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Camonsertib

CAS No. : 2417489-10-0

MCE 国际站：Camonsertib

产品活性：Camonsertib (RP-3500) 是一种口服有效的，选择性 ATR 激酶抑制剂 (ATRi)，在生化试验中的 IC₅₀ 为 1.00 nM。Camonsertib 对 ATR 的选择性是 mTOR 的 30 倍 (IC₅₀=120 nM)，是 ATM、DNA-PK 和 PI3Kα 激酶的 > 2,000 倍。Camonsertib 具有有效的抗肿瘤活性。

研究领域：Cell Cycle/DNA Damage | PI3K/Akt/mTOR

作用靶点：ATM/ATR | mTOR

In Vitro: Camonsertib (RP-3500; 1 µM; 1-24 hours) inhibits CHK1(Ser345) phosphorylation from 1 to 3 hours.
Camonsertib inhibits Gemcitabine stimulated ATR phosphorylation of its substrate pCHK1(Ser345) with an IC₅₀ of 0.33 nM in a LoVo cell-based assay.

In Vivo: Camonsertib (RP-3500; 3, 7, 15 mg/kg; Orally; once daily for 18 days) produces dose-dependent tumor growth inhibition with a minimum effective dose (MED) of 7 mg/kg in LoVo xenografts.
Camonsertib (5, 10 mg/kg; Orally; once daily) produces statistically significant tumor growth inhibition in the CW-2 colon xenograft model.
Camonsertib (7 mg/kg; for 7 days) results in 8.1- ａnd 2.7-fold inductions of KAP1 ａnd DNA-PKcs phosphorylation in mice bearing LoVo tumors.
Camonsertib has a more profound anti-tumor effect occurred at higher doses on the 3 days on/4 days off (30 mg/kg) ａnd 5 days on/2 days off (25 mg/kg) schedules compared with consecutive daily administrations (10 mg/kg) at a lower dose for 14 days.
Camonsertib (15mg/kg) combined PARPi Olaparib (80mg/kg; both agents days 1-3 on/4 days off) or sequential (PARPi for 3 days followed by RP-3500 for 3 days then 1 day off) schedules produces greater antiTumor effects compared with sequential administration without affecting tolerability.

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