Detail of "158681-13-1"

CAS Number:
158681-13-1
Name:
Rimonabant hydrochloride
Molecular Structure:
Formula:
C₂₂H₂₁Cl₃N₄O^.HCl
Molecular Weight:
500.25
Synonyms:
1H-Pyrazole-3-carboxamide,5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-N-1-piperidinyl-,monohydrochloride (9CI);5-(4-Chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-N-(1-piperidinyl)-1H-pyrazole-3-carboxamide hydrochloride (1:1);Ribafit;Riomont;N-(Piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride;5-(4-Chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-N-1-piperidinyl-1H-pyrazole-3-carboxamide monohydrochloride;
Melting Point:
230-240 °C
Boiling Point:
627.6 °C at 760 mmHg
Flash Point:
333.3 °C
Appearance:
White to Off-White Crystalline Solid

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Reference

Cannabinoid CB1 receptor antagonism modulates plasma corticosterone in rodents: All Rights Reserved. Cannabinoid CB1 receptor antagonism modulates plasma corticosterone in rodents. Wade, Mark R.; Degroot, Aldemar; Nomikos, George G. (Lilly Research Laboratories, Neuroscience Discovery Research, Eli Lilly and Company, Indianapolis, IN 46285-0510, USA). European Journal of Pharmacology, 551(1-3), 162-167 (English) 2006 Elsevier B.V. CODEN: EJPHAZ. ISSN: 0014-2999. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Although the involvement of cannabinoids and the endogenous cannabinoid system in the regulation of the hypothalamo-pituitary-adrenal axis in rodents is well documented, the precise role played by the cannabinoid type one (CB1) receptor in this effect has not been fully elucidated. Consequently, we investigated the role of CB1 receptor in modulating plasma corticosterone concns. through use of the potent and selective CB1 receptor antagonist SR141716A and CB1 receptor knockout mice. Rats were administered SR141716A (0.1, 0.3, and 1 mg/kg, i.v.) and blood was sampled at 0, 15, 60, 90 and 120 min postinjection. SR141716A dose- and time-dependently increased plasma corticosterone levels and max. effects were obtained with the 1 mg/kg dose 60 min postinjection. In mice, SR141716A (0.1, 0.3, 1, 3, and 10 mg/kg, i.p.) also induced a dose-dependent rise in corticosterone levels 60 min postinjection; this rise reached plateau levels with the 0.3-1 mg/kg doses. The stimulatory effect of SR141716A (1 mg/kg, i.p.) on plasma corticosterone 60 min postinjection was abolished in the CB1 receptor knockout mice, which did not show any difference in basal corticosterone levels as compared to their wild-type controls. Finally, the stimulatory effects of SR141716A (10 mg/kg, i.p.) on plasma corticosterone 60 min postinjection were retained after subchronic dosing (5 days, once daily) in mice.In this experiment, several chemicals are used like 158681-13-1 and 50-22-6 The present results indicate that SR141716A increases plasma corticosterone in rats and mice possibly through blockade of CB1 receptors, an effect that is retained after subchronic dosing in mice. These data provide support for the notion that changes in plasma corticosterone concns. may be used in the lab. and the clinic to assess the effects of CB1 receptor antagonism. .

Blockade of cannabinoid CB1 receptor function protects against in vivo disseminating brain damage following NMDA-induced excitotoxicity: Blockade of cannabinoid CB1 receptor function protects against in vivo disseminating brain damage following NMDA-induced excitotoxicity. Hansen, Henrik H.; Azcoitia, Inigo; Pons, Sebastian; Romero, Julian; Garcia-Segura, Luis Miguel; Ramos, Jose Antonio; Hansen, Harald S.; Fernandez-Ruiz, Javier (Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, Madrid 28040, Spain). Journal of Neurochemistry, 82(1), 154-158 (English) 2002 Blackwell Science Ltd. CODEN: JONRA9. ISSN: 0022-3042. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The ability of cannabinoid CB1 receptors to influence glutamatergic excitatory neurotransmission has fueled interest in how these receptors and their endogenous ligands may interact in conditions of excitotoxic insults. The present study characterized the impact of stimulated and inhibited CB1 receptor function on NMDA-induced excitotoxicity. Neonatal (6-day-old) rat pups received a systemic injection of a mixed CB1/CB2 receptor agonist (WIN55,212-2) or their resp. antagonists (SR141716A for CB1 and SR144528 for CB2) prior to an unilateral intrastriatal microinjection of NMDA. The NMDA-induced excitotoxic damage in the ipsilateral forebrain was not influenced by agonist-stimulated CB1 receptor function. In contrast, blockade of CB1, but not CB2, receptor activity evoked a robust neuroprotective response by reducing the infarct area and the no. of cortical degenerating neurons. These results suggest a crit. involvement of CB1 receptor tonus on neuronal survival following NMDA receptor-induced excitotoxicity in vivo.Except for chemicals metioned above, 131543-22-1 and 158681-13-1 are also used. .

Detail of "158681-13-1"

Rimonabant hydrochloride

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CAS No.158681-13-1 Rimonabant hydrochloride

CAS No.158681-13-1 Rimonabant hydrochloride

CAS No.158681-13-1 Rimonabant hydrochloride

Reference