LRRK2-IN-14 (Compound 8), an orally active inhibitor of LRRK2, exhibits an IC 50 of 6.3 nM against LRRK2(G2019S) cell activity and demonstrates inhibitory effects on hERG with an IC 50 of 22 μM. Additionally, LRRK2-IN-14 is permeable to the blood-brain barrier [1].

LRRK2-IN-14 exhibits high metabolic stability in liver microsomes, with a stability rate of 79.3% when administered at a concentration of 1 μM for 30 minutes [1].

LRRK2-IN-14（30 mg/kg；p.o.；单次剂量）在 ICR 小鼠中抑制了大脑中 G2019S 突变的 LRRK2 的磷酸化 [1]。在ICR小鼠中的药代动力学分析 [1]：Route Dose (mg/kg) C 0 (ng/mL) C max (ng/mL) T max (h) t 1/2 (h) Vd ss (mL/kg) Cl obs (mL/min/kg) AUC 0-last (ng·h/mL) AUC 0-INF (ng·h/mL) MRT 0-INF (h) F (%) i.v. 5 4101 / / 0.905 1233 16.3 5122 5181 1.27 / p.o. 5 / 2803 0.083 0.709 / / 3657 3672 1.22 70.9 brain 5 / 837 0.292 0.648 / / 1230 1233 1.14 / 动物模型：ICR小鼠 [1]；剂量：30 mg/kg；给药方式：p.o.；单次剂量；结果：磷酸化LRRK2水平下降至34%。