Febuxostat-d7 is deuterium labeled Febuxostat. Febuxostat (TEI 6720) is selective xanthine oxidase inhibitor with a Ki of 0.6 nM[1].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
323.42
Formula
C16H9D7N2O3S
CAS 号
1285539-74-3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Takano Y, et al. Selectivity of febuxostat, a novel non-purine inhibitor of xanthine oxidase/xanthine dehydrogenase. Life Sci, 2005, 76(16), 1835-1847.
[3]. Sanchez-Lozada LG, et al. Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome. Am J Physiol Renal Physiol, 2008, 294(4), F710-F718.
[4]. Sanchez-Lozada LG, et al. Effect of febuxostat on the progression of renal disease in 5/6 nephrectomy rats with and without hyperuricemia. Nephron Physiol, 2008, 108(4), p69-p78.
[5]. Xu X, et al. Xanthine oxidase inhibition with febuxostat attenuates systolic overload-induced left ventricular hypertrophy and dysfunction in mice. Card Fail, 2008, 14(9), 746-753.
Febuxostat (TEI 6720) is selective xanthine oxidase inhibitor with a Ki of 0.6 nM[1].
IC50 & Target
Ki: 0.6 nM (Xanthine oxidase)[1]
体外研究 (In Vitro)
Febuxostat displays potent mixed-type inhibition of the activity of purified bovine milk xanthine oxidase, with Ki and Ki‘ values of 0.6 nM and 3.1 nM respectively, indicating inhibition of both the oxidized and reduced forms of xanthine oxidase[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Febuxostat (5-6 mg/kg/day) combined with fructose significantly lowers blood pressure, UA, triglycerides, and insulin in rats compared with fructose alone. Febuxostat (5–6 mg/kg/day) combined with fructose also reduces glomerular pressure, renal vasoconstriction, and afferent arteriolar area in rats compared with fructose alone[2]. Febuxostat prevents hyperuricemia in 5/6 nephrectomy (5/6 Nx)+oxonic acid (OA)+Febuxostat(Fx) rats and ameliorates proteinuria, preserves renal function and prevents glomerular hypertension in both 5/6 nephrectomy (5/6 Nx)+vehicle (V)+Febuxostat(Fx) and 5/6 nephrectomy (5/6 Nx)+oxonic acid (OA)+Febuxostat(Fx) groups[3]. Febuxostat (5 mg/kg/d by gavage for 8 days) treatment after transverse aortic constriction (TAC) attenuates the TAC-induced left ventricular (LV) hypertrophy and dysfunction. Febuxostat blunts the TAC-induced increases in nitrotyrosine (indicating reduced myocardial oxidative stress), p-Erk(Thr202/Tyr204), and p-mTOR(Ser2488), with no effect on total Erk or total mTOR[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
316.37
Formula
C16H16N2O3S
CAS 号
144060-53-7
中文名称
非布司他
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Takano Y, et al. Selectivity of febuxostat, a novel non-purine inhibitor of xanthine oxidase/xanthine dehydrogenase. Life Sci, 2005, 76(16), 1835-1847.
[2]. Sanchez-Lozada LG, et al. Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome. Am J Physiol Renal Physiol, 2008, 294(4), F710-F718.
[3]. Sanchez-Lozada LG, et al. Effect of febuxostat on the progression of renal disease in 5/6 nephrectomy rats with and without hyperuricemia. Nephron Physiol, 2008, 108(4), p69-p78.
[4]. Xu X, et al. Xanthine oxidase inhibition with febuxostat attenuates systolic overload-induced left ventricular hypertrophy and dysfunction in mice. Card Fail, 2008, 14(9), 746-753.
