Clinical cautions1 sources
STOP: NSAIDs in Chronic Kidney Disease
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Search: “NSAIDs”
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Mechanisms5 sources
Arachidonic Acid
Arachidonic acid (AA) is a 20-carbon omega-6 polyunsaturated fatty acid (20:4n-6) that serves as the primary substrate for prostaglandin and leukotriene synthesis via COX-2 and 5-LOX pathways. It is the dominant pro-inflammatory lipid mediator — and its balance with ant…
Mechanisms3 sources
Aspirin
Aspirin (acetylsalicylic acid) is a non-steroidal anti-inflammatory drug (NSAID) that irreversibly inhibits cyclooxygenase (COX) enzymes, suppressing prostaglandin synthesis. While widely used as an antiplatelet and anti-inflammatory agent, aspirin carries significant i…
Mechanisms6 sources
COX-2 (Cyclooxygenase-2)
Cyclooxygenase-2 (COX-2) is the inducible enzyme that converts arachidonic acid to prostaglandin H₂ — the precursor of prostaglandin E₂ (PGE₂), prostacyclin, and thromboxane. Unlike COX-1 (constitutive, homeostatic), COX-2 is transcriptionally induced by nf kappa b duri…
Mechanisms5 sources
Drug Repurposing
Drug repurposing (also called drug repositioning) is the strategy of identifying new therapeutic uses for existing approved drugs. It dramatically accelerates the path from bench to bedside because safety, pharmacokinetics, and manufacturing are already established. In …
Mechanisms5 sources
Pharmacomicrobiomics
Pharmacomicrobiomics is the study of bidirectional interactions between drugs and the microbiome. The gut microbiome is not a passive bystander in pharmacology -- it actively metabolizes drugs, alters their bioavailability, and modulates therapeutic efficacy. Conversely…