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MK 383

Known as: MK-383 
National Institutes of Health

Papers overview

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2005
2005
OBJECTIVE We tested the hypothesis that simultaneous inhibition of the endothelial integrin alpha(v)beta(3) and the platelet… Expand
2004
2004
Several preclinical studies have found a poor correlation between the ex vivo platelet inhibitory potency and the in vivo… Expand
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2002
2002
The platelet integrin αIIb β3 (GPIIb/IIIa) acts as a receptor for fibrinogen, playing a critical role in platelet aggregation… Expand
Review
1999
Review
1999
  • C. Dyke
  • American heart journal
  • 1999
  • Corpus ID: 33198754
Platelet-mediated coronary thrombosis is the primary pathophysiologic mechanism of acute coronary syndromes (ACS) and acute… Expand
1999
1999
In vivo antithrombotic efficacy of GPIIb/IIIa receptor antagonists (m7E3, MK-383 and DMP-728) was studied with respect to their… Expand
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Highly Cited
1996
Highly Cited
1996
OBJECTIVES The objectives of this double-blind, placebo-controlled, randomized dose-ranging study were 1) to examine the safety… Expand
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Highly Cited
1994
Highly Cited
1994
MK‐383 (L‐tyrosine, N‐n‐butylsulfonyl)‐O‐[4‐butyl(4‐piperidinyl)], monohydrochloride monohydrate) is a potent and specific… Expand
1994
1994
MK-383 is a novel, non-peptide fibrinogen receptor antagonist. A sensitive and specific radioimmunoassay has been developed for… Expand
Highly Cited
1993
Highly Cited
1993
BackgroundFibrinogen-dependent cross-linking of glycoprotein (GP) lIb/IIIa on activated platelets is the final mechanism leading… Expand
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