platelet

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

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

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

Z-Gly-Gly-Arg-AMC TFA (66216-78-2 free base) is a thrombin-specific fluorogenic substrate for testing thrombin generation in PRP and platelet-poor plasma (PPP).

tcY-NH2 TFA is a selective PAR4 antagonist peptide. Inhibits endostatin release and platelet aggregation induced by thrombin.

Arg-Gly-Asp-Cys acetate inhibits platelet aggregation and fibrinogen binding. Arg-Gly-Asp-Cys acetate is the binding motif of fibronectin to cell adhesion molecules.

Fibrinogen-Binding Peptide (designed by anticomplementarity hypothesis) is a presumptive peptide mimic of the vitronectin binding site on the fibrinogen receptor. Fibrinogen-Binding Peptide binds fibrinogen and inhibits both the adhesion of platelets to fibrinogen and platelet aggregation, and also inhibits the adhesion of platelets to vitronectin

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].

Potent irreversible αVβ3 integrin antagonist (Ki = 0.27 nM). Disrupts attachment of osteoclasts to bone and inhibits bone reabsorption (IC50 = 0.1 nM). Prevents ADP-induced platelet aggregation via inhibition of glycoprotein IIb/IIIa (GpIIb/IIIa, αIIbβ3)

Fibrinogen-Binding Peptide (designed by anticomplementarity hypothesis) is a presumptive peptide mimic of the vitronectin binding site on the fibrinogen receptor. Fibrinogen, a soluble plasma protein, is a cofactor in platelet activation. It is converted

Z-Gly-Gly-Arg-AMC is a specific fluorogenic substrate utilized for assessing thrombin generation in Platelet-Rich Plasma (PRP) and Platelet-Poor Plasma (PPP), with a particular focus on thrombin activity.

Selective PAR4 antagonist peptide. Inhibits endostatin release and platelet aggregation induced by thrombin.

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].

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

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

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).

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.

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].

Arg-Gly-Asp-Cys is the binding motif of fibronectin and cell adhesion molecules, which can inhibit platelet aggregation and fibrinogen binding.

LAU-0901, a platelet-activating factor (PAF) receptor antagonist, demonstrates efficacy in reducing infarct volume and enhancing neurological function in rats subjected to middle cerebral artery occlusion (MCAO)-induced cerebral ischemia, at doses of 30, 60, and 90 mg/kg. Furthermore, it diminishes microglial infiltration while promoting astrocytic and neuronal survival in the same model. Additionally, at a dose of 30 mg/kg, LAU-0901, either alone or combined with atorvastatin, shows a capability to inhibit tumor growth in a U87MG glioblastoma mouse orthotopic tumor model.

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.

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

Fibrinogen Binding Inhibitor Peptide, a synthetic dodecapeptide, represents the specific platelet receptor recognition site of the human fibrinogen g-chain (residues 400-411).

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

Z-Gly-Gly-Arg-AMC acetate is a thrombase-specific fluorescent matrix for the detection of thrombin production in PRP and poor platelet plasma (PPP).

Pam2CSK4 TFA (PUL-042 TFA) is a potent dual agonist of TLR2 and TLR6, a peptide that mimics bacterial lipoproteins.Pam2CSK4 TFA promotes platelet aggregation, and can be used to study the effects of lipoproteins on the periodontium.

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.

Aviptadil Acetate (Vasoactive Intestinal Peptide acetate salt) induces pulmonary vasodilation and inhibits the proliferation of vascular SMCs and platelet aggregation. Avitadil acetate can be used for research on pulmonary fibrosis, pulmonary hypertension (PAH), and respiratory failure caused by SARS-CoV-2.

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].

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.

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 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].

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