Description

Product Description

Pep-10L peptide is a synthetic research peptide identified as a selective antagonist of glycoprotein VI (GPVI)—a critical platelet receptor for collagen involved in thrombus formation and hemostasis. By binding competitively to GPVI and blocking its interaction with collagen or collagen-mimetic ligands, Pep-10L peptide inhibits platelet activation and aggregation, thereby exerting anti-thrombotic activity without severely impairing normal hemostasis.

Scientific Background

Platelets play an essential role in maintaining vascular integrity, responding to endothelial injury through adhesion, activation, and aggregation. While this process is vital for preventing bleeding, excessive or uncontrolled platelet activation leads to pathological thrombosis, contributing to diseases such as myocardial infarction, ischemic stroke, and venous thromboembolism.

Among the receptors on platelet membranes, glycoprotein VI (GPVI) is the principal signaling receptor for collagen and collagen-like structures such as convulxin, CRP (collagen-related peptide), and GPO (glycoprotein-binding peptides). GPVI-mediated activation triggers downstream signaling cascades involving Src-family kinases, Syk, and PLCγ2, ultimately resulting in intracellular calcium release and platelet aggregation.

Pep-10L peptide functions as a competitive inhibitor of GPVI, preventing the receptor from binding to collagen fibrils. By disrupting this interaction, Pep-10L peptide effectively attenuates platelet activation and reduces thrombus formation in experimental settings, without the extensive bleeding risks often associated with other platelet inhibitors such as aspirin or P2Y₁₂ antagonists.

Product Specifications

Mechanism of Action

Pep-10L peptide’s mechanism of action centers on selective inhibition of GPVI-collagen binding, which is critical for platelet activation during vascular injury and thrombus formation.

1. GPVI-Collagen Interaction Blockade

GPVI is a type I transmembrane glycoprotein found exclusively on platelets and megakaryocytes. It functions as the primary collagen receptor, triggering signal transduction when platelets encounter exposed collagen following endothelial disruption.

Pep-10L peptide binds to the extracellular domain of GPVI, occupying or sterically hindering the collagen-binding interface. This interference blocks the association between GPVI and its natural ligands—CRP, GPO-1, and Type I collagen—each of which contributes to different aspects of platelet adhesion and activation.

2. Signal Transduction Inhibition

By antagonizing GPVI, Pep-10L peptide disrupts downstream phosphorylation events mediated by Src-family kinases (Fyn and Lyn) and Syk kinase, thereby inhibiting the activation of PLCγ2 and reducing cytosolic Ca²⁺ mobilization. The end result is diminished platelet granule release and reduced integrin αIIbβ3 activation, both essential for platelet aggregation.

3. Functional Outcomes in Research Models

• Inhibition of Platelet Aggregation: Demonstrates significant inhibition of collagen-induced platelet clumping in vitro.

• Reduction in Thrombus Formation: Reduces thrombus size and stability in collagen-dependent thrombosis models.

• Maintenance of Hemostasis: Exhibits minimal prolongation of bleeding time, highlighting its selectivity for GPVI over other platelet pathways.

• Reversibility: Inhibition is reversible upon peptide removal, making it suitable for controlled experimental designs.

4. Therapeutic and Research Potential

The unique selectivity of Pep-10L peptide makes it a valuable research tool for:

• Investigating GPVI signaling mechanisms in platelet activation.

• Developing novel anti-thrombotic strategies with lower bleeding risks.

• Studying platelet-collagen interactions in cardiovascular pathology.

• Screening potential GPVI-targeting compounds or combination therapies.

  

Side Effects

Pep-10L peptide has not been evaluated for clinical use, but research observations and in vitro data suggest potential laboratory effects:

• Reduced Platelet Aggregation: Expected due to GPVI antagonism; reversible upon peptide withdrawal.

• Minor Bleeding Propensity: Prolonged clotting time may be observed in overexposed samples.

• No Cytotoxicity: No significant cytotoxic or off-target cellular effects have been reported at research concentrations.

• Protein Binding Interference: May interfere with collagen-binding assays or other peptide-protein binding studies if used in high concentrations.

Proper laboratory handling and dosage optimization are recommended to maintain experimental accuracy.

Disclaimer

For research use only. Not intended for human or veterinary use. Do not use in diagnostic or therapeutic applications. Handle with appropriate laboratory safety procedures.

Keywords

Pep-10L peptide, GPVI antagonist, anti-thrombotic peptide, platelet activation inhibitor, collagen-binding inhibitor, cardiovascular research peptide, platelet aggregation blockade, thrombus formation research.

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