RGDS peptide (Synonyms: Fibronectin Inhibitor, HArgGlyAspSerOH) |
| Katalog-Nr.GC16385 |
Das RGDS-Peptid ist eine Integrin-Bindungssequenz, die die Funktion des Integrin-Rezeptors hemmt.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 91037-65-9
Sample solution is provided at 25 µL, 10mM.
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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.
| 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 | |
| Überlieferungen | Fibronectin Inhibitor, HArgGlyAspSerOH | ||
| Chemical Name | (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 | ||
| Formula | C15H27N7O8 | M.Wt | 433.42 |
| Löslichkeit | ≥ 21.65mg/mL in Water | Storage | Desiccate at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
|
1 mg | 5 mg | 10 mg |
| 1 mM | 2.3072 mL | 11.5362 mL | 23.0723 mL |
| 5 mM | 461.4 μL | 2.3072 mL | 4.6145 mL |
| 10 mM | 230.7 μL | 1.1536 mL | 2.3072 mL |
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Quality Control & SDS
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- Purity: >98.50%
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Average Rating: 5 (Based on Reviews and 25 reference(s) in Google Scholar.)
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