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0.03 mM causes 100% inhibition
-
90% inhibition at 0.1 mM
-
strong inhibition at 0.2 mM
-
abolishes inhibitory effect upon collagen- and ADP-induced platelet aggregation and the edematogenic effect
abolishes inhibitory effect upon collagen- and ADP-induced platelet aggregation and the edematogenic effect
abolishes inhibitory effect upon collagen- and ADP-induced platelet aggregation and the edematogenic effect
BthTX-II: loses most of its catalytic, indirect haemolytic, anticoagulant, myotoxic and cytotoxic activity, BthTX-I: myotoxic activity reduced to 50% and the cytotoxic activity reduced to 13%
BthTX-II: loses most of its catalytic, indirect haemolytic, anticoagulant, myotoxic and cytotoxic activity, BthTX-I: myotoxic activity reduced to 50% and the cytotoxic activity reduced to 13%
BthTX-II: loses most of its catalytic, indirect haemolytic, anticoagulant, myotoxic and cytotoxic activity, BthTX-I: myotoxic activity reduced to 50% and the cytotoxic activity reduced to 13%
suppresses anticoagulant activity, indirect haemolytic activity and inhibition of platelet aggregation, does not inhibit the induction of edema
suppresses anticoagulant activity, indirect haemolytic activity and inhibition of platelet aggregation, does not inhibit the induction of edema
suppresses anticoagulant activity, indirect haemolytic activity and inhibition of platelet aggregation, does not inhibit the induction of edema
1.8 mM, prevents myotoxicity caused by the enzyme
1.8 mM, prevents myotoxicity caused by the enzyme
1.8 mM, prevents myotoxicity caused by the enzyme
enzymatic activity of bromophenacylated PLA2 is approximate 0.06% of that of PLA2
enzymatic activity of bromophenacylated PLA2 is approximate 0.06% of that of PLA2
enzymatic activity of bromophenacylated PLA2 is approximate 0.06% of that of PLA2
selectively and irreversibly modifies the His48 residue in the active site
selectively and irreversibly modifies the His48 residue in the active site
selectively and irreversibly modifies the His48 residue in the active site
4-bromophenacyl bromide treatment irreversibly abolishes the neurotoxic effect induced by secretory phospholipase A2
4-bromophenacyl bromide treatment irreversibly abolishes the neurotoxic effect induced by secretory phospholipase A2
4-bromophenacyl bromide treatment irreversibly abolishes the neurotoxic effect induced by secretory phospholipase A2
alkylation with 4-bromophenacyl bromide leads to the complete loss of its enzymatic activity signifying the crucial role of histidine residue in catalysis
alkylation with 4-bromophenacyl bromide leads to the complete loss of its enzymatic activity signifying the crucial role of histidine residue in catalysis
alkylation with 4-bromophenacyl bromide leads to the complete loss of its enzymatic activity signifying the crucial role of histidine residue in catalysis
-
133879, 133892, 133897, 133906, 133910, 133912, 133915, 133916, 133917, 133922, 133924, 133926, 133927
-
133879, 133892, 133897, 133906, 133910, 133912, 133915, 133916, 133917, 133922, 133924, 133926, 133927
-
133879, 133892, 133897, 133906, 133910, 133912, 133915, 133916, 133917, 133922, 133924, 133926, 133927
complete loss of both catalytic activity and platelet aggregation inhibitory activity
complete loss of both catalytic activity and platelet aggregation inhibitory activity
complete loss of both catalytic activity and platelet aggregation inhibitory activity
loss of both catalytic activity and neurotoxicity
loss of both catalytic activity and neurotoxicity
loss of both catalytic activity and neurotoxicity
loss of both enzymatic and toxic properties
loss of both enzymatic and toxic properties
loss of both enzymatic and toxic properties
abolishes the enzymatic activity of PLA2 without affecting its anti-tumor effect, suggesting the presence of pharmacological sites distinct from the catalytic site
abolishes the enzymatic activity of PLA2 without affecting its anti-tumor effect, suggesting the presence of pharmacological sites distinct from the catalytic site
abolishes the enzymatic activity of PLA2 without affecting its anti-tumor effect, suggesting the presence of pharmacological sites distinct from the catalytic site
inhibits both the catalytic and anticoagulant activities. Inhibition of catalytic activity is approximately 6fold higher compared with inhibition of anticoagulant activity
inhibits both the catalytic and anticoagulant activities. Inhibition of catalytic activity is approximately 6fold higher compared with inhibition of anticoagulant activity
inhibits both the catalytic and anticoagulant activities. Inhibition of catalytic activity is approximately 6fold higher compared with inhibition of anticoagulant activity
i.e. pBPB, 3.3 mM, 95% inhibition of isoenzyme NK-PLA2-I, 89% inhibition of isoenzyme NK-PLA2-II
i.e. pBPB, 3.3 mM, 95% inhibition of isoenzyme NK-PLA2-I, 89% inhibition of isoenzyme NK-PLA2-II
i.e. pBPB, 3.3 mM, 95% inhibition of isoenzyme NK-PLA2-I, 89% inhibition of isoenzyme NK-PLA2-II
i.e. pBpb, 0.1 mM, 60% inhibition
i.e. pBpb, 0.1 mM, 60% inhibition
i.e. pBpb, 0.1 mM, 60% inhibition
intracellular enzyme form Ib from brain
-
60% inhibition at 5 mM, isozyme II from cerebrospinal fluid
-
complete inhibition at 4 mM
-
78.5% residual activity at 2 mM
-
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