Platelet

Platelet Factor 4 (58-70), human, is a polypeptide comprising the 58-70 amino acid sequence of Platelet Factor 4 (PF-4) residues.

GPRP acetate (Pefabloc FG) is fibrinogen-related peptides, which inhibit the interaction of fibrinogen with the platelet membrane glycoprotein IIbIIIa complex (GPIIbIIIa).

GPllb is composed of a 125 Kd heavy chain that is disulfide-linked to a 23 Kd light chain. Hydropathicity analysis of the cDNA sequence indicates that GPllb is anchored to the platelet through a single transmembrane domain located within 20 amino acids of

Platelet factor 4 (59-70) elicits human neutrophil & monocyte chemotaxis.

Bivalirudin (BG-8967) is a reversible inhibitor of α- and ζ-thrombin (Kis = 2.56 and 1.84 nM, respectively), enzymes that exhibit high fibrinogen-clotting activities.

TRAP-6 (Thrombin Receptor Activator Peptide 6)(2TFA) is an agonist of protease-activated receptor 1 (PAR1).

Arg-Gly-Asp-Ser (RGDS peptide) is a conserved tetrapeptide sequence found on fibronectin, fibrinogen α, and von Willebrand factor. It binds to integrins on the cell surface, inhibiting thrombin-induced platelet-fibrinogen interaction.

PPACK is a synthetic peptide derivative. It also irreversibly and specifically inhibits thrombin-mediated platelet activation by binding with high affinity to the active site of thrombin (Ki = 0.24 nM).

GPRP (Gly-Pro-Arg-Pro) is a fibrin polymerization inhibitor that inhibits the interaction between fibrinogen and the platelet membrane glycoprotein IIb/IIIa complex (glycoprotein IIb/IIIa receptor).

Arg-Gly-Asp-Cys TFA serves as the binding motif through which fibronectin interacts with cell adhesion molecules. This compound has the ability to hinder platelet aggregation and fibrinogen binding.

Bivalirudin TFA, a synthetic 20-residue peptide, serves as a reversible inhibitor of thrombin. Its IC50 value highlights its target specificity in vitro, where, combined with Eptifibatide (8 mg/mL) at a low concentration (70 ng/mL), it significantly reduces platelet aggregation induced by thrombin (0.2 U/mL) by approximately 90% [1]. The compound demonstrates no effect on thrombin generation assay (TGA) parameters up to 10 μmol/L [2]. Additionally, it facilitates the binding of MPO to BAEC, leading to functional alterations such as increased NO consumption and enhanced MPO-mediated redox modifications [3]. In vivo studies reveal its efficacy in preventing the rise of antiheparin/PF4 antibody IgG levels in rats, with significant findings from the toxicokinetic assessment signaling its safety profile at tested doses, although higher doses resulted in fatalities [4][5]. In clinical trials, its antithrombotic effects were explored, comparing it with alternatives like Ticagrelor and Clopidogrel in a Phase 4 study.

tcY-NH2 (trans-Cinnamoyl)-YPGKF-NH2) TFA is a selective PAR4 antagonist peptide with potent properties. It effectively inhibits thrombin- and AY-NH2-induced platelet aggregation and endostatin release. This compound finds utility in inflammation and immunology research [1] [2] [6].

CD31, also known as platelet endothelial cell adhesion molecule-1 (PECAM-1), is a receptor on endothelial cells for clostridium perfringens beta-Toxin (CPB). It also functions as an ER-MP12 antigen and connects mechanical stress, metabolism, and inflammation. The CD31 peptide promotes phosphorylation of CD31 ITIM 686 and SHP2, thereby inhibiting TCR-induced T-cell activation [1]-[5].

CD31 TFA, also known as platelet endothelial cell adhesion molecule-1 (PECAM-1), functions as the specific receptor for Clostridium perfringens beta-Toxin (CPB) in endothelial cells. It is recognized as an ER-MP12 antigen and plays a pivotal role in connecting mechanical stress, metabolism, and inflammation. Additionally, the CD31 TFA peptide facilitates the phosphorylation of CD31 ITIM 686 and SHP2, further inhibiting TCR-induced T-cell activation [1]-[5].

Cys-Arg-Gly-Asp-Phe-Pro-Ala-Ser-Ser-Cys (Disulfide bridge: Cys1-Cys10), a decapeptide with a cyclic RGD active sequence, functions as an Integrin αIIbβ3 antagonist, effectively inhibiting platelet adhesion and proMMP-13 adhesion [1].

C18G, a synthetic α-helical peptide derived from human platelet factor IV, exhibits biological activity with pronounced antibacterial properties against Salmonella.

Thrombostatin cont-1, an analogue of the bradykinin metabolite thrombostatin, has been shown to reduce platelet activation in the canine carotid artery following balloon angioplasty (BA) injury [1].

Thrombospondin-1 (TSP-1)-derived CD36 binding motif is a bioactive peptide cyclized by a disulfide bond, critical for TSP-1-CD36 interaction. Involved in cancer metastasis, tumor adhesion, and angiogenesis, this matrix-bound glycoprotein-origin peptide competitively inhibits platelet aggregation and tumor metastasis.

S-(1,2-Dicarboxyethyl)glutathione is a peptide recognized for its inhibitory effects on blood coagulation and platelet aggregation [1].

RGDV functions as a platelet aggregation inhibitor and disrupts platelet-dependent thrombus formation. Additionally, it serves in tumor recognition due to its targeting effect [1] [2].

K-Casein (106-116), bovine, is a peptide that impedes platelet aggregation and fibrinogen binding, significantly contributing to the pathophysiology of atherosclerosis [1].

Integrin Signaling Inhibitor mP13 is a compound that impedes both inside-out and outside-in integrin-mediated signaling processes, such as fibrinogen binding, platelet adhesion, and clot retraction [1].

Batifiban TFA, a cyclic peptide and antagonist of the platelet glycoprotein GPⅡb/Ⅲa, inhibits platelet aggregation by blocking the binding of circulating vitronectin to integrin ανβ3 [1].

Azurin (50-77) is a peptide fragment derived from the copper-containing bacterial protein azurin, present in P. aeruginosa. It exhibits properties that regulate the cell cycle, inhibit cancer proliferation, and manage angiogenesis, proving its potential as an anticancer agent. Specifically, this compound acts as a VEGFR2 inhibitor with an IC20 of approximately 10.7 µM. At a concentration of 20 µM, it effectively induces cell cycle arrest at the G2/M phase in MCF-7 breast cancer cells, while a higher concentration of 50 µM significantly reduces the proliferation of both MCF-7 and ZR-75-1 breast cancer cell lines. Furthermore, Azurin (50-77) impedes VEGF-A-induced capillary tube formation with an IC50 of 12 µM, and alters the cellular and extracellular levels of critical signaling and structural proteins such as F-actin, focal adhesion kinase (FAK), paxillin, and platelet endothelial cell adhesion molecule-1 (PECAM-1) in human umbilical vein endothelial cells (HUVECs) at a concentration of 25 µM. Demonstrating its efficacy in vivo, Azurin (50-77) administered at 10 mg/kg per day notably reduces tumor volume in an MCF-7 mouse xenograft model, highlighting its therapeutic potential.