Abstract
The pyridazine moiety is an important structural feature of various pharmacological active compounds. Synthetic pyridazine compounds have been reported as effective antiprostaglandins (PGs), 5-lipoxygenase (5-LOX), and antiplatelet agents, that is, inhibitors of prostaglandin or cyclooxygenase (COX-I & COX-II) enzyme, platelet cAMP phosphodiesterase, and thromboxane A2 (TXA2) synthase. These compounds are selective and nonselective COX inhibitors and showed analgesic, anti-inflammatory, and antipyretic activity. Pyridazine compounds with antiplatelet agents inhibited TXA2enzyme. Pyridazines also exhibited antirheumatoid activity. These pyridazine compounds hold considerable interest relative to the preparation of organic intermediates and other anticipated biologically active compounds.
Highlights
Most biologically active compounds are heterocyclic in nature
Level through inhibiting cyclic AMP (cAMP) PDE activity. These findings demonstrate that PC-09 is an inhibitor of platelet aggregation, which may be associated with mechanisms including inhibition of THX-A2 formation, intracellular calcium mobilization, and platelet surface GPIIb/IIIa expression accompanied by increasing cAMP level [42]
nonsteroidal anti-inflammatory drugs (NSAIDs) have been used in familial adenomatous polyposis (FAP), an inherited disorder characterized by multiple adenomatous colon polyps developing during adolescence and the inevitable occurrence of colon cancer
Summary
Most biologically active compounds are heterocyclic in nature. Due to this finding, nitrogen heteroatom containing compounds are becoming more popular in the current research and so is development of new more potent drugs and newer derivatives of existing or currently used drugs with minimum or without adverse effects. Nonsteroidal anti-inflammatory drugs (NSAIDs) have huge therapeutic value in the management of pain and inflammation These compounds inhibit the cyclooxygenase enzymes (COX-1 and COX-2), which catalyze the conversion of arachidonic acid (AA) to PGs and prevent the formation of PGs and 5-lipoxygenase (5-LOX) [10,11,12]. Aspirin inhibits platelet aggregation and prolongs bleeding time It is useful for preventing coronary thrombosis in patients with unstable angina, as an adjunct to thrombolytic therapy, and in reducing recurrence of thrombotic stroke. It acetylates and irreversibly inhibits primarily COX1 both in platelets, preventing the formation of TXA2 , and in endothelial cells, inhibiting the synthesis of PGI2 (anticoagulant, antiplatelet, and fibrinolytic (thrombolytic)). Aspirin inhibits platelet COX to produce a mild clotting defect [16,17,18,19,20]
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