99%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

盐酸利莫那班；利莫那班盐酸盐; SR 141716A；SR 151716A

white to beige powder

DMSO : 33.33 mg/mL (66.63 mM; Need ultrasonic)

Cannabinoid Receptor

Rimonabant hydrochloride (SR 141716A) binds selectively to central cannabinoid receptors (CB1) with high affinity (Ki=2 nM), and blocks the inhibitory effects of cannabinoid receptor agonists in the mouse vas deferens, dopamine-stimulated adenylyl cyclase and WIN 55212-stimulated GTPγS binding. Rimonabant dose-dependently inhibited CO synthesis in Raw 264.7 macrophages, with 1 µM producing a significant (~40%) decrease compared to untreated controls and concentrations ≥ 5 µM producing near complete inhibition. A small, but significant, reduction of TG and DG synthesis is also observed with Rimonabant at concentrations ≥ 10 µM. Inhibition of CO synthesis in Raw 264.7 macrophages by Rimonabant (IC50 value 2.9±0.38 µM) is very similar to that of AM251 and SR144528 (IC50 value 2.6±0.26 µM and 2.5±0.32 µM, respectively), two related compounds previously demonstrated to be potent ACAT inhibitors. Mouse peritoneal macrophages also displayed significantly reduced CO synthesis in response to Rimonabant treatment. Rimonabant at concentrations ≥ 1 µM significantly inhibits CO synthesis in CHO-ACAT1 and CHO-ACAT2 cells in a concentration-dependent manner with similar efficiency (IC50s of 1.5±1.2 µM and 2.2±1.1 µM, respectively).

Pretreatment with Rimonabant hydrochloride (SR 141716A) blocks the antinociceptive, discriminative stimulus, memory impairing and hypolocomotor effects produced by Δ-9-THC. SR 141716A also precipitates a withdrawal syndrome in rats treated chronically with Δ-9-THC. Pretreatment of mice with 0.1 mg/kg of WIN 55212-2 is effective in increasing the CPP induced by MDMA , while 1 mg/kg of Rimonabant specifically blocks CB1 receptors and does not act as an inverse agonist.