Preclinical Pharmacokinetics and In Vitro Metabolism of BMS-690514, a Potent Inhibitor of EGFR and VEGFR2

2010 ◽  
Vol 99 (8) ◽  
pp. 3579-3593 ◽  
Author(s):  
Punit Marathe ◽  
Yuwei Tang ◽  
Bogdan Sleczka ◽  
David Rodrigues ◽  
Ashvinikumar Gavai ◽  
...  
Keyword(s):  
Potent Inhibitor ◽  
In Vitro Metabolism ◽  
Preclinical Pharmacokinetics

Preclinical Pharmacokinetics and In Vitro Metabolism of Asunaprevir (BMS-650032), a Potent Hepatitis C Virus NS3 Protease Inhibitor

2015 ◽  
Vol 104 (9) ◽  
pp. 2813-2823 ◽  
Author(s):  
Kathleen W. Mosure ◽  
Jay O. Knipe ◽  
Marc Browning ◽  
Vinod Arora ◽  
Yue-Zhong Shu ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protease Inhibitor ◽  
In Vitro Metabolism ◽  
Preclinical Pharmacokinetics ◽  
Ns3 Protease

Preclinical Pharmacokinetics and In Vitro Metabolism of BMS-605339: A Novel HCV NS3 Protease Inhibitor

2014 ◽  
Vol 103 (6) ◽  
pp. 1891-1902 ◽  
Author(s):  
Susan Jenkins ◽  
Paul Scola ◽  
Fiona Mcphee ◽  
Jay Knipe ◽  
Christoph Gesenberg ◽  
...  
Keyword(s):  
Protease Inhibitor ◽  
In Vitro Metabolism ◽  
Preclinical Pharmacokinetics ◽  
Ns3 Protease

Preclinical pharmacokinetics and in vitro metabolism of brivanib (BMS-540215), a potent VEGFR2 inhibitor and its alanine ester prodrug brivanib alaninate

2009 ◽  
Vol 65 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Punit H. Marathe ◽  
Amrita V. Kamath ◽  
Yueping Zhang ◽  
Celia D’Arienzo ◽  
Rajeev Bhide ◽  
...  
Keyword(s):  
In Vitro Metabolism ◽  
Preclinical Pharmacokinetics ◽  
Brivanib Alaninate ◽  
Ester Prodrug

A Thiazole Compound with Potential Antithrombotic Activity

1982 ◽  
Vol 47 (02) ◽  
pp. 173-176 ◽  
Author(s):  
E E Nishizawa ◽  
A R Mendoza ◽  
T Honohan ◽  
K A Annis
Keyword(s):  
Platelet Aggregation ◽  
Potent Inhibitor ◽  
Platelet Rich Plasma ◽  
Development Program ◽  
Antithrombotic Agent ◽  
Antithrombotic Activity ◽  
Thiazole Derivative ◽  
Cyclooxygenase Activity ◽  
Drug Development Program

SummaryA thiazole derivative, 4,5-bis(p-methoxyphenyl)-2-(trifluoromethyl)-thiazole was found to be a potent inhibitor of collagen-induced platelet aggregation, in vitro, using platelets from at least six species, including man. It was active in human platelet-rich plasma at a concentration of 1 ng/ml. While its antiplatelet activity was greater than that of flurbiprofen, its cyclooxygenase activity was equivalent to that of flurbiprofen. Also, compared to flurbiprofen, the thiazole had less anti-inflammatory activity in the hind-paw edema test. The thiazole derivative inhibited platelet aggregation following oral administration in five laboratory species. In the guinea pig it was active at 0.5 mg/kg. The LD50 in mice was greater than 1000 mg/kg (i.p.). This compound, which was designed through a systematic drug development program, may have high potential as an antithrombotic agent.

Tridegin, a Novel Peptidic Inhibitor of Factor XIIIa from the Leech, Haementeria ghilianii, Enhances Fibrinolysis In Vitro

1997 ◽  
Vol 77 (05) ◽  
pp. 0959-0963 ◽  
Author(s):  
Lisa Seale ◽  
Sarah Finney ◽  
Roy T Sawyer ◽  
Robert B Wallis
Keyword(s):  
Potent Inhibitor ◽  
Platelet Rich Plasma ◽  
Factor Xiiia ◽  
Cross Linking ◽  
Fibrinolytic Enzymes ◽  
Small Polypeptide ◽  
Tissue Plasminogen ◽  
Protein Cross Linking

SummaryTridegin is a potent inhibitor of factor Xllla from the leech, Haementeria ghilianii, which inhibits protein cross-linking. It modifies plasmin-mediated fibrin degradation as shown by the absence of D-dimer and approximately halves the time for fibrinolysis. Plasma clots formed in the presence of Tridegin lyse more rapidly when either streptokinase, tissue plasminogen activator or hementin is added 2 h after clot formation. The effect of Tridegin is markedly increased if clots are formed from platelet-rich plasma. Platelet-rich plasma clots are lysed much more slowly by the fibrinolytic enzymes used and if Tridegin is present, the rate of lysis returns almost to that of platelet- free clots. These studies indicate the important role of platelets in conferring resistance to commonly used fibrinolytic enzymes and suggest that protein cross-linking is an important step in this effect. Moreover they indicate that Tridegin, a small polypeptide, may have potential as an adjunct to thrombolytic therapy.

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