RGDS peptide
(Synonyms: RGDS peptide; Fibronectin tetrapeptide) 目录号 : GC16385
RGDS peptide含有可介导细胞外基质蛋白与细胞整合素相互作用的Arg-Gly-Asp(RGD)序列,被广泛用于研究整合素功能。
Cas No.:91037-65-9
Sample solution is provided at 25 µL, 10mM.
RGDS peptide contains the Arg-Gly-Asp (RGD) motif that mediates the interaction between extracellular matrix proteins and cell integrins and is widely used to probe integrin function[1]. RGDS peptide demonstrates significant antibacterial potential as an antibiotic adjuvant[2]. RGDS peptide covalently functionalized ND (NDCO-RGDS) can also be a tumor-targeting carrier of VEGF-siRNA[3].
In vitro, treatment of osteoblast-like cells with 0.2mM RGDS peptide for three days completely blocked apoptosis induced by staurosporine, the Ca2+·Pi ion pair, and sodium nitroprusside[4]. Following 500μg/mL RGDS peptide treatment for 2, 6, 16, and 24h, SK-MEL-110 cells internalized RGDS peptide in a time-dependent manner and exhibited marked anti-proliferative and pro-apoptotic effects independent of any extracellular anti-adhesive action[5].
In vivo, a single intraperitoneal injection of RGDS peptide 1h before lipopolysaccharide (LPS) challenge (1, 2.5, or 5mg/kg) dose-dependently suppressed the LPS-induced increases in neutrophil and macrophage counts, total protein content, TNF-α and macrophage inflammatory protein (MIP)-2 levels, and matrix metalloproteinase-9 activity in bronchoalveolar lavage fluid[6]. In Balb/c mice, a single intraperitoneal injection of RGDS peptide (5mg/kg) 30min before LPS (50μg/kg) and D-GalN (800mg/kg) markedly reduced hepatic injury and mortality[7].
References:
[1] Ortega-Velázquez R, Díez-Marqués ML, Ruiz-Torres MP, et al. Arg-Gly-Asp-Ser (RGDS) peptide stimulates transforming growth factor beta1 transcription and secretion through integrin activation. FASEB J. 2003;17(11):1529-1531.
[2] Feng Y, Xie W, Wan Z, et al. Harnessing RGDS peptides to regulate bacterial-host interfaces for targeted antimicrobial therapy. J Control Release. 2025;384:113922.
[3] Cui C , Wang Y , Zhao W , et al. RGDS covalently surfaced nanodiamond as a tumor targeting carrier of VEGF-siRNA: synthesis, characterization and bioassay. J Mater Chem B. 2015;3(48):9260-9268.
[4] Grigoriou V, Shapiro IM, Cavalcanti-Adam EA, et al. Apoptosis and survival of osteoblast-like cells are regulated by surface attachment. J Biol Chem. 2005;280(3):1733-1739.
[5] Aguzzi MS, Fortugno P, Giampietri C, et al. Intracellular targets of RGDS peptide in melanoma cells. Mol Cancer. 2010;9:84.
[6] Moon C, Han JR, Park HJ, et al. Synthetic RGDS peptide attenuates lipopolysaccharide-induced pulmonary inflammation by inhibiting integrin signaled MAP kinase pathways. Respir Res. 2009;10(1):18.
[7] Yin X, Gong X, Jiang R, et al. Synthetic RGDS peptide attenuated lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure in mice. J Gastroenterol Hepatol. 2014;29(6):1308-1315.
RGDS peptide含有可介导细胞外基质蛋白与细胞整合素相互作用的Arg-Gly-Asp(RGD)序列,被广泛用于研究整合素功能[1]。RGDS peptide作为抗生素佐剂亦表现出显著的抗菌潜力[2]。共价修饰的RGDS peptide功能化纳米金刚石(NDCO-RGDS)还可作为VEGF-siRNA的肿瘤靶向递送载体[3]。
在体外,0.2mM的RGDS peptide处理类成骨细胞3天,可完全阻断由星形孢菌素、Ca2+·Pi离子对和硝普钠诱导的细胞凋亡[4]。以500μg/mL的RGDS peptide处理SK-MEL-110细胞2、6、16和24小时后,RGDS peptide被细胞以时间依赖性方式摄取,并表现出显著的抗增殖和促凋亡效应,且该效应独立于其胞外抗黏附作用[5]。
在体内,于脂多糖(LPS)刺激前1小时单次腹腔注射1、2.5或5mg/kg的RGDS peptide,可剂量依赖性地抑制LPS诱导的支气管肺泡灌洗液中中性粒细胞和巨噬细胞数量、总蛋白含量、TNF-α和巨噬细胞炎症蛋白(MIP)-2水平以及基质金属蛋白酶-9活性的升高[6]。在Balb/c小鼠中,于LPS(50μg/kg)和D-GalN(800mg/kg)刺激前30分钟单次腹腔注射5mg/kg的RGDS peptide,可显著减轻肝损伤并降低死亡率[7]。
Cell experiment [1]: | |
Cell lines | Osteoblast-like cells |
Preparation Method | To evaluate cell death, osteoblast-like cells were plated on experimental (RGDS peptide) and control (Arg-Gly-Glu-Ser (RGES)) substrates in 12- or 24-well plates at a density of 50,000/well or 25,000/well, respectively. After 3 days in culture in complete media, the osteoblasts were incubated overnight with sublethal doses of staurosporine (0.1 and 0.5μM), the Ca2+ (2.4 and 2.9mM) and Pi (3mM) ion pair, or sodium nitroprusside (0.5 and 0.1mM). |
Reaction Conditions | 0.2mM; 3 days |
Applications | Cells were grown on the RGDS peptide substrate and treated with 0.1 and 0.5μM staurosporine; no significant cell killing was observed. In contrast, staurosporine killed osteoblasts maintained on the RGES surface in a dose-dependent manner. Although 3mM Pi and 2.4mM Ca2+ did not kill osteoblasts grown on the RGDS peptide surface, there was a significant increase in cell death on the RGES surface. A further increase in cell death was apparent when osteoblasts were treated with 3mM Pi and 2.9mM Ca2+. Again, there was no significant increase in death among osteoblasts maintained on the RGDS peptide surface. The effect of the Nitric Oxide (NO) donor sodium nitroprusside on osteoblast apoptosis was similar to that of the Ca2+·Pi ion pair and staurosporine. At concentrations of 0.1 and 0.5mM, sodium nitroprusside killed 45 and 65% of osteoblasts cultured on the RGES surface, respectively. These concentrations of sodium nitroprusside failed to kill osteoblasts on the RGDS peptide surface. |
Animal experiment [2]: | |
Animal models | Male BALB/C mice |
Preparation Method | Animals were anesthetized with a mixture of ketamine and xylazine (45mg/kg and 8mg/kg; i.p.; respectively). Test solution (30μl) containing lipopolysaccharide (LPS) (1.5mg/kg) was placed posterior to the throat and aspirated into the lungs. Control mice were administered sterile saline (0.9% NaCl). Animals were administered with RGDS peptide or Arg-Gly-Glu-Ser (RGES) peptide (1, 2.5, or 5mg/kg; i.p.) one hour before LPS treatment and sacrificed 4h post-LPS. Animals were also administered RGDS peptide or RGES peptide (5mg/kg; i.p.) once at different time points (1h before or 2h after LPS treatment) and sacrificed 24h post-LPS. |
Dosage form | 1, 2.5, or 5mg/kg; i.p. |
Applications | A pretreatment with RGDS peptide inhibited LPS-induced increases in neutrophil and macrophage numbers, total protein levels, and TNF-α and macrophage inflammatory protein (MIP)-2 levels, and matrix metalloproteinase-9 activity in bronchoalveolar lavage (BAL) fluid in a dose-dependent manner at 4 or 24h post-LPS treatment. RGDS peptide inhibited LPS-induced phosphorylation of focal adhesion kinase and mitogen-activated protein (MAP) kinases, including ERK, JNK, and p38 MAP kinase, in lung tissue. Importantly, the inhibition of the inflammatory responses and the kinase pathways was still evident when this peptide was administered 2h after LPS treatment. |
References: |
Cas No. | 91037-65-9 | SDF | |
别名 | RGDS peptide; Fibronectin tetrapeptide | ||
化学名 | (6R,12S,15R)-1,1,6-triamino-12-(carboxymethyl)-15-(hydroxymethyl)-7,10,13-trioxo-2,8,11,14-tetraazahexadec-1-en-16-oic acid | ||
Canonical SMILES | O=C([C@@H](CCC/N=C(N)\N)N)NCC(N[C@H](C(N[C@@H](C(O)=O)CO)=O)CC(O)=O)=O | ||
分子式 | C15H27N7O8 | 分子量 | 433.42 |
溶解度 | ≥ 21.65mg/mL in Water | 储存条件 | Desiccate at -20°C |
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1 mg | 5 mg | 10 mg |
1 mM | 2.3072 mL | 11.5362 mL | 23.0723 mL |
5 mM | 0.4614 mL | 2.3072 mL | 4.6145 mL |
10 mM | 0.2307 mL | 1.1536 mL | 2.3072 mL |
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2.
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- Purity: >98.50%
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