| Description | L-Sepiapterin, also known as Sepiapterin, is a precursor compound crucial for the production of tetrahydrobiopterin (BH4), which serves as a coenzyme for endothelial nitric oxide synthase (eNOS). This compound demonstrates its efficacy by improving endothelial dysfunction in small mesenteric arteries from db/db mice and promoting angiogenesis. Moreover, L-Sepiapterin exerts inhibitory effects on cellular proliferation and migration in ovarian cancer cells through the down-regulation of p70S6K-dependent vascular endothelial growth factor receptor-2 (VEGFR-2) expression[1][2]. |
| In vitro | 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 |
| In vivo | 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] |
| molecular weight | 237.22 |
| Molecular formula | C9H11N5O3 |
| CAS | 17094-01-8 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
| References | 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. |