A potent CB1 receptor antagonist
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AVE-1625

Item No. 10009021

Product Insert (PDF)Safety Data Sheet (SDS) (PDF)
Technical Information
Formal Name
N-[1-[bis(4-chlorophenyl)methyl]-3-azetidinyl]-N-(3,5-difluorophenyl)-methanesulfonamide
CAS Number
358970-97-5
Synonyms
  • Drinabant
Molecular Formula
C23H20Cl2F2N2O2S
Formula Weight
497.4
Purity
≥98%
Formulation (Request formulation change)
A crystalline solid
Solubility(Learn about Variance in Solubility)
DMF: 15 mg/mlDMSO: 15 mg/mlDMSO:PBS (pH 7.2) (1:2): 0.3 mg/mlEthanol: 0.15 mg/ml
λmax
231 nm
SMILES
Clc1ccc(cc1)C(c1ccc(Cl)cc1)N1CC(C1)N(c1cc(F)cc(F)c1)S(=O)(=O)C
InChi Code
InChI=1S/C23H20Cl2F2N2O2S/c1-32(30,31)29(21-11-19(26)10-20(27)12-21)22-13-28(14-22)23(15-2-6-17(24)7-3-15)16-4-8-18(25)9-5-16/h2-12,22-23H,13-14H2,1H3
InChi Key
IQQBRKLVEALROM-UHFFFAOYSA-N
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    1 mg

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    10 mg

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    Cayman Chemical
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    OBESITY RESEARCH SOLUTIONS
    Product 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.1 Signaling through the CB1 receptor is implicated in attentional and working memory deficits as well as obesity.2,3,4 AVE-1625 is a highly potent, selective antagonist for the CB1 receptor with Ki values of 0.16-0.44 nM.4 At 1-3 mg/kg, AVE-1625 significantly improves the performance of rodents in working memory tasks.4 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.5

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Howlett, A.C., Song, C., Berglund, B.A., et al. Characterization of CB1 cannabinoid receptors using receptor peptide fragments and site-directed antibodies. Mol. Pharmacol. 53(3), 504-510 (1998).

    2. Gómez, R., Navarro, M., Ferrer, B., et al. A peripheral mechanism for CB1 cannabinoid receptor-dependent modulation of feeding. J. Neurosci. 22(21), 9612-9617 (2002).

    3. Mackie, K. Cannabinoid receptors as therapeutic targets. Annu. Rev. Pharmacol. Toxicol. 46, 101-122 (2006).

    4. Borowsky, B., Stevens, R., Mark, B., et al. AVE1625, a cannabinoid CB1 antagonist, as a co-treatment for Schizophrenia: Improvement in cognitive function and reduction of antipsychotic-side effects in animal models. Neuropsychopharmacology 30, S116-S117 (2005).

    5. Herling, A.W., Gossel, M., Haschke, G., et al. The CB1 receptor antagonist AVE1625 affects primarily metabolic parameters independently of reduced food intake in wistar rats. Am. J. Physiol. Endocrinol. Metab. 293(3), E826-E832 (2007).