VGX-1027 Immunology & Inflammation related modulator

Cat.No.S7515

VGX-1027 (GIT 27) is an orally active immunomodulator. Phase 1.
VGX-1027 Immunology & Inflammation related modulator Chemical Structure

Chemical Structure

Molecular Weight: 205.21

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Quality Control

Batch: S751501 DMSO]41 mg/mL]false]Ethanol]41 mg/mL]false]Water]Insoluble]false Purity: 99.92%
99.92

Solubility

In vitro
Batch:

DMSO : 41 mg/mL (199.79 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 41 mg/mL

Water : Insoluble

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
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Chemical Information, Storage & Stability

Molecular Weight 205.21 Formula

C11H11NO3

Storage (From the date of receipt)
CAS No. 6501-72-0 Download SDF Storage of Stock Solutions

Synonyms GIT 27 Smiles C1C(ON=C1C2=CC=CC=C2)CC(=O)O

Mechanism of Action

In vitro
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. This compound inhibits both proliferation of enterobacterial antigen-reactive CD4+CD25− T cells in vitro.
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. This compound also reduces clinical signs of MLD-STZ-induced diabetes and suppresses pathohistological changes of pancreas. It 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), this chemical ameliorates the course of the disease with higher percent survival and improved clinical and histopathological signs.
References

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