DC Chemicals Limited
China
Product Name: AVE1625
Price: $Inquiry/100mg $Inquiry/250mg $Inquiry/500mg
Purity: 98.0%
Stocking Period: 3 Day
Contact: Tony Cao

358970-97-5

358970-97-5 structure

Name: AVE 1625
Chemical Name: N-[1-[bis(4-chlorophenyl)methyl]azetidin-3-yl]-N-(3,5-difluorophenyl)methanesulfonamide
CAS Number: 358970-97-5
Molecular Formula: C₂₃H₂₀Cl₂F₂N₂O₂S
Molecular Weight: 497.385
Catalog: Signaling Pathways GPCR/G Protein Cannabinoid Receptor
Create Date: 2018-09-12 22:14:35
Modify Date: 2024-01-09 15:16:46
Drinabant (AVE1625) is an orally active CB1 receptor antagonist. Drinabant (AVE1625) inhibits the agonist-stimulated calcium signal with IC50 values of 25 nM and 10 nM for the hCB1-R and rCB1-R, respectively, and is ineffective for the hCB2-R[1].

Name	N-[1-[bis(4-chlorophenyl)methyl]azetidin-3-yl]-N-(3,5-difluorophenyl)methanesulfonamide
Synonyms	AVE-1625 Drinabant N-{1-[Bis(4-chlorophenyl)methyl]-3-azetidinyl}-N-(3,5-difluorophenyl)methanesulfonamide Methanesulfonamide, N-[1-[bis(4-chlorophenyl)methyl]-3-azetidinyl]-N-(3,5-difluorophenyl)- UNII-61S98RLL5I

Description	Drinabant (AVE1625) is an orally active CB1 receptor antagonist. Drinabant (AVE1625) inhibits the agonist-stimulated calcium signal with IC50 values of 25 nM and 10 nM for the hCB1-R and rCB1-R, respectively, and is ineffective for the hCB2-R[1].
Related Catalog	Research Areas >> Metabolic Disease Signaling Pathways >> GPCR/G Protein >> Cannabinoid Receptor
Target	hCB1-R:25 nM (IC50) rCB1-R:10 nM (IC50) CB2:10000 nM (IC50)
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 intheir 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. 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.
References	[1]. Andreas W Herling, et al. CB1 receptor antagonist AVE1625 affects primarily metabolic parameters independently of reduced food intake in Wistar rats. Am J Physiol Endocrinol Metab. 2007 Sep;293(3):E826-32. [2]. Michaela Liebig, et al. Profiling of energy metabolism in olanzapine-induced weight gain in rats and its prevention by the CB1-antagonist AVE1625. Obesity (Silver Spring). 2010 Oct;18(10):1952-8. [3]. Mark D Black, et al. AVE1625, a cannabinoid CB1 receptor antagonist, as a co-treatment with antipsychotics for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in rodents. Psychopharmacology (Berl). 2011 May;215(1):149-63.

Density	1.5±0.1 g/cm3
Boiling Point	581.7±60.0 °C at 760 mmHg
Molecular Formula	C₂₃H₂₀Cl₂F₂N₂O₂S
Molecular Weight	497.385
Flash Point	305.6±32.9 °C
Exact Mass	496.059052
PSA	49.00000
LogP	5.46
Vapour Pressure	0.0±1.6 mmHg at 25°C
Index of Refraction	1.646
Storage condition	-20°C

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