COX-2 selective NSAIDs were developed to maintain analgesia efficacy while minimizing the side effects associated with COX-1 inhibition. The cyclooxygenase enzyme is anchored to the endoplasmic reticulum membrane. Above it, released prostaglandin hormones soar into the cell. The COX-2 selective NSAID is blocked from the channel of access for COX-1, but gains entry at COX-2 site, and thereby inhibits the active site for pain prostaglandin creation.
Keywords: Airbrush, Color, 3D, Editorial, Cell biology / Histology, Disease Management, Molecular Biology, Pharmacology
© Cynthia Turner