Arg-Gly-Asp-Ser is an integrin binding sequence that inhibits integrin receptor function. Arg-Gly-Asp-Ser directly and specifically bind pro-caspase-8, pro-caspase-9 and pro-caspase-3, while it does not bind pro-caspase-1.

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 (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^[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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 tumor necrosis factor (TNF)-α and macrophage inflammatory protein (MIP)-2 production, and decreases myeloperoxidase (MPO) and NF-κB activity^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

433.42

C₁₅H₂₇N₇O₈

91037-65-9

Arg-Gly-Asp-Ser

RGDS

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

Powder	-80deg;C	2 years
	-20deg;C	1 year

*In solvent : -80deg;C, 6 months; -20deg;C, 1 month (sealed storage, away from moisture)

In Vitro:;

DMSO : ≥ 55 mg/mL (126.90 mM)

H₂O : ≥ 25 mg/mL (57.68 mM)

* “≥” means soluble, but saturation unknown.

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

• [1]. Grigoriou V, et al. Apoptosis and survival of osteoblast-like cells are regulated by surface attachment. J Biol Chem. 2005 Jan 21;280(3):1733-9.

  [2]. Moon C, et al. Synthetic RGDS peptide attenuates lipopolysaccharide-induced pulmonary inflammation by inhibiting integrin signaled MAP kinase pathways. Respir Res. 2009 Mar 9;10:18.

  [3]. Yin X, et al. Synthetic RGDS peptide attenuated lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure in mice. J Gastroenterol Hepatol. 2014 Jun;29(6):1308-15.

  [4]. Aguzzi MS, et al. Intracellular targets of RGDS peptide in melanoma cells. Mol Cancer. 2010 Apr 22;9:84.

Cell death is measured using the MTT analysis. This assay is based on the ability of mitochondrial dehydrogenases to oxidize thiazolyl blue (MTT), a tetrazolium salt (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenylterazolium bromide), to an insoluble blue formazan product. The cells are incubated with the MTT reagent (120 μg/mL) at 37°C for 2 h. After the supernatant is removed, 400 μL of 0.04mol/LHCl in isopropanol is added to each well, and the optical density of the solution is read at 590 nm in an enzyme-linked immunosorbent assay plate reader. As the generation of the blue product is proportional to the dehydrogenase activity, a decrease in the absorbance at 590 nm provides a direct measurement of the number of viable cells. To determine the contribution of the PI3K pathway to inhibition of apoptosis, some cell populations are pretreated with 50 μM LY294002, a PI3K inhibitor. Following this pretreatment, cell death is determined as described above.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Mice pharyngeal aspiration is performed as described. Animals are anesthetized with a mixture of ketamine and xylazine (45 mg/kg and 8 mg/kg, i.p., respectively). Test solution (30 μL) containing LPS (1.5 mg/kg) is placed posterior in the throat and aspirated into the lungs. Control mice are administrated sterile saline (0.9% NaCl). Animals are administered with Arg-Gly-Asp-Ser or RGES peptide (1, 2.5 or 5 mg/kg, i.p.) once one hour before LPS treatment and sacrificed 4 h post-LPS. Animals are also administered Arg-Gly-Asp-Ser or RGES peptide (5 mg/kg, i.p.) once at different time points (1 h before or 2 h after LPS treatment) and sacrificed 24 h post-LPS. In addition, animals are administered with αvβ3-blocking mAbs, anti-αv, or anti-β3 (5 mg/kg, i.p.) once 1 h before and sacrificed 4 h post-LPS. Animals administered with these mAbs 2 h after LPS treatment are sacrificed 24 h post-LPS

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Grigoriou V, et al. Apoptosis and survival of osteoblast-like cells are regulated by surface attachment. J Biol Chem. 2005 Jan 21;280(3):1733-9.

  [2]. Moon C, et al. Synthetic RGDS peptide attenuates lipopolysaccharide-induced pulmonary inflammation by inhibiting integrin signaled MAP kinase pathways. Respir Res. 2009 Mar 9;10:18.

  [3]. Yin X, et al. Synthetic RGDS peptide attenuated lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure in mice. J Gastroenterol Hepatol. 2014 Jun;29(6):1308-15.

  [4]. Aguzzi MS, et al. Intracellular targets of RGDS peptide in melanoma cells. Mol Cancer. 2010 Apr 22;9:84.