L-Sepiapterin |
Catalog No.GC61007 |
La L-sépiaptérine (sépiaptérine) est un précurseur du cofacteur endothélial de l'oxyde nitrique synthase (eNOS) tétrahydrobioptérine (BH4). La L-sépiaptérine améliore la dysfonction endothéliale dans les petites artères mésentériques des souris db/db et induit l'angiogenèse. La L-sépiaptérine inhibe la prolifération cellulaire et la migration des cellules cancéreuses de l'ovaire via une régulation À la baisse de l'expression du VEGFR-2 dépendant de p70S6K.
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Cas No.: 17094-01-8
Sample solution is provided at 25 µL, 10mM.
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.
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