RGDS peptideIntegrin binding sequence; inhibits integrin receptor function CAS# 91037-65-9 |
2D Structure
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Quality Control & MSDS
3D structure
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Cas No. | 91037-65-9 | SDF | Download SDF |
PubChem ID | 107775 | Appearance | Powder |
Formula | C15H27N7O8 | M.Wt | 433.42 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | RGDS peptide | ||
Solubility | DMSO : ≥ 55 mg/mL (126.90 mM) H2O : ≥ 25 mg/mL (57.68 mM) *"≥" means soluble, but saturation unknown. | ||
Sequence | RGDS | ||
Chemical Name | (3S)-3-[[2-[[(2S)-2-amino-5-(diaminomethylideneamino)pentanoyl]amino]acetyl]amino]-4-[[(1S)-1-carboxy-2-hydroxyethyl]amino]-4-oxobutanoic acid | ||
SMILES | C(CC(C(=O)NCC(=O)NC(CC(=O)O)C(=O)NC(CO)C(=O)O)N)CN=C(N)N | ||
Standard InChIKey | NNRFRJQMBSBXGO-CIUDSAMLSA-N | ||
Standard InChI | InChI=1S/C15H27N7O8/c16-7(2-1-3-19-15(17)18)12(27)20-5-10(24)21-8(4-11(25)26)13(28)22-9(6-23)14(29)30/h7-9,23H,1-6,16H2,(H,20,27)(H,21,24)(H,22,28)(H,25,26)(H,29,30)(H4,17,18,19)/t7-,8-,9-/m0/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Integrin binding sequence that inhibits integrin receptor function. Decreases systemic inflammation via inhibition of collagen-triggered activation of leukocytes and attenuates expression of inflammatory cytokines, iNOS and MMP-9. Promotes cell attachment and abrogates apoptosis via the mitochondrial pathway in osteoblasts in vitro. |
RGDS peptide Dilution Calculator
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Arg-Gly-Asp-Ser is an integrin binding sequence that inhibits integrin receptor function, decreases systemic inflammation via inhibition of collagen-triggered activation of leukocytes and attenuates expression of inflammatory cytokines, iNOS and MMP-9.
In Vitro: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. 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].
In Vivo: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].
References:
[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.
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Synthetic RGDS peptide attenuates mechanical ventilation-induced lung injury in rats.[Pubmed:22452721]
Exp Lung Res. 2012 May;38(4):204-10.
Pulmonary inflammation is the key pathological presentation of mechanical ventilation-induced lung injury (VILI), and synthetic RGDS peptide has been suggested to attenuate pulmonary inflammation. The present study aimed to determine whether RGDS peptide has protective effects on VILI. Rats received 4 hours of high tidal volume mechanical ventilation with or without pretreatment with RGDS. Rats that were kept on spontaneous respiration served as controls. At the end of 4 hours, rats that received 4 hours of mechanical ventilation exhibited serious pulmonary pathological changes, more polymorphonulear and mononuclear leukocyte recruitment, more tumor necrosis factor (TNF-alpha) and interleukin-6 (IL-6) production, higher total protein contents in the bronchoalveolar lavage fluids (BALFs) and more lung phosphorylation of integrin beta3 and nuclear factor-kappaB inhibitor (I-kappaB), and increased NF-kappaB p65 binding activity than did the control group. Administration of RGDS peptide tended to significantly inhibit all these changes induced by mechanical ventilation. These results suggested that RGDS pretreatment might improve VILI in rats by attenuating inflammatory cascade related to integrin alphaVbeta3 and NF-kappaB.
Detection of synthetic RGDS(PO3H2)PA peptide adsorption using a titanium surface plasmon resonance biosensor.[Pubmed:21221730]
J Mater Sci Mater Med. 2011 Mar;22(3):657-61.
The purpose of this study was to measure the time-dependent chemical interaction between synthetic RGDS(PO(3)H(2))PA (P-RGD) peptide and titanium surfaces using a titanium surface plasmon resonance (SPR) biosensor and to determine the degree of peptide immobilization on the surfaces. An SPR instrument for 'single-spot' analysis was used for nanometer-scale detection of biomolecular adsorption using a He-Ne laser light according to Knoll's method. The oxidized titanium surface was etched when exposed to H(3)PO(4) solutions with a pH of 2.0 or below. The amount of P-RGD adsorbed at pH 1.9 was approximately 3.6 times as much as that at pH 3.0 (P < 0.05). P-RGD naturally adsorbed on the oxidized titanium surface as a consequence of the bonding and dissociation mechanism of the phosphate functional group. Furthermore, the control of pH played a very important role in the interaction between P-RGD and the surface. These findings show that pH control may promote progressive binding of biomolecules with the phosphate functional group to the titanium surface.
Synthetic RGDS peptide attenuated lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure in mice.[Pubmed:24476051]
J Gastroenterol Hepatol. 2014 Jun;29(6):1308-15.
BACKGROUND AND AIM: Fulminant hepatic failure (FHF) is a serious clinic syndrome with extremely poor prognosis and no effective treatment except for liver transplantation. Synthetic RGDS peptide, an inhibitor of integrins, was proved to suppress integrin signals. In this study, we investigated the protection effects of RGDS peptide on lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced FHF and the underlying molecular mechanisms. METHODS: Synthetic RGDS peptide was given intraperitoneally 30 min before LPS/D-GalN injection. Liver function and the extent of liver injury were analyzed biochemically and pathologically respectively. Enzyme-linked immunosorbent assay, real-time polymerase chain reaction and Western blotting were used to detect effectors and signaling molecules. RESULTS: Pretreatment with synthetic RGDS peptide significantly improved LPS/D-GalN-induced mortality, and liver injury as determined by alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, as well as pathological analysis. In addition, RGDS peptide significantly reduced tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MIP)-2 production, and decreased myeloperoxidase (MPO) and NF-kappaB activity. Furthermore, Western blotting indicated that the levels of phospho-integrin beta3, phospho-focal adhesion kinase (FAK) and phospho-p38 mitogen-activated protein kinases (MAPK) decreased with RGDS peptide pretreatment. CONCLUSION: Together, these data suggest that synthetic RGDS peptide protect against LPS/D-GalN-induced FHF by inhibiting inflammatory cells migration and blocking the integrin alphaVbeta3-FAK-p38 MAPK and NF-kappaB signaling.
Matrix metalloproteinase-2-deficient fibroblasts exhibit an alteration in the fibrotic response to connective tissue growth factor/CCN2 because of an increase in the levels of endogenous fibronectin.[Pubmed:19276073]
J Biol Chem. 2009 May 15;284(20):13551-61.
Matrix metalloproteinase-2 (MMP-2) is an important extracellular matrix remodeling enzyme, and it has been involved in different fibrotic disorders. The connective tissue growth factor (CTGF/CCN2), which is increased in these pathologies, induces the production of extracellular matrix proteins. To understand the fibrotic process observed in diverse pathologies, we analyzed the fibroblast response to CTGF when MMP-2 activity is inhibited. CTGF increased fibronectin (FN) amount, MMP-2 mRNA expression, and gelatinase activity in 3T3 cells. When MMP-2 activity was inhibited either by the metalloproteinase inhibitor GM-6001 or in MMP-2-deficient fibroblasts, an increase in the basal amount of FN together with a decrease of its levels in response to CTGF was observed. This paradoxical effect could be explained by the fact that the excess of FN could block the access to other ligands, such as CTGF, to integrins. This effect was emulated in fibroblasts by adding exogenous FN or RGDS peptides or using anti-integrin alpha(V) subunit-blocking antibodies. Additionally, in MMP-2-deficient cells CTGF did not induce the formation of stress fibers, focal adhesion sites, and ERK phosphorylation. Anti-integrin alpha(V) subunit-blocking antibodies inhibited ERK phosphorylation in control cells. Finally, in MMP-2-deficient cells, FN mRNA expression was not affected by CTGF, but degradation of (125)I-FN was increased. These results suggest that expression, regulation, and activity of MMP-2 can play an important role in the initial steps of fibrosis and shows that FN levels can regulate the cellular response to CTGF.
Synthetic RGDS peptide attenuates lipopolysaccharide-induced pulmonary inflammation by inhibiting integrin signaled MAP kinase pathways.[Pubmed:19272161]
Respir Res. 2009 Mar 9;10:18.
BACKGROUND: Synthetic peptides containing the RGD sequence inhibit integrin-related functions in different cell systems. Here, we investigated the effects of synthetic Arg-Gly-Asp-Ser (RGDS) peptide on key inflammatory responses to intratracheal (i.t.) lipopolysaccharide (LPS) treatment and on the integrin signaled mitogen-activated protein (MAP) kinase pathway during the development of acute lung injury. METHODS: Saline or LPS (1.5 mg/kg) was administered i.t. with or without a single dose of RGDS (1, 2.5, or 5 mg/kg, i.p.), anti-alphav or anti-beta3 mAb (5 mg/kg, i.p.). Mice were sacrificed 4 or 24 h post-LPS. RESULTS: A pretreatment with RGDS inhibited LPS-induced increases in neutrophil and macrophage numbers, total protein levels and TNF-alpha and MIP-2 levels, and matrix metalloproteinase-9 activity in bronchoalveolar lavage (BAL) fluid at 4 or 24 h post-LPS treatment. RGDS inhibited LPS-induced phosphorylation of focal adhesion kinase and MAP kinases, including ERK, JNK, and p38 MAP kinase, in lung tissue. Importantly, the inhibition of the inflammatory responses and the kinase pathways were still evident when this peptide was administered 2 h after LPS treatment. Similarly, a blocking antibody against integrin alphav significantly inhibited LPS-induced inflammatory cell migration into the lung, protein accumulation and proinflammatory mediator production in BAL fluid, at 4 or 24 h post-LPS. Anti-beta3 also inhibited all LPS-induced inflammatory responses, except the accumulation of BAL protein at 24 h post-LPS. CONCLUSION: These results suggest that RGDS with high specificity for alphavintegrins attenuates inflammatory cascade during LPS-induced development of acute lung injury.
Apoptosis and survival of osteoblast-like cells are regulated by surface attachment.[Pubmed:15522882]
J Biol Chem. 2005 Jan 21;280(3):1733-9.
We tested the hypothesis that RGDS peptides regulate osteoblast survival in culture. Osteoblast-like MC3T3-E1 cells were allowed to attach to RGDS peptides that had been tethered to a silicone surface utilizing a previously described grafting technique. The RGDS-modified surface caused up-regulation of alpha(v)beta(3) integrin. We noted that there was an increase in expression of activated focal adhesion kinase and activated Akt. There was no change in the expression level of the anti-apoptotic protein Bcl-2, the pro-apoptotic protein Bad, or the inactivated form of Bad, pBad. Attachment to the RGDS-treated membrane completely abolished apoptosis induced by staurosporine, the Ca(2+).P(i) ion pair, and sodium nitroprusside. However, the surface modification did not interfere with apoptosis mediated by the free RGDS peptide or serum-free medium. When the activity of the phosphatidylinositol 3-kinase pathway was inhibited, RGDS-dependent resistance to apoptosis was eliminated. These results indicated that the binding of cells to RGDS abrogated apoptosis via the mitochondrial pathway and that the suppression of apoptosis was dependent on the activity of phosphatidylinositol 3-kinase.