Maximal blockade of TxA2 without compromised PGI2 formation; a superior profile of the TxA2 receptor blocking drug GR32191 over aspirin.
Lumley
P
P
Department of Peripheral Pharmacology, Glaxo Group Research Ltd., Ware, Hertfordshire, U.K.
Keery
R J
RJ
Wharton
K A
KA
White
B P
BP
Watts
I S
IS
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000328:Adult; D001241:Aspirin / Q000494:pharmacology*; D001713:Biphenyl Compounds / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000096:biosynthesis*; D006538:Heptanoic Acids / Q000494:pharmacology*; D006801:Humans; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D011982:Receptors, Prostaglandin / Q000037:antagonists & inhibitors*; D017482:Receptors, Thromboxane; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors*; D013929:Thromboxane B2 / Q000097:blood
D001713:Biphenyl Compounds; D006538:Heptanoic Acids; D011982:Receptors, Prostaglandin; D017482:Receptors, Thromboxane; D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; C060013:vapiprost; D001241:Aspirin