ACP-5862 是 Acalabrutinib 的主要活性的，循环的，吡咯烷开环代谢产物，对 Bruton 酪氨酸激酶 (BTK) 的 IC₅₀ 为 5.0 nM。ACP-5862 是时间依赖性的 CYP3A4 和 CYP2C8 弱抑制剂。Acalabrutinib 是一种口服有效的，选择性的 BTK 抑制剂，IC₅₀ 和 EC₅₀ 分别为 3 nM 和 8 nM。

ACP-5862 is a major active, circulating, pyrrolidine ring-opened metabolite of Acalabrutinib with an IC 50 of 5.0 nM for Bruton tyrosine kinase (BTK). ACP‐5862 is a weak time‐dependent inactivator of CYP3A4 and CYP2C8. Acalabrutinib is an orally active, irreversible, and highly selective BTK inhibitor, with an IC 50 of 3 nM and EC 50 of 8 nM.

Solid

CYP2C8 CYP3A4

Following a single oral dose of 100 mg Acalabrutinib, the half‐life of ACP‐5862 is 6.9 hours and the mean exposure is approximately twofold to threefold higher than that of Acalabrutinib.
ACP-5862 (M27) is the major single metabolite in the systemic circulation and accountes for 57.4% and 42.1% of the AUC 0-t total radioactivity in male and female rat plasma, respectively. ACP-5862, the major human metabolite, is a relatively minor component in the systemic circulation and accountes for 6.1% and 8.1% of the AUC 0-t total radioactivity in male and female dog plasma, respectively.
ACP-5862 (1 or 10 μM) has reversible protein binding of 98.6%, 99.8%, 94.3%, 98.6% in mouse, rat, dog, and human plasma.
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]. Herman SE, et al. The Brutons tyrosine kinase (BTK) inhibitor acalabrutinib demonstrates potent on-target effects and efficacy in two mouse models of chronic lymphocytic leukemia. Clin Cancer Res. 2016 Nov 30
[2]. Diansong Zhou, et al. Evaluation of the Drug-Drug Interaction Potential of Acalabrutinib and Its Active Metabolite, ACP-5862, Using a Physiologically-Based Pharmacokinetic Modeling Approach. CPT Pharmacometrics Syst Pharmacol. 2019 Jul;8(7):489-499.

In Vitro: DMSO : 250 mg/mL (519.20 mM; Need ultrasonic)配制储备液