MCOPPB (trihydrochloride)

MCOPPB trihydrochloride is a NOP/ORL1 G protein-coupled receptor agonist and autophagy inhibitor that can cross the blood-brain barrier. MCOPPB trihydrochloride clears senescent cells, regulates locomotion, lipid storage and immune responses, and inhibits fibrosis and angiogenesis. MCOPPB trihydrochloride blocks autophagic flux, induces changes in locomotion and lipid storage, and activates the stress-responsive immune transcription network, thereby improving post-infarction cardiac function and exerting anxiolytic effects. MCOPPB trihydrochloride can be applied to research fields such as aging-related diseases and ischemic heart failure^[1][2][3]. In Vitro:MCOPPB trihydrochloride (10 μM; 5 days) preferentially reduces viability of Aphidicolin (HY-N6733)-induced senescent human MRC5 fibroblasts while having less effect on non-senescent proliferating human MRC5 fibroblasts^[1].
MCOPPB trihydrochloride (0.125-5 μM; 24 h) reduces viability of doxorubicin-induced senescent human HepG2 and Huh-7 hepatocellular carcinoma cells in a dose-dependent manner, with significant effects observed at concentrations ≥0.75 μM^[1].
MCOPPB trihydrochloride (0.5 µM; 3 days total) downregulates NPPA and NPPB gene expression in ET-1-stimulated neonatal rat cardiomyocytes, an effect that is mediated via the ORL1 receptor^[3].
MCOPPB trihydrochloride (0.5 µM; 3 days total) reduces ET-1-induced nuclear NFATc4 accumulation in H9C2 cells, an effect that is mediated via the ORL1 receptor^[3]. In Vivo:MCOPPB trihydrochloride (2.5-5 mg/kg; i.p.; 5 consecutive days followed by 2 days rest; 21 days) exerts potent, tissue-specific senolytic effects in peripheral tissues (white adipose tissue and liver) of aging male C57BL/6 mice^[1].
MCOPPB trihydrochloride (2.5 mg/kg/day; i.p.; 5 days per week; 3 months) significantly improves cardiac function, reduces fibrosis, increases cardiomyocyte diameter, and induces angiogenesis in rats with post-myocardial infarction heart failure, with an ejection fraction of 67% at euthanasia^[3].