Product Data Sheet
Product Name:WIN 55,212-2 Mesylate
Cat. No.:GC37935
Chemical Properties
Cas No.131543-23-2
Chemical
Name
N/A
Canonical SMILES O=C(C1=C2C=CC=CC2=CC=C1)C3=C(N4[C@@H](COC5=C4C3=CC=C5)CN6CCOCC6)C.CS(=O)(O)= O
Formula C28H30N2O6S M.Wt522.61 Solubility Soluble in DMSO Storage Store at -20°C
General tips For obtaining a higher solubility , plea warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for veral months.
相信的反义词Shipping Condition Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request.
Structure
台式电脑电源
Background
WIN 55,212-2 Mesylate is a potent aminoalkylindole cannabinoid (CB) receptor agonist with Kis of 62.3 and 3.3 nM for human recombinant CB1 and CB2 receptors, respectively. Ki: 62.3 nM (human recombinant CB1), 3.3 nM (human
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斯的意思Product Data Sheet
recombinant CB2)京骂
WIN 55,212-2 is more potent in CHO-CB2 cells than in CHO-CB1 cells by a factor of 6O. WIN 55,212-2 has no effect on arachidonic acid relea in CHO-CB2 or control CHO cells. WIN 55,212-2
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叛逆的青春fails to stimulate any increa in intracellular Ca2+ up to 10 μM[1]. In primary cultures of rat cerebral cortex neurons, WIN 55,212-2 (0.01--100 nM) increas extracellular glutamate levels, displaying a bell-shaped concentration-respon curve. The facilitatory
effect of WIN 55,212-2 (1 nM) is fully counteracted by SR141716A (10 nM), by the replacement of the normal Krebs Ringer-bicarbonate buffer with a low Ca2+ medium (0.2 mM) and by the IP(3) receptor antagonist xestospongin C (1μM)[2]. WIN 55,212-2 evokes CGRP relea from TG neurons in vitro (EC50=26 μM) in a concentration- and calcium-dependent manner. WIN 55,212-2-2 neither inhibits capsaicin-evokes CGRP relea nor does it inhibit forskolin-, isoproteranol- or prostaglandin E2-stimulated cAMP accumulation. WIN 55,212-2 significantly inhibits (EC50=1.7 μM) 50 mm K+-evoked CGRP relea by approximately 70%. WIN 55,212-2 inhibition of 50 mm K+-evoked CGRP relea is not reverd by antagonists of cannabinoid type 1 (CB1) receptor, but is mimicks in magnitude and potency
(EC50=2.7 μM) by its cannabinoid-inactive enantiomer WIN 55,212-2-3[3].
In the prefrontal cortex WIN 55,212-2 (0.1 and 1 mg/kg i.p.) increas dialysate glutamate levels from of the awake rat, while the lower (0.01 mg/kg) and the higher (2 mg/kg) dos are ineffective. F
urthermore, the WIN 55,212-2 (0.1 mg/kg)- induced increa of dialysate glutamate levels is counteracted by pretreatment with the lective CB(1) receptor antagonist SR141716A (0.1 mg/kg, i.p.) and by the local perfusion with a low-calcium Ringer solution (Ca2+ 0.2 mM)[2]. WIN 55,212-2 (0.5, 1, 3, 5, 10 and 15 mg/kg, i.p.) does not alter the izure threshold at low dos, while higher dos of the drug significantly increas the threshold in a do-dependent manner. The anticonvulsant effect of WIN 55,212-2, which is obrved with dos as high as 5 mg/kg, can be obrved with dos as low as 0.5 mg/kg in groups pre-treated with 20 mg/kg of pioglitazone[4].
[1]. Felder CC, et al. Comparison of the pharmacology and signal transduction of the human cannabinoid CB1 and CB2 receptors. Mol Pharmacol. 1995 Sep;48(3):443-50. [2]. Ferraro L, et al. The cannabinoid receptor agonist WIN 55,212-2 regulates glutamate transmission in rat cerebral cortex: an in vivo and in vitro study. Cereb Cortex. 2001 Aug;11(8):728-33. [3]. Price TJ, et al. Cannabinoid receptor-independent actions of the aminoalkylindole WIN
55,212-2 on trigeminal nsory neurons. Br J Pharmacol. 2004 May;142(2):257-66. [4]. Payandemehr B, et al. Involvement of PPAR receptors in the anticonvulsant effects of a cannabinoid agonist, WIN 55,212-2. Prog Neuropsychopharmacol Biol Psychiatry. 2015 Mar 3;57:140-5
