thrombin

Thrombin Receptor Activator for Peptide is also called Coagulation Factor II Receptor (1-5) or Proteinase Activated Receptor 1 (1-5), used in the research of coronary heart disease (CHD).

Thrombin Receptor Activator for Peptide 5 (TRAP-5), also known as Coagulation Factor II Receptor (1-5) or Proteinase Activated Receptor 1 (1-5), is employed in coronary heart disease (CHD) research.

Thrombin is a trypsin-like serine protease that is encoded by the F2 gene in humans. Thrombin is produced by the enzymatic cleavage of two sites on prothrombin by activated Factor X (Xa). Thrombin in turn acts as a serine protease that converts soluble

Thrombin Inhibitor 6, with an IC 50 of 1 nM, acts as a potent anticoagulant by inhibiting thrombin.

Thrombin receptor agonist peptide (TRAP-14) is a 14-amino acid peptide agonist of the α-thrombin receptor. It induces aggregation of washed platelets as well as platelets in citrated and hirudin plasma. TRAP-14 (100 μM) increases the cytosolic calcium concentration in isolated guinea pig pulmonary smooth muscle cells 5-fold over baseline. It increases pulmonary arterial pressure in isolated guinea pig lung when used at a concentration of 1 μM, which is comparable to the effect induced by 10 nM α-thrombin. TRAP-14 also induces contraction of isolated rat aortic rings and increases endothelin-1 (ET-1) levels in a dose-dependent manner, an effect that is reversed by the ETA antagonist BQ-123 and the nitric oxide synthase (NOS) inhibitor L-NNA .

Thrombin inhibitor 1 is a potent inhibitor of thrombin (Ki: 0.66 nM, 2xaPTT=0.43 μM).

Thrombin inhibitor 5 (compound 385) is a thrombin inhibitor with IC 50s ranging from 0.1 μM to 1 μM. Thrombin inhibitor 5 can be used for venous thromboembolism research[1].

Thrombin (MW 37kDa) is a trypsin-like allosteric serine protease.

Thrombin receptor peptide ligand is antagonist of the thrombin receptor (EC50s = 16-33 μM to inhibit platelet aggregation in vitro). It inhibits α-thrombin and platelet aggregation induced by thrombin receptor activating peptide in vitro when used at a concentration of 32 μM but does not affect platelet aggregation induced by ADP or collagen. It also inhibits thrombin- and TRAP-induced proliferation of vascular smooth muscle cells (VSMCs). Thrombin receptor peptide ligand (100 μmol/kg bolus, i.v., plus 900 μmol/kg infusion) inhibits arterial thrombosis in a rabbit model of partial carotid artery occlusion without increasing bleeding time.

Thrombin Inhibitor 2 is a small molecule direct thrombin inhibitor. Thrombin Inhibitor 2 has antithrombotic activity.

Thrombin receptor peptide ligand, a thrombin receptor antagonist, serves as an antithrombotic agent [1].

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

Tirofiban hydrochloride monohydrate (MK-383 Hydrochloride) is a potent non-peptide, glycoprotein IIb/IIIa (integrins alphaIIbbetaIII) antagonist.

Flovagatran (TGN 255) is an orally active, potent, and selective inhibitor of thrombin and parenteral direct factor II.Flovagatran is used to study venous thromboembolism.

Melagatran, a direct and orally active thrombin inhibitor, specifically inhibits thrombin without affecting other enzymes in the coagulation cascade or fibrinolytic enzymes. It does not rely on endogenous co-factors to exert its antithrombin effect, and may alleviate the harmful effects of endotoxemia. As a result, Melagatran offers a promising strategy for the prevention of arterial occlusion.

AEBSF hydrochloride (Pefabloc SC) is an irreversible inhibitor of serine proteases, such as chymotrypsin, kallikrein, thrombin, plasmin, and trypsin.

Prothrombin (coagulation factor II) is produced in the liver and is post-translationally modified in a vitamin K-dependent reaction that converts ten glutamic acids on prothrombin into gamma-carboxyglutamic acid. Prothrombin is proteolytically cleaved to

Fibrinopeptide A, human acetate (Human fibrinopeptide A acetate) is a 16-residue short polypeptide cleaved from fibrinogen by thrombin. Fibrinopeptide A (FPA) is produced from the N-terminal Aα region of fibrinogen protein, on cleavage by thrombin.

Patamostat HCl is a highly potent and selective small molecule protease (protease) inhibitor that inhibits trypsin, fibrinolytic enzymes, and thrombin with IC50 values of 39 nM, 950 nM, and 1.9 μM, respectively.Patamostat HCl is used in the study of acute pancreatitis.

YRGDS Fibronectin Fragment acetate (YRGDS Fibronectin Fragment acetate (134282-68-1 free base))(134282-68-1 free base) is a fibronectin fragment acetate, an adhesion peptide that displays strong binding affinity to thrombin-stimulated platelets. It is RGD consisting of sequence.

H-D-Phe-Pip-Arg-pNA dihydrochloride (S-2238 dihydrochloride), a chromogenic substrate, mimics the N-terminal fragment of the A alpha chain of fibrinogen, the native substrate of thrombin. Specifically designed for thrombin detection, H-D-Phe-Pip-Arg-pNA dihydrochloride is employed for the quantification of antithrombin-heparin cofactor (AT-III). The AT-III assay utilizing this substrate is characterized by its sensitivity, accuracy, and ease of implementation.

IQB-782 is a mucolytic agent with mucolytic expectorant activity.IQB-782 inhibits thrombin-activating fibrinolytic inhibitor (TAFI), protects rats from tobacco smoke-induced respiratory obstruction, reduces the viscosity of gastric mucin suspensions in vitro, and may be useful in studies of obstructive lung disease.IQB-782 has been shown to reduce the viscosity of gastric mucin suspensions in vitro.

Efegatran sulfate (LY294468 sulfate) is a potent thrombin inhibitor used in the treatment of thrombotic disorders.

Protease-Activated Receptor-1, PAR-1 Agonist acetate is a selective proteinase-activated receptor1 (PAR-1) agonist peptide. Protease-Activated Receptor-1, PAR-1 Agonist acetate corresponds to PAR1 tethered ligand and which can selectively mimic theactions of thrombin via this receptor[1][2].

Boc-Val-Pro-Arg-MCA TFA is a sensitive fluorescent substrate that is a thrombin substrate for the determination of trypsin-like serine protease activity.

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.

TRAP-6 amide acetate is a PAR-1 thrombin receptor agonist peptide[1].

Atopaxar (E5555), a reversible PAR-1 thrombin receptor antagonist, interferes with platelet signaling. Atopaxar has been investigated for the treatment of Coronary Artery Disease and Acute Coronary Syndrome.

Patamostat (E-3123) is a potent protease inhibitor that effectively inhibits trypsin, plasmin, and thrombin, exhibiting IC50 values of 39 nM, 950 nM, and 1.9 µM, respectively. Research suggests that Patamostat might suppress the pathogenesis and development of acute pancreatitis [1] [2].

Dibutyryl-cGMP sodium (Bt2cGMP sodium) is a cell-permeable cGMP analog. Dibutyryl-cGMP sodium preferentially activates cGMP-dependent protein kinase (PKG). Dibutyryl-cGMP sodium inhibits [3H]-arachidonic acid release in human platelets stimulated by gamma

Patamostat (E-3123) mesylate is a histone deacetylase (HDAC) inhibitor.Patamostat mesylate increases the accumulation of acetylated histones and microtubule proteins in tumor cells, contributing to cell cycle termination and apoptosis.Patamostat mesylate has antitumor activity and can be used in the study of multiple myeloma.

Vorapaxar (MK-5348) (SCH 530348) is an effective and orally active thrombin receptor (PAR-1) antagonist (Ki: 8.1 nM).

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.

Leupeptin is a competitive protease inhibitor produced by actinomycetes. Leupeptin can inhibit cysteine, serine and threonine peptidases. Leupeptin inhibits serine proteinases (trypsin (Ki=3.5 nM), plasmin (Ki= 3.4 nM), porcine kallikrein), and cysteine p

Atopaxar, a reversible PAR-1 thrombin receptor antagonist, interferes with platelet signaling. Atopaxar has been investigated for the treatment of Coronary Artery Disease and Acute Coronary Syndrome.

Parmodulin 2 (ML 161) is the inhibitor of protease-activated receptor 1 (PAR1)-mediated platelet activation (IC50: 0.26 μM for the inhibition of platelet P-selectin expression on human platelets). It also inhibits thrombin-induced platelet activation.

TP508 is a 23 amino acid synthetic peptide representing residues 508-530 of human prothrombin which is identified as a potential receptor-binding domain based on competition for high-affinity thrombin binding to fibroblasts.TP508 (Chrysalin) is an investi

Ser-parafluoroPhe-Aad-Leu-Arg-Asn-Pro-NH2 is a biologically active peptide. Structure-activity studies of the thrombin receptor-tethered ligand SFLLRNP underscored the pivotal role of the Phe-2-phenyl group in receptor recognition, while substitution with para-fluorophenylalanine [(p-F)Phe] augmented its activity.

12(S)-HETrE is produced by 12-lipoxygenase oxidation of dihomo-γ-linolenic acid (DGLA). 12(S)-HETrE is reported to inhibit agonist-mediated platelet activation (IC50 = 40 μM), α granule secretion, integrin αIIbβ3 activation, Rap1 activation, and thrombin-induced clot retraction in vitro.

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).

Cycloolivil (Isoolivil) is a natural polyphenolic compound with a significant radical scavenging activity present in olive trees. Cycloolivil has antioxidant activity, it may prevent thrombotic complications associated to platelet hyperaggregability and be the base

SCH 38519 is an isochromanequinone fungal metabolite originally isolated from Thermomonospora. It inhibits aggregation induced by thrombin , as well as inhibits serotonin secretion in human platelets (IC50s = 68 and 61 μg/ml, respectively). It inhibits the growth of various Gram-negative and Gram-positive bacteria (mean MICs = 122.1 and 0.92 μg/ml, respectively).

Acetyl-Hirudin (54-65) (sulfated) directly binds to thrombin-rHCII(L444R) and hinders the interaction between the N-terminal acidic domain of rHCII and anion-binding exosite I of thrombin, which stabilizes the complex.

(-)-Denudatin B (Denudatin B) is derived from Magnolia fargesii. (-)-Denudatin B has nonspecific antiplatelet action at high concentration by inhibiting phosphoinositides breakdown induced by collagen and thrombin.

RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 dihydrochloride inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective relative to U46619 . RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis[1][2]. Proteinase-activated receptors (PARs) are a family of G protein-coupled receptors activated by the proteolytic cleavage of their N-terminal extracellular domain, exposing a new amino terminal sequence that functions as a tethered ligand to activate the receptors.RWJ56110 inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM) while being quite selective relative to collagen and the thromboxane mimetic U46619 [1].RWJ-56110 dihydrochloride is fully inhibits thrombin-induced RASMC proliferation with an IC50 value of 3.5 μM. RWJ-56110 dihydrochloride shows blockade of thrombin's action with RASMC calcium mobilization (IC50=0.12 μM), as well as with HMVEC (IC50=0.13 μM) and HASMC calcium mobilization (IC50=0.17 μM)[1].RWJ56110 (0.1-10 μM; 24-96 hours) inhibits endothelial cell growth dose-dependently, with half-maximal inhibitory concentration of RWJ56110 is approximately 10 μM[2].RWJ56110 (0.1-10 μM; 6 hours) inhibits DNA synthesis of endothelial cells in a thymidine incorporation assays. Endothelial cells are in fast-growing state (50-60% confluence), RWJ56110 inhibits cell DNA synthesis in a dose-dependent manner, but when cells that are in the quiescent state (100% confluent), the inhibitory effect of PAR-1 antagonists is much less pronounced[2].RWJ56110 (0.1-10 μM; pretreatment for 15 min) inhibits thrombin-induced Erk1/2 activation in a concentration-dependent manner. However, when endothelial cells are stimulated by FBS (final concentration 4%), it reduces partially the activated levels of Erk1/2[2].RWJ56110 (30 μM; 24 hours) has an inhibitory effect on endothelial cell cycle progression. It reduces the percentage of cells in the S phase, while alterations in the percentages of G1 and G2/M cells are less pronounced[2]. Western Blot Analysis[2] Cell Line: Endothelial cells [1]. Andrade-Gordon, et al.Design, synthesis, and biological characterization of a peptide-mimetic antagonist for a tethered-ligand receptor. oc Natl Acad Sci U S A. 1999 Oct 26;96(22):12257-62. [2]. Panagiota Zania, et al. Blockade of angiogenesis by small molecule antagonists to protease-activated receptor-1: association with endothelial cell growth suppression and induction of apoptosis. J Pharmacol Exp Ther. 2006 Jul;318(1):246-54.

TFLLR-NH2(2TFA) is an agonist of PAR1 (EC50 :1.9 μM).

JAMM protein inhibitor 2 (Acetamide, 2-(2-ethylphenoxy)-N-[2-methyl-4-(1-pyrrolidinyl)phenyl]-) is an inhibitor of JAMM protease and can be used for anticancer studies. The IC50s are 10 μM, 46 μM, and 89 μM for thrombin, Rpn11, and MMP2, respectively.

S 2238 is a chromogenic substrate for thrombin that is used in amidolytic assay.

Rosenonolactone shows inhibitory activity against prolyl endopeptidase and thrombin.