1.14.99.1	1,10-phenanthroline	weak	62	
1.14.99.1	1-Mercapto-9,11,15-trihydroxyprosta-5,13-diene	inhibition of prostaglandin G1 synthesis	90540	
1.14.99.1	1-Mercapto-9-oxo-11,15-dihydroxyprosta-5,13-dione	inhibition of prostaglandin G1 synthesis	90541	
1.14.99.1	12-nitroarachidonic acid	nitro-fatty acid inhibition is due to a slow, tightly binding mechanism, it inhibits oxygenase and peroxidase activity PGHS-1, kinetics, overview. Inactivation of PGHS by nitroarachidonic acid involves two sequential steps: an initial reversible binding event, followed by a practically irreversible event leading to an inactivated enzyme. Inactivation is associated with irreversible disruption of heme binding to the protein, the inhibitor induces heme release from Fe2+-protoporphyrin-PGHS-1. In activated human platelets, nitroarachidonic acid significantly decreases PGHS-1-dependent thromboxane B2 formation in parallel with a decrease in platelet aggregation	194323	
1.14.99.1	14-nitroarachidonic acid	nitro-fatty acid inhibition is due to a slow, tightly binding mechanism, it inhibits oxygenase and peroxidase activity PGHS-1, kinetics, overview. Inactivation of PGHS by nitroarachidonic acid involves two sequential steps: an initial reversible binding event, followed by a practically irreversible event leading to an inactivated enzyme. Inactivation is associated with irreversible disruption of heme binding to the protein, the inhibitor induces heme release from Fe2+-protoporphyrin-PGHS-1. In activated human platelets, nitroarachidonic acid significantly decreases PGHS-1-dependent thromboxane B2 formation in parallel with a decrease in platelet aggregation	194324	
1.14.99.1	15-nitroarachidonic acid	nitro-fatty acid inhibition is due to a slow, tightly binding mechanism, it inhibits oxygenase and peroxidase activity PGHS-1, kinetics, overview. Inactivation of PGHS by nitroarachidonic acid involves two sequential steps: an initial reversible binding event, followed by a practically irreversible event leading to an inactivated enzyme. Inactivation is associated with irreversible disruption of heme binding to the protein, the inhibitor induces heme release from Fe2+-protoporphyrin-PGHS-1. In activated human platelets, nitroarachidonic acid significantly decreases PGHS-1-dependent thromboxane B2 formation in parallel with a decrease in platelet aggregation	194325	
1.14.99.1	2,2'-bipyridyl	weak	1706	
1.14.99.1	2,3-Dimercaptopropanol	inhibition of prostaglandin G1 synthesis	2535	
1.14.99.1	2-hydroxybutyric acid	weak	15496	
1.14.99.1	3,6-bis(3-[[(furan-2-yl)methyl]amino]propyl)-9H-xanthen-9-one	-	222505