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Merck
CN

SML3640

Sigma-Aldrich

GS-6201

≥98% (HPLC)

Synonym(s):

3-Ethyl-3,9-dihydro-1-propyl-8-[1-[[3-(trifluoromethyl)phenyl]methyl]-1H-pyrazol-4-yl]-1H-purine-2,6-dione, 3-ethyl-1-propyl-8-[1-(3-trifluoromethylbenzyl)-1H-pyrazol-4-yl]-3,7-dihydropurine-2,6-dione, CVT 6883, CVT-6883

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About This Item

Empirical Formula (Hill Notation):
C21H21F3N6O2
CAS Number:
Molecular Weight:
446.43
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.21
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Quality Level

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear (Warmed)

storage temp.

-10 to -25°C

Biochem/physiol Actions

GS-6201 (CVT-6883) is a potent and selective A2B adenosine receptor (A2BAdoR) antagonist. GS-6201 reduces caspase-1 activity in the heart and leads to a more favorable cardiac remodeling in a mouse model of non-reperfused myocardial infarction. Also GS-6201 attenuated vascular remodeling and hypertension in mouse model.
Potent and selective A2B adenosine receptor (A2BAdoR) antagonist

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Role of A2B adenosine receptor-dependent adenosine signaling in multi-walled carbon nanotube-triggered lung fibrosis in mice
Journal of Nanobiotechnology, 17(1), 45-45 (2019)
S Jamal Mustafa et al.
The Journal of pharmacology and experimental therapeutics, 320(3), 1246-1251 (2006-12-13)
It has been previously proposed that adenosine plays an important role in the pathogenesis of asthma. The proposed mechanism of action for nucleoside adenosine is to activate A(2B) adenosine receptors (AR) and to indirectly modulate levels of mediators in the
Stefano Toldo et al.
The Journal of pharmacology and experimental therapeutics, 343(3), 587-595 (2012-08-28)
Adenosine (Ado) is released in response to tissue injury, promotes hyperemia, and modulates inflammation. The proinflammatory effects of Ado, which are mediated by the A(2B) Ado receptor (AdoR), may exacerbate tissue damage. We hypothesized that selective blockade of the A(2B)

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