SCH 50911

SCH 50911 is a selective, orally active, blood-brain barrier permeable GABA-B receptor (GABA-B Receptor) antagonist with an IC₅₀ of 1.1 μM in rats. SCH 50911 blocks baclofen-induced antitussive effects, regulates neuronal firing and GABA release. SCH 50911 promotes spontaneous seizures during withdrawal in ethanol-dependent rats, alters reward-related neurotransmission, and reduces or suppresses lever responding and self-administration behaviors of alcohol and sucrose in rats. SCH 50911 is applicable to research related to ethanol withdrawal syndrome, absence epilepsy and alcohol use disorder^[1][2][3][4]. In Vitro:SCH 50911 (1.1-2.2 μM) potently inhibits GABA binding to GABA-B receptors in rat brain with an IC₅₀ of 1.1 μM, and shows no binding affinity for most tested non-GABA-B receptors aside from weak activity in a nonspecific muscarinic binding assay^[1]. In Vivo:SCH 50911 (100-300 mg/kg; i.p.; single acute dose) produces a significant, dose-dependent proconvulsive effect in rats undergoing ethanol withdrawal syndrome, with the 300 mg/kg dose inducing tonic-clonic seizures in 44% of treated rats^[2].
Sch 50911 suppresses multiple forms of absence seizures in lethargic (lh/lh) mutant mice^[3].
Sch 50911 (systemic) crosses the blood-brain barrier and blocks baclofen-induced central antitussive and respiratory depressant effects in Felis catus and Cavia porcellus^[3].
SCH 50911 (25-100 mg/kg; i.p.; single dose; 30 minutes before test session) reduces operant alcohol self-administration in male sP rats, with statistically significant ~35% and ~65% reductions in alcohol lever-responses at 50 and 100 mg/kg, respectively, and marked interindividual response variability^[4].
SCH 50911 (100 mg/kg; i.p.; single dose; 30 minutes before test session) produces a statistically significant ~70% reduction in operant sucrose self-administration in male sP rats, with marked interindividual response variability^[4].