For research use only. Not for therapeutic Use.
GS-6201 (CVT-6883) is a selective adenosine A2B receptor antagonist. GS-6201 displays high affinity and selectivity for the human adenosine A2B receptors (Ki=22 nM)[1]. GS-6201 reduces caspase-1 activity in the heart, and attenuates cardiac remodeling after acute myocardial infarction (AMI) in the mouse[2]. GS-62013 attenuates the airway reactivity induced by NECA, AMP, or allergen in sensitized mice[3].
GS-6201 (CVT-6883) (4 mg/kg; i.p.; every 12 h for 14 days) significantly reduces IL-6, TNF-α, E-selectin, ICAM-1, and VCAM plasma levels[2].
GS-6201 (4 mg/kg; i.p.; every 12 h for 14 days) leads to a significant attenuation of left and right ventricular enlargement and dysfunction at 7 days, which was maintained at 14 days and also at 28 days[2].
GS-6201 (2 mg/kg; p.o.) treatment shows the Cmax, dAUC and t1/2 are 1110 ng/mL, 6500 ng h/mL, and 4.25 hours, respectively[1].
| Catalog Number | I011872 |
| CAS Number | 752222-83-6 |
| Synonyms | 3-ethyl-1-propyl-8-[1-[[3-(trifluoromethyl)phenyl]methyl]pyrazol-4-yl]-7H-purine-2,6-dione |
| Molecular Formula | C21H21F3N6O2 |
| Purity | ≥95% |
| InChI | InChI=1S/C21H21F3N6O2/c1-3-8-30-19(31)16-18(29(4-2)20(30)32)27-17(26-16)14-10-25-28(12-14)11-13-6-5-7-15(9-13)21(22,23)24/h5-7,9-10,12H,3-4,8,11H2,1-2H3,(H,26,27) |
| InChIKey | KOYXXLLNCXWUNF-UHFFFAOYSA-N |
| SMILES | CCCN1C(=O)C2=C(N=C(N2)C3=CN(N=C3)CC4=CC(=CC=C4)C(F)(F)F)N(C1=O)CC |
| Reference | [1]. Elzein E, et al. Discovery of a novel A2B adenosine receptor antagonist as a clinical candidate for chronic inflammatory airway diseases. J Med Chem. 2008 Apr 10;51(7):2267-78. [2]. Toldo S, et al. GS-6201, a selective blocker of the A2B adenosine receptor, attenuates cardiac remodeling after acute myocardial infarction in the mouse. J Pharmacol Exp Ther. 2012 Dec;343(3):587-95. [3]. Mustafa SJ, et al. Effect of a specific and selective A(2B) adenosine receptor antagonist on adenosine agonist AMP and allergen-induced airway responsiveness and cellular influx in a mouse model of asthma. J Pharmacol Exp Ther. 2007 Mar;320(3):1246-51. |
