Betrixaban (PRT054021) hydrochloride is a highly potent, selective, and orally efficacious factor Xa (fXa) inhibitor with an IC50 of 1.5 nM. Betrixaban hydrochloride shows antithrombotic effect[1][3].
Osocimab (BAY 1213790), an anti-FXIa antibody (Ki=2.4 nM; EC50=0.2 nM). FXI inhibition may reduce the risk of thrombosis. Osocimab inhibits thrombin generation, and prolongs activated partial thromboplastin time. Osocimab exhibits anticoagulant effects[1].
5-R-Rivaroxaban is (R)-enantiomer of Rivaroxaban. Rivaroxaban (BAY 59-7939) is a highly potent and selective, direct Factor Xa (FXa) inhibitor, achieving a strong gain in anti-FXa potency (IC50 0.7 nM; Ki 0.4 nM).
FXIa-IN-13 (example 1) is an Factor Xa inhibitor with antithrombotic activity. FXIa-IN-13 inhibits arteriovenous thrombosis in vivo and in vitro[1].
EMD 495235 is a potent and orally active coagulation factor Xa inhibitor with an IC50 of 5.5 nM and a Ki of 6.8 nM. EMD 495235 shows anticoagulant activities[1].
RWJ-445167 is a dual inhibitor of thrombin and factor Xa with Ki of 4.0 nM and 230 nM, respectively, exhibiting potent antithrombotic activity.
Zifaxaban is a novel, potent, selective, direct and oral factor Xa inhibitor with IC50 of 11.1 nM (human FXa), displays > 10,000-fold selectivity than other serine proteases; also deoes not impair platelet aggregation induced by collagen, adenosine diphosphate (ADP) or arachidonic acid; significantly prolongs clotting time, prothrombin time (PT), and activated partial thromboplastin time (APTT) in the plasma of humans, rabbits, and rats, with a relatively weak effect on thrombin time; strongly suppresses thrombus formation with ED50 values of 3.09 mg/kg in venous thrombosis models in rats.
Ozagrel(OKY-046) is an antiplatelet agent working as a thromboxane A2 synthesis inhibitor.Target: Thromboxane A2 SynthaseOzagrel was selected as the best compound of highly selective inhibitors of TXA2 synthase. The inhibition of TXA2 synthase by ozagrel was more effective on human and rabbit enzymes than those of other species. Ozagrel increased 6-keto-PGF1 alpha, one of stable metabolites of PGI2, in various isolated cells and tissues perhaps via accumulated PG endoperoxides resulted by the inhibition of TXA2 synthase [1]. Ozagrel was estimated to be a reversible mixed-type inhibitor of diphenolase activity with the constants (K (S1), K (S2), K (i1), and K (i2)) determined to be 2.21, 3.89, 0.454, and 0.799 mM, repectively [2]. Infusion of OKY-046 significantly inhibited pulmonary thromboxane B2 delivery, attenuated the early increase in pulmonary vascular resistance, and blocked the increase in systemic vascular resistance. In addition, OKY-046 blunted and delayed the decrease in cardiac output and maintained end-systolic pressure-diameter relation, +dp/dt, and lung lymph flow at baseline values [3].
Methoxycarbonyl-D-Nle-Gly-Arg-pNA is a synthetic trypsin that can serve as a substrate for coagulation factors IXa (FIXa) and Xa (FXa)[1][2][3].
Denecimig (Mim8) is a novel activated coagulation factor VIII-mimetic human bispecific antibody with anti-FIXa and anti-FX arms that potently stimulates FX activation resulting in efficacious haemostasis in vitro and in vivo[1].
Fondaparinux sodium is an antithrombin-dependent factor Xa inhibitor.
Milvexian (BMS-986177), an effective antithrombotic agent, is an orally-bioavailable, reversible and direct inhibitor of human and rabbit factor XIa (FXIa) with Ki of 0.11, and 0.38 nM, respectively[1].
FXIa-IN-6 is a potent FXIa inhibitor with selectivity against most of the relevant serine proteases (Ki = 0.3 nM).
Edoxaban(DU-176) is an oral factor Xa (FXa) inhibitor in clinical development for stroke preventionIC50 Value:Target: factor XaEdoxaban is an oral factor Xa (FXa) inhibitor in clinical development for stroke prevention in patients with atrial fibrillation, an elderly population that frequently receives aspirin (ASA) and/or nonsteroidal anti-inflammatory drugs for concurrent illnesses[1].in vitro: Edoxaban PK was not affected by concomitant low-dose ASA or naproxen, but high-dose ASA increased systemic exposure of edoxaban by approximately 30%. The effects of edoxaban on prothrombin time, activated partial thromboplastin time, international normalized ratio, anti-FXa, and intrinsic FXa activity were not influenced by administration with ASA or naproxen. Inhibition of platelet aggregation by high-dose ASA, low-dose ASA, or naproxen was not affected by edoxaban[1].in vivo: Forty-eight subjects, aged 18 to 45 years, received either edoxaban 60 mg once daily × 7 days (n = 24) or digoxin 0.25 mg twice daily × 2 days and once daily × 5 days (n = 24) and then concomitantly for 7 days. Serial blood and urine samples were collected for digoxin and edoxaban concentrations on days 7 and 14. Serial coagulation assays were measured for edoxaban on days 7 and 14. Edoxaban PK parameters demonstrated mild increases in area under the curve and peak concentrations of 9.5% and 15.6%, respectively[2],Clinical trial: Pharmacokinetics, biotransformation, and mass balance of edoxaban, a selective, direct factor Xa inhibitor, in humans was reported[3].
Edoxaban(DU-176) is an oral factor Xa (FXa) inhibitor in clinical development for stroke preventionIC50 Value:Target: factor XaEdoxaban is an oral factor Xa (FXa) inhibitor in clinical development for stroke prevention in patients with atrial fibrillation, an elderly population that frequently receives aspirin (ASA) and/or nonsteroidal anti-inflammatory drugs for concurrent illnesses[1].in vitro: Edoxaban PK was not affected by concomitant low-dose ASA or naproxen, but high-dose ASA increased systemic exposure of edoxaban by approximately 30%. The effects of edoxaban on prothrombin time, activated partial thromboplastin time, international normalized ratio, anti-FXa, and intrinsic FXa activity were not influenced by administration with ASA or naproxen. Inhibition of platelet aggregation by high-dose ASA, low-dose ASA, or naproxen was not affected by edoxaban[1].in vivo: Forty-eight subjects, aged 18 to 45 years, received either edoxaban 60 mg once daily × 7 days (n = 24) or digoxin 0.25 mg twice daily × 2 days and once daily × 5 days (n = 24) and then concomitantly for 7 days. Serial blood and urine samples were collected for digoxin and edoxaban concentrations on days 7 and 14. Serial coagulation assays were measured for edoxaban on days 7 and 14. Edoxaban PK parameters demonstrated mild increases in area under the curve and peak concentrations of 9.5% and 15.6%, respectively[2],Clinical trial: Pharmacokinetics, biotransformation, and mass balance of edoxaban, a selective, direct factor Xa inhibitor, in humans was reported[3].
Betrixaban D6 is a deuterium labeled Betrixaban. Betrixaban is a highly potent, selective, and orally efficacious factor Xa (fXa) inhibitor[1].
Rivaroxaban is a highly potent and selective, direct Factor Xa (FXa) inhibitor, achieving a strong gain in anti-FXa potency (IC50 0.7 nM; Ki 0.4 nM).
Betrixaban (PRT054021) maleate is a highly potent, selective, and orally efficacious factor Xa (fXa) inhibitor with an IC50 of 1.5 nM. Betrixaban maleate shows antithrombotic effect[1][3].
Delparantag (PMX-60056) is a salicylamide derivative and an effective unfractionated heparin (UFH) and low molecular weight heparin (LMWH) reversing agent. Delparantag shows ability to neutralize the anticoagulation and bleeding effects of UFH and LMWH[1][2].
ARC19499 is an aptamer that inhibits tissue factor pathway inhibitor (TFPI) , thereby enabling clot initiation and propagation via the extrinsic pathway. The core aptamer binds tightly and specifically to TFPI. ARC19499 blocks TFPI inhibition of both factor Xa and the TF/factor VIIa complex. ARC19499 corrects thrombin generation in hemophilia A and B plasma and restores clotting in FVIII-neutralized whole blood.
Heparin sodium salt is an anticoagulant which binds reversibly to antithrombin III (ATIII) and greatly accelerates the rate at which ATIII inactivates coagulation enzymes thrombin factor IIa and factor Xa.