Arg-Gly-Asp-Ser is an integrin-binding sequence that inhibits integrin receptor function. It decreases systemic inflammation via inhibition of collagen-triggered activation of leukocytes and attenuates expression of inflammatory cytokines, MMP-9, and iNOS.

The Arg-Gly-Asp-Ser-modified surface causes up-regulation of αvβ3 integrin. Attachment to the Arg-Gly-Asp-Ser-treated membrane completely abolishes apoptosis induced by staurosporine, the Ca2+·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 [1]. 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 (Kd: 27.5 μM) and locates at the survivin C-terminus [4].

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 [2]. Arg-Gly-Asp-Ser peptide significantly reduces TNF-α and macrophage inflammatory protein (MIP)-2 production and decreases myeloperoxidase (MPO) and NF-κB activity [3].