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| Cas No.: | 91037-65-9 |
| Chemical Name: | Arg-gly-asp-ser |
| Synonyms: | L-Serine,L-arginylglycyl-L-a-aspartyl-;Arg-Gly-Asp-Ser;arginyl-glycyl-aspartyl-serine;H-Arg-Gly-Asp-Ser-OH;RGDS;RGDS peptide;2ACOH 2H2O;Arg-Gly-Asp-Ser-OH;fibronectin active fragment;FIBRONECTIN INHIBITOR;L-ARG-GLY-ASP-SER;L-Arg-Gly-L-Asp-L-Ser-OH;RGDS 1;Palmitoyl Oligopertide;Fibronectin tetrapeptide;C15H27N7O8;L-Arginylglycyl-L-alpha-aspartyl-L-serine;L-Serine, L-arginylglycyl-L-alpha-aspartyl-;L-Serine, N-(N-(N-L-arginylglycyl)-L-alpha-aspartyl)-;AK163508;3-[(S)-2-((S)-2-Amino-5-guanidino-pentanoylamino)-acetylamino]-N-(1-carboxy-2-hydroxy-ethyl)-succinamic acid;BDBM50241180;3450AH;AKO;L-Arginylglycyl-L-α-aspartyl-L-serine (ACI);L-Serine, N-[N-(N-L-arginylglycyl)-L-α-aspartyl]- (ZCI);102: PN: WO2008113030 SEQID: 103 unclaimed sequence;10: PN: JP2003089648 SEQID: 11 unclaimed;10: PN: WO03099465 SEQID: 11 claimed protein;10: PN: WO2020081717 SEQID: 10 claimed protein;110: PN: US20100136614 SEQID: 111 unclaimed sequence;11: PN: US20050142094 SEQID: 11 unclaimed sequence;11: PN: WO2013007839 SEQID: 52 claimed protein;12: PN: JP2004000070 SEQID: 14 unclaimed protein;12: PN: WO0044808 TABLE: 4 unclaimed sequence;12: PN: WO03089607 SEQID: 12 claimed sequence;13: PN: US20100028387 SEQID: 13 claimed protein;13: PN: US20140004158 SEQID: 14 claimed sequence;13: PN: US6111069 SEQID: 6 claimed protein;13: PN: WO2017072759 SEQID: 13 claimed sequence;14: PN: JP2003210166 SEQID: 14 claimed protein;14: PN: JP2004049921 SEQID: 14 unclaimed protein;16: PN: EP3415165 SEQID: 16 claimed protein;16: PN: KR20140027031 SEQID: 17 claimed protein;16: PN: WO0105991 SEQID: 17 unclaimed sequence;16: PN: WO2022027020 PAGE: 57 claimed sequence;172: PN: US20080107614 SEQID: 134 unclaimed sequence;18: PN: US20040228913 SEQID: 11 claimed sequence;18: PN: US6147189 SEQID: 6 claimed protein;18: PN: WO2011163398 SEQID: 15 unclaimed protein;1: PN: JP2002369878 SEQID: 11 unclaimed sequence;1: PN: JP2007230891 SEQID: 1 claimed protein;1: PN: JP2008195682 SEQID: 1 unclaimed protein;1: PN: JP2008195683 SEQID: 1 unclaimed protein;1: PN: JP2023038840 SEQID: 1 claimed sequence;1: PN: KR20150027940 SEQID: 2 claimed sequence;1: PN: US20040023391 PAGE: 9 claimed protein;1: PN: US20150064143 SEQID: 1 claimed sequence;1: PN: US6013628 SEQID: 16 unclaimed protein;1: PN: US6043216 SEQID: 1 claimed sequence;1: PN: WO0178529 PAGE: 26 unclaimed sequence;1: PN: WO0187071 SEQID: 2 unclaimed sequence;1: PN: WO2012124998 SEQID: 3 claimed protein;1: PN: WO2012135813 PAGE: 8 claimed protein;1: PN: WO2014172355 SEQID: 1 claimed protein;1: PN: WO2017036533 SEQID: 1 claimed protein;1: PN: WO2017040335 SEQID: 210 claimed sequence;1: PN: WO2017059312 SEQID: 1 claimed sequence;1: PN: WO2017160862 SEQID: 7 claimed protein;1: PN: WO2018201051 SEQID: 383 claimed protein;1: PN: WO2019104154 SEQID: 1 claimed protein;1: PN: WO2020097235 SEQID: 31 claimed sequence;1: PN: WO2022234536 SEQID: 1 claime... |
| SMILES: | [C@@H](CC(=O)O)(NC(=O)CNC(=O)[C@@H](N)CCCNC(N)=N)C(=O)N[C@@H](CO)C(=O)O |
| Formula: | C15H27N7O8 |
| M.Wt: | 433.416982889175 |
| Purity: | >98% |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | 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 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]. |
| 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]. |
| Cell Assay: | 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. |
| Animal Administration: | 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 |
| 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. |