| Identification | Back Directory | [Name]
Drinabant | [CAS]
358970-97-5 | [Synonyms]
AVE-1625
drinabant
N-[1-[Bis(4-chlorophenyl)methyl]azetidin-3-yl]-N-(3,5-difluorophenyl)methanesulfonamide
Methanesulfonamide, N-[1-[bis(4-chlorophenyl)methyl]-3-azetidinyl]-N-(3,5-difluorophenyl)- | [Molecular Formula]
C23H20Cl2F2N2O2S | [MDL Number]
MFCD10567084 | [MOL File]
358970-97-5.mol | [Molecular Weight]
497.38 |
| Chemical Properties | Back Directory | [Boiling point ]
581.7±60.0 °C(Predicted) | [density ]
1.458 | [storage temp. ]
Store at -20°C | [solubility ]
≤0.15mg/ml in ethanol;15mg/ml in DMSO;15mg/ml in dimethyl formamide | [form ]
crystalline solid | [pka]
5.44±0.10(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Description]
The central cannabinoid (CB1) receptor is a G protein-coupled receptor that is widely distributed in the central nervous system and several peripheral tissues and binds the active component of cannabis, Δ9-tetrahydrocannabinol. Signaling through the CB1 receptor is implicated in attentional and working memory deficits as well as obesity. AVE-1625 is a highly potent, selective antagonist for the CB1 receptor with Ki values of 0.16-0.44 nM. At 1-3 mg/kg, AVE-1625 significantly improves the performance of rodents in working memory tasks. At 30 mg/kg, AVE-1625 reduces caloric intake by more than 50% of controls and significantly increases lipolysis from fat tissues and reduces hepatic glycogen levels in rodents. | [Uses]
AVE-1625 is a selective antagonist for the CB1 receptor. | [in vivo]
AVE1625 (10 mg/kg orally once daily), combined with Olanzapine (HY-14541) attenuates body weight gain, diminishing the enhanced food intake while maintaining increased energy expenditure and decreased motility[2].
AVE1625 (1, 3, and 10 mg/kg ip), reverses abnormally persistent LI induced by MK-801 (HY-15084B) or neonatal nitric oxide synthase inhibition in rodents, and improves both working and episodic memory[3].
| Animal Model: | Rats[1]. | | Dosage: | 30 mg/kg. | | Administration: | Oral gavage, single dose. | | Result: | Had free access to food during the preceding night (postprandial state) caused a pronounced reduction of food intake during the subsequent 10-12 h without differences in
their locomotor activity relative to that of the control group.
Caused an increase in FFA and glycerol, indicating increased lipolysis from fat tissue.
Immediately resulted in a pronounced increase in VCO2 and VO2, indicating increased oxidation of energetic substrates and increased TEE.
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| Animal Model: | Female Hanover Wistar rats weighing 225 ± 8.6 g[2]. | | Dosage: | 10 mg/kg. | | Administration: | Orally once daily. | | Result: | Reduced their weight markedly within the first 3 days of treatment where upon animals maintained lower body weight, although they lost about 7.3 ± 1.3 g fat during the 12 days of treatment.
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| [IC 50]
hCB1-R: 25 nM (IC50); rCB1-R: 10 nM (IC50); CB2: 10000 nM (IC50) | [storage]
Store at -20°C | [References]
[1] borowsky b, stevens r, mark b, et al. ave1625, a cannabinoid cbi antagonist, as a co-treatment for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in animal models[c]//neuropsychopharmacology. macmillan building, 4 crinan st, london n1 9xw, england: nature publishing group, 2005, 30: s116-s117.
[2] herkenham m, lynn a b, little m d, et al. cannabinoid receptor localization in brain[j]. proceedings of the national academy of sciences, 1990, 87(5): 1932-1936.
[3] herling a w, gossel m, haschke g, et al. cb1 receptor antagonist ave1625 affects primarily metabolic parameters independently of reduced food intake in wistar rats[j]. american journal of physiology-endocrinology and metabolism, 2007, 293(3): e826-e832. |
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BOC Sciences
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Energy Chemical
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Alfa Chemistry
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