| Cas No.: | 158681-13-1 |
| Chemical Name: | 5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-N-piperidin-1-ylpyrazole-3-carboxamide |
| Synonyms: | Rimonabant free base, SR141716; SR 141716; SR-141716; A 281; A-281; A281; Rimonabant, Acomplia, Zimulti |
| SMILES: | CC1=C(C2=CC=C(Cl)C=C2)N(N=C1C(NN3CCCCC3)=O)C4=C(Cl)C=C(Cl)C=C4.Cl |
| Formula: | C22H21Cl3N4O |
| M.Wt: | 463.787 |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Rimonabant hydrochloride is a cannabinoid receptor (CB) antagonist which binds selectively to CB1 with a Ki of 2 nM. |
| In Vivo: | 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[1]. 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[3]. |
| In Vitro: | 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[1]. 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)[2]. |
MSDS
COA
| LOT NO. | DOWNLOAD |
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| 2018-0101 |
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| 2018-0101 |
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