Molecular Formula | C15H27N7O8
|
Molar Mass | 433.42 |
Density | 1.65±0.1 g/cm3(Predicted) |
Melting Point | 183-187℃ |
Water Solubility | Soluble in water at 1mg/ml |
Appearance | White to off-white powder |
pKa | 2.84±0.10(Predicted) |
Storage Condition | -20°C |
Sensitive | Easily absorbing moisture |
MDL | MFCD00076452 |
Use | This product is for scientific research only and shall not be used for other purposes. |
In vitro study | The Arg-Gly-Asp-Ser-modified surface causes up-regulation of αvβ3integrin. Attachment to the Arg-Gly-Asp-Ser-treated membrane completely abolishes apoptosis induced by staurosporine, the Ca 2+ ·Pi ion pair, and sodium nitroprusside. Arg-Gly-Asp-Ser-dependent resistance to apoptosis is eliminated, when the activity of the phosphatidylinositol 3-kinase pathway is inhibited. Arg-Gly-Asp-Ser interacts with survivin, as well as with procaspase-3, -8 and -9. Arg-Gly-Asp-Ser-peptide binding to survivin is found to be specific, at high affinity (K d 27.5 μM) and locates at the survivin C-terminus. Arg-Gly-Asp-Ser-survivin interaction appears to play a key role, since Arg-Gly-Asp-Ser lost its anti-mitogenic effect in survivin-deprived cells with a specific siRNA. |
In vivo study | Arg-Gly-Asp-Ser (2.5 or 5 mg/kg, 1 h before LPS) significantly inhibits LPS-induced MMP-9 activity in BAL fluid 4 h post-LPS. Arg-Gly-Asp-Ser (1, 2.5 or 5 mg/kg, i.p.) administers 1 h before LPS inhibited LPS-induced increases in TNF-α and MIP-2 levels in BAL fluid at 4 h post-LPS. Arg-Gly-Asp-Ser peptide significantly reduces tumor necrosis factor (TNF)-α and macrophage inflammatory protein (MIP)-2 production, and decreases myeloperoxidase (MPO) and NF-κB activity. |