Fadraciclib (CYC065) 是第二代口服有效的 ATP 竞争性的 CDK2/CDK9 激酶抑制剂，IC₅₀ 分别为 5 和 26 nM。

Fadraciclib (CYC065) is a second-generation, orally available ATP-competitive inhibitor of CDK2/CDK9 kinases with IC 50 s of 5 and 26 nM, respectively.

Solid

CDK2 CDK9

Fadraciclib blocks cells in the G1 phase of the cell cycle and inhibits cell growth specifically in cyclin E1 (CCNE1)-overexpressing uterine serous carcinomas (USCs). USC cell lines expressing high CCNE1 mRNA and protein levels to be significantly more sensitive to treatment with Fadraciclib in vitro when compared with low CCNE1-expressing cell lines (IC50: mean±s.d.=124.1±57.8?nM in CCNE1-overexpressing USC cell lines vs 415±117.5?nM in CCNE1 low expressors, respectively; P=0.0003). Importantly, low concentrations of Fadraciclib (i.e., 100?nM) causes an arrest in the G1 phase of the cell cycle only in the CCNE1-overexpressing USC cell lines (i.e., USC-ARK-2, USC-ARK-7) . has not independently confirmed the accuracy of these methods. They are for reference only.

To evaluate the therapeutic potential of Fadraciclib as a single agent, USC-ARK-2-derived xenografts are treated daily with Fadraciclib (22.5?mg/kg) for a 3-week period. Tumor size and mouse weight are recorded two times a week. The daily administration of Fadraciclib results in a significant reduction of tumor growth compared with the vehicle-treated mice (P=0.012 starting at day 9 of the treatment). No significant weight loss is reported during the entire treatment period. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Cocco E, et al. Dual CCNE1/PIK3CA targeting is synergistic in CCNE1-amplified/PIK3CA-mutated uterine serous carcinomas in vitro and in vivo. Br J Cancer. 2016 Jul 26;115(3):303-11.
[2]. Sumana Devata, et al. Molecular markers and venous thromboembolism (VTE) in acute myelogenous leukemia (AML)

In Vitro: DMSO : ≥ 100 mg/mL (251.56 mM)配制储备液