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L-Sepiapterin
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
L-Sepiapterin图片
CAS NO:17094-01-8
包装:1mg
市场价:10350元

产品介绍
L-Sepiapterin(Sepiapterin)是内皮型一氧化氮合酶(eNOS)辅因子四氢生物喋呤(BH4)的前体。L-Sepiapterin改善db/db小鼠肠系膜小动脉内皮功能障碍,诱导血管生成。L-Sepiapterin通过下调p70S6K依赖性VEGFR-2表达抑制卵巢癌细胞增殖和迁移。
Cas No.17094-01-8
别名L-墨蝶呤,Sepiapterin
Canonical SMILESO=C1NC(N)=NC2=C1N=C(C([C@@H](O)C)=O)CN2
分子式C9H11N5O3
分子量237.22
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

L-Sepiapterin (Sepiapterin) is a precursor of the endothelial nitric oxide synthase (eNOS) cofactor tetrahydrobiopterin (BH4). L-Sepiapterin improves endothelial dysfunction in small mesenteric arteries from db/db mice, and induces angiogenesis. L-Sepiapterin inhibits cell proliferation and migration of ovarian cancer cells via down-regulation of p70S6K-dependent VEGFR-2 expression[1][2].

L-Sepiapterin (Sepiapterin) (0.1-10 μM; 24 hpurs) Iinduces cell proliferation in a dose-dependent manner[1].L-Sepiapterin (1-50 μM; 20 minutes) significantly inhibits the phosphorylation of VEGF-A-induced (50 ng/ml) p70S6K[1].L-Sepiapterin inhibits VEGF-A-induced cell proliferation and migration through NO-independent mechanism[1]. Cell Proliferation Assay[1] Cell Line: SKOV-3 cells

Sepiapterin (10 mg/kg; p.o. (powder chow); daily for or 8 weeks) significantly improves the relaxation to Ach in small mesenteric arteries (SMA) from db/db mice[2]. Animal Model: Male C57BL/KsJ diabetic mice (db/db)[2]

[1]. Pannirselvam M, et al. Chronic oral supplementation with sepiapterin prevents endothelial dysfunction and oxidative stress in small mesenteric arteries from diabetic (db/db) mice. Br J Pharmacol. 2003;140(4):701‐706. [2]. Cho YR, et al. Sepiapterin inhibits cell proliferation and migration of ovarian cancer cells via down-regulation of p70S6K-dependent VEGFR-2 expression. Oncol Rep. 2011;26(4):861‐867.