Powder: -20°C for 3 years | In solvent: -80°C for 1 year
Rimonabant hydrochloride (SR 141716A) is a cannabinoid receptor antagonist, binding selectively to central cannabinoid receptors (CB1) with high affinity.
Pack Size | Availability | Price/USD | Quantity |
---|---|---|---|
5 mg | In stock | $ 38.00 | |
10 mg | In stock | $ 61.00 | |
25 mg | In stock | $ 118.00 | |
50 mg | In stock | $ 217.00 | |
100 mg | In stock | $ 327.00 | |
500 mg | In stock | $ 783.00 | |
1 mL * 10 mM (in DMSO) | In stock | $ 68.00 |
Description | Rimonabant hydrochloride (SR 141716A) is a cannabinoid receptor antagonist, binding selectively to central cannabinoid receptors (CB1) with high affinity. |
Targets&IC50 | CB1 receptor:1.8 nM(ki) |
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]. |
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]. |
Kinase Assay | Raw 264.7 cells (2×106/well) in 12-well plates are rinsed with PBS and refed culture media supplemented with varying amounts of Rimonabant 1h prior to supplementation with 7-ketocholesterol (7KC). All wells are adjusted to receive equal amounts of vehicle. Following a 16 h incubation, caspase-3 and caspase 3-like activity is determined[2]. |
Synonyms | SR 151716A, SR 141716A |
Molecular Weight | 500.25 |
Formula | C22H22Cl4N4O |
CAS No. | 158681-13-1 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
DMSO: 50 mg/mL(100 mM)
You can also refer to dose conversion for different animals. More
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Rimonabant hydrochloride 158681-13-1 GPCR/G Protein Microbiology/Virology Antibacterial Cannabinoid Receptor Rimonabant Bacterial Rimonabant Hydrochloride Inhibitor SR 151716A SR 141716A inhibit inhibitor