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VGX-1027(GIT 27)
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。
VGX-1027(GIT 27)图片
CAS NO:6501-72-0
规格:≥98%
包装与价格:
包装价格(元)
50mg电议
100mg电议
250mg电议
500mg电议

产品介绍
理化性质和储存条件
Molecular Weight (MW)205.21
FormulaC11H11NO3
CAS No.6501-72-0
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 41 mg/mL (199.8 mM)
Water: <1 mg/mL
Ethanol: 41 mg/mL (199.8 mM)
Solubility (In vivo)2% DMSO+30% PEG 300+5% Tween 80+ddH2O: 10mg/mL
SynonymsVGX-1027; GIT-27; VGX 1027; GIT 27; VGX1027; GIT27
实验参考方法
In Vitro

In vitro activity: VGX-1027 significantly inhibits both IL-1β/IFN-γ-induced TNF-α and nitrite accumulation, and causes a significant increase in cell survival by interfering with the cytotoxic effects of the cytokines. VGX-1027 inhibits both proliferation of enterobacterial antigen-reactive CD4+CD25– T cells in vitro.


Cell Assay: In microarray analysis, VGX-1027 modulated the expression of genes that involved in immune activation and the antigen processing and presentation in response to lipopolysaccharide (LPS) stimulation. In CD4+CD25– T cells, VGX-1027 inhibited cell proliferation induced by enterobacterial antigen.

In VivoVGX-1027 prevents development of spontaneous type 1 diabetes in NOD Mice and counteracts accelerated diabetogenesis induced by cyclophosphamide challenge or adoptive transfer of diabetogenic spleen cells in NOD Mice. VGX-1027 also reduces clinical signs of MLD-STZ-induced diabetes and suppresses pathohistological changes of pancreas. VGX-1027 suppresses the development of clinical, histological and immunological signs of DNBS-induced colitis in CD1 mice. In NZB/NZW F1 model of systemic lupus erythematosus (SLE), VGX-1027 ameliorates the course of the disease with higher percent survival and improved clinical and histopathological signs.
Animal modelNOD Mice with MLD-STZ-induced diabetes
Formulation & DosageDissolved in 500 mM Na2HPO4; 20 mg/kg b.wt. i.p. and 100 mg/kg b.wt. p.o.; i.p. or p.o.
References

J Pharmacol Exp Ther. 2007 Mar;320(3):1038-49; Eur J Pharmacol. 2008 May 31;586(1-3):313-21.