product name AM251
Description: AM251 is a cannabinoid receptor antagonist that blocks the inhibitory effects of endocannabinoids and synthetic cannabinoid agonists on transmitter release through an action at presynaptic cannabinoid 1 receptors in brain. AM251 improves recognition memory in rats and produces nocifensive behavior via activation of ERK signaling pathway. Moreover, AM251 alters mitochondrial physiology via proteolytic degradation of ERRα and attenuates mechanical allodynia and thermal hyperalgesia after burn injury.
References: Basic Clin Pharmacol Toxicol. 2004 Feb;94(2):73-8; Physiol Behav. 2004 Oct 15;82(5):863-9.
555.24
Formula
C22H21Cl2IN4O
CAS No.
183232-66-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 40 mg/mL (72.0 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
1% DMSO+30% polyethylene glycol+1% Tween 80: 8 mg/mL
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19404257
| In Vitro |
In vitro activity: AM251 reduces veratridine-dependent (tetrodotoxin suppressible) release of L-glutamic acid and GABA from synaptosomes with IC50 of 8.5 μM and 9.2 μM, respectively. AM251 increases (by 2.3 times) the Kd of radioligand without altering Bmax. AM251 inhibits equilibrium binding by allosterically accelerating the dissociation of the [3H]-batrachotoxinin A 20-alpha-benzoate:sodium channel complex. AM251 reduces cholesteryl ester synthesis in unstimulated and acetylated LDL-stimulated Raw 264.7 macrophages, CB2+/+ and CB2 −/− peritoneal macrophages. Kinase Assay: Macrophages are seeded (2 × 106/well) in 12-well culture plates. AM-251 are added from 4 mM stock solutions prepared in DMSO, 1 hour prior to the addition of 7-ketocholesterol from a 2 mg/mL ethanol stock solution. Controls are adjusted to receive equivalent volumes of DMSO and ethanol. After 16 hours, caspase-3 activity is determined. All treatments are done in triplicate and the data presented as the mean RFLU/mg protein± SD. Cell Assay: Treatment with AM251 (5 μmol/l) induced apoptosis, G2/M cell cycle arrest, and cAMP increase in A375 human melanoma cells. Moreover, AM-251 inhibited 7-ketocholesterol induced apoptosis of Raw 264.7 macrophages. |
|---|---|
| In Vivo | AM251 causes a sustained reduction of daily food intake in the rat. AM251 produces food avoidance and behaviors associated with nausea but does not impair feeding efficiency in rats. AM251 disrupts memory consolidation of the inhibitory avoidance task. AM251 has caused a significative decrease in the test step-down latency when compared to the control group, but no differences are detected in the open field habituation task, including the number of crossings, i.e. there are no motor effects. AM251 (4.0 mg/kg) reduces freezing during a conditioned tone cue played within a novel context. |
| Animal model | Moderately obese male Lewis rats |
| Formulation & Dosage | Dissolved in 2% DMSO,1% Tween 80 and 97% physiological saline; 1.25, 2.5,5mg/kg; i.p. injection |
| References | Basic Clin Pharmacol Toxicol. 2004 Feb;94(2):73-8; Physiol Behav. 2004 Oct 15;82(5):863-9. |
Related Posts
product name AM251
Description: AM251 is a cannabinoid receptor antagonist that blocks the inhibitory effects of endocannabinoids and synthetic cannabinoid agonists on transmitter release through an action at presynaptic cannabinoid 1 receptors in brain. AM251 improves recognition memory in rats and produces nocifensive behavior via activation of ERK signaling pathway. Moreover, AM251 alters mitochondrial physiology via proteolytic degradation of ERRα and attenuates mechanical allodynia and thermal hyperalgesia after burn injury.
References: Basic Clin Pharmacol Toxicol. 2004 Feb;94(2):73-8; Physiol Behav. 2004 Oct 15;82(5):863-9.
555.24
Formula
C22H21Cl2IN4O
CAS No.
183232-66-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 40 mg/mL (72.0 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
1% DMSO+30% polyethylene glycol+1% Tween 80: 8 mg/mL
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19404257
| In Vitro |
In vitro activity: AM251 reduces veratridine-dependent (tetrodotoxin suppressible) release of L-glutamic acid and GABA from synaptosomes with IC50 of 8.5 μM and 9.2 μM, respectively. AM251 increases (by 2.3 times) the Kd of radioligand without altering Bmax. AM251 inhibits equilibrium binding by allosterically accelerating the dissociation of the [3H]-batrachotoxinin A 20-alpha-benzoate:sodium channel complex. AM251 reduces cholesteryl ester synthesis in unstimulated and acetylated LDL-stimulated Raw 264.7 macrophages, CB2+/+ and CB2 −/− peritoneal macrophages. Kinase Assay: Macrophages are seeded (2 × 106/well) in 12-well culture plates. AM-251 are added from 4 mM stock solutions prepared in DMSO, 1 hour prior to the addition of 7-ketocholesterol from a 2 mg/mL ethanol stock solution. Controls are adjusted to receive equivalent volumes of DMSO and ethanol. After 16 hours, caspase-3 activity is determined. All treatments are done in triplicate and the data presented as the mean RFLU/mg protein± SD. Cell Assay: Treatment with AM251 (5 μmol/l) induced apoptosis, G2/M cell cycle arrest, and cAMP increase in A375 human melanoma cells. Moreover, AM-251 inhibited 7-ketocholesterol induced apoptosis of Raw 264.7 macrophages. |
|---|---|
| In Vivo | AM251 causes a sustained reduction of daily food intake in the rat. AM251 produces food avoidance and behaviors associated with nausea but does not impair feeding efficiency in rats. AM251 disrupts memory consolidation of the inhibitory avoidance task. AM251 has caused a significative decrease in the test step-down latency when compared to the control group, but no differences are detected in the open field habituation task, including the number of crossings, i.e. there are no motor effects. AM251 (4.0 mg/kg) reduces freezing during a conditioned tone cue played within a novel context. |
| Animal model | Moderately obese male Lewis rats |
| Formulation & Dosage | Dissolved in 2% DMSO,1% Tween 80 and 97% physiological saline; 1.25, 2.5,5mg/kg; i.p. injection |
| References | Basic Clin Pharmacol Toxicol. 2004 Feb;94(2):73-8; Physiol Behav. 2004 Oct 15;82(5):863-9. |