Administration: | Oral gavage; daily; for 14 days | | Result: | At day 14, tumor growth was inhibited by 60%. |
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| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |
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