Guanylhydrazones of 3-substituted 2-pyridinecarboxaldehyde and of (2-substituted 3-pyridinyloxy) acetaldehyde as prostanoid biosynthesis and platelet aggregation inhibitors
摘要:
Some guanylhydrazones of (3-benzyloxy)-2-pyridinecarboxaldehyde and of (2-substituted 3-pyridinyloxy)acetaldehyde were prepared in order to evaluate their possible activity as inhibitors of prostanoid biosynthesis in human serum. Only those products of the second group without the carboxylic function reduced prostanoid generation in vitro at the highest concentration; they also inhibited platelet aggregation induced by arachidonic acid and U-46619. The results suggest that these compounds are both inhibitors of cyclooxygenase and cyclic endoperoxides/TxA2 platelet receptor antagonists.
Guanylhydrazones of 3-substituted 2-pyridinecarboxaldehyde and of (2-substituted 3-pyridinyloxy) acetaldehyde as prostanoid biosynthesis and platelet aggregation inhibitors
摘要:
Some guanylhydrazones of (3-benzyloxy)-2-pyridinecarboxaldehyde and of (2-substituted 3-pyridinyloxy)acetaldehyde were prepared in order to evaluate their possible activity as inhibitors of prostanoid biosynthesis in human serum. Only those products of the second group without the carboxylic function reduced prostanoid generation in vitro at the highest concentration; they also inhibited platelet aggregation induced by arachidonic acid and U-46619. The results suggest that these compounds are both inhibitors of cyclooxygenase and cyclic endoperoxides/TxA2 platelet receptor antagonists.
Guanylhydrazones of 3-substituted 2-pyridinecarboxaldehyde and of (2-substituted 3-pyridinyloxy) acetaldehyde as prostanoid biosynthesis and platelet aggregation inhibitors
Some guanylhydrazones of (3-benzyloxy)-2-pyridinecarboxaldehyde and of (2-substituted 3-pyridinyloxy)acetaldehyde were prepared in order to evaluate their possible activity as inhibitors of prostanoid biosynthesis in human serum. Only those products of the second group without the carboxylic function reduced prostanoid generation in vitro at the highest concentration; they also inhibited platelet aggregation induced by arachidonic acid and U-46619. The results suggest that these compounds are both inhibitors of cyclooxygenase and cyclic endoperoxides/TxA2 platelet receptor antagonists.