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Arg-Gly-Glu-Ser TFA

Cat No.:V77242 Purity: ≥98%
Arg-Gly-Glu-Ser TFA is a RGD-related peptide that controls the inhibitory activity of RGDS on the binding of fibrinogen to activated platelets.
Arg-Gly-Glu-Ser TFA
Arg-Gly-Glu-Ser TFA Chemical Structure Product category: Peptides
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
5mg
10mg
50mg
Other Sizes

Other Forms of Arg-Gly-Glu-Ser TFA:

  • Cyclo(Gly-Arg-Gly-Glu-Ser-Pro) (c(GRGESP))
  • Arg-Gly-Glu-Ser
Official Supplier of:
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Top Publications Citing lnvivochem Products
Product Description
Arg-Gly-Glu-Ser TFA is a RGD-related peptide that controls the inhibitory activity of RGDS on the binding of fibrinogen to activated platelets.
Arg-Gly-Glu-Ser TFA (RGES) is a synthetic tetrapeptide that serves as a non-adhesive control in cell adhesion experiments. It is a variant of the RGDS (Arg-Gly-Asp-Ser) cell adhesion motif where aspartic acid (Asp) is replaced by glutamic acid (Glu). RGES is inactive in integrin binding and is used to verify specificity in adhesion studies.
Biological Activity I Assay Protocols (From Reference)
Targets
Integrins (specifically those recognizing RGD motifs) - RGES lacks the critical aspartic acid residue required for integrin binding. It does not activate or bind to integrin receptors with high affinity, making it an ideal negative control for experiments involving RGDS-mediated cell adhesion.
ln Vitro
RGES binds to neonatal rat calvarial osteoblasts with an average Kd of approximately 3.0 × 10-⁴ M. In contrast to RGDS (55-60% inhibition), RGES has minimal effect on cell attachment to fibronectin-coated surfaces. It shows no significant inhibition of fibrinogen binding to activated platelets.
ln Vivo
In comparison to LPS- or saline-treated mice, respectively, Arg-Gly-Glu-Ser (5 mg/kg) in conjunction with LPS or saline + RGDS has no effect on protein accumulation, neutrophil and macrophage cell counts, or both[1].
In mouse models, RGES (5 mg/kg combined with LPS or saline) does not affect neutrophil or macrophage recruitment, unlike RGDS which alters immune cell trafficking. Its lack of in vivo activity makes it a suitable control peptide for studies involving RGDS-mediated effects.
Enzyme Assay
Receptor binding assays using radiolabeled RGDS or RGES and membrane preparations from integrin-expressing cells (e.g., osteoblasts) are used to measure binding affinity. Cells are incubated with labeled peptide at varying concentrations, and bound radioactivity is quantified after washing. RGES is used as a competitor to demonstrate specificity.
Cell Assay
Cell adhesion assays: Cells are seeded onto fibronectin- or vitronectin-coated microtiter plates in serum-free medium containing RGES or RGDS (0-1 mM). After incubation (30-60 min), non-adherent cells are removed by washing. Adherent cells are fixed, stained (e.g., with crystal violet), and quantified by absorbance measurement.
Animal Protocol
In animal studies, RGES is administered intraperitoneally or intravenously at 5 mg/kg together with LPS or other inflammatory stimuli in mouse models. Endpoints include quantification of immune cell infiltration (neutrophils, macrophages) in tissues by flow cytometry or immunohistochemistry, compared to RGDS-treated controls.
ADME/Pharmacokinetics
No detailed pharmacokinetic data available. As a small tetrapeptide, RGES is expected to be rapidly cleared from circulation by proteolytic degradation and renal filtration. Its short half-life (minutes) makes it suitable only for acute experimental interventions.
Toxicity/Toxicokinetics
No toxicity data specific to RGES. As an endogenous amino acid sequence and a control peptide with minimal biological activity, RGES is generally considered non-toxic at research concentrations. Standard laboratory safety practices are sufficient.
References

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

Additional Infomation
RGES is a standard negative control peptide for RGD-dependent cell adhesion experiments. The substitution of aspartic acid (D) with glutamic acid (E) abolishes integrin recognition. It is not FDA-approved and is strictly for research use. Molecular weight: ~561.5 g/mol as TFA salt.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C18H30F3N7O10
Molecular Weight
561.47
Related CAS #
Arg-Gly-Glu-Ser;93674-97-6
Appearance
White to off-white solid powder
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
H2O :~20 mg/mL (~35.62 mM)
Solubility (In Vivo)
Solubility in Formulation 1: 100 mg/mL (178.10 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 1.7810 mL 8.9052 mL 17.8104 mL
5 mM 0.3562 mL 1.7810 mL 3.5621 mL
10 mM 0.1781 mL 0.8905 mL 1.7810 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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