CAS NO: | 6501-72-0 |
规格: | ≥98% |
包装 | 价格(元) |
50mg | 电议 |
100mg | 电议 |
250mg | 电议 |
500mg | 电议 |
Molecular Weight (MW) | 205.21 |
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Formula | C11H11NO3 |
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 |
Synonyms | VGX-1027; GIT-27; VGX 1027; GIT 27; VGX1027; GIT27 |
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. |
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In Vivo | VGX-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 model | NOD Mice with MLD-STZ-induced diabetes |
Formulation & Dosage | Dissolved 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. |