Mefuparib hydrochloride induces apoptosis and possesses prominent anticancer activity in vitro and in vivo. Mefuparib hydrochloride (MPH) is an orally active, substrate-competitive and selective PARP1/2 inhibitor with IC50s of 3.2 nM and 1.9 nM, respectively.

Mefuparib hydrochloride (1-10 μM; 24 hours) causes the accumulation of DSB marked by the increased levels of γH2AX in the MDA-MB-436 (BRCA1?/?) cells in a concentration-dependent manner[1]. Mefuparib hydrochloride exerts potent in vitro proliferation-inhibitory effects on cancer cells derived from different human tissues with an average IC50 of 2.16 μM (0.12 μM~3.64 μM)[1]. Mefuparib hydrochloride inhibits PARP3 (IC50>10 μM), PARP6 (IC50>10 μM), TNKS1 (IC50=1.6 μM), TNKS2 (IC50=1.3 μM)[1].Mefuparib hydrochloride (1-10 μM;?48 hours) causes cell apoptosis[1].??Mefuparib hydrochloride (MPH;?1-10 μM;?24 hours) causes V-C8 cells into typical G2/M arrest[1].

Mefuparib hydrochloride (10, 20, 40 mg/kg; oral) has a T1/2 of 1.07-1.3 hours and a C max of 116-725 ng/mL for SD rats[1]. Mefuparib hydrochloride (5, 10, 20 mg/kg; oral) has a T1/2 of 2.16-2.7 hours and a C max of 114-608 ng/mL for cynomolgus monkeys[1].?Mefuparib hydrochloride (MPH;?40-160 mg/kg;?orally;?once every other day;?for 21 days) displays dose- and time-dependent killing on V-C8 xenografts accompanied by complete disappearance of some xenografts, especially in the high-dose group[1].??Mefuparib hydrochloride (160 mg/kg;?orally;?once every other day;?for 21 days) inhibits the growth of the BR-05-0028 breast patient-derived xenograft (PDX) without obvious loss of body weight[1].

1449746-00-2

C17H16ClFN2O2

334.77

MPH

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years