Bromfenac Pathway


The mechanism of action of Bromfenac is thought to be due to its ability to block prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2 (COX-1 and -2), also called prostaglandin G/H synthase 1 and 2. COX-1 and -2 catalyze the conversion of arachidonic acid to prostaglandin G2 and prostaglandin G2 to prostglandin H2. Prostaglandin H2 is the precursor to a number of prostaglandins (e.g. PGE2) involved in fever, pain, swelling, inflammation, and platelet aggregation. Bromfenac antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. Prostaglandins have been shown in many animal models to be mediators of certain kinds of intraocular inflammation. In studies performed in animal eyes, prostaglandins have been shown to produce disruption of the blood-aqueous humor barrier, vasodilation, increased vascular permeability, leukocytosis, and increased intraocular pressure. The analgesic and anti-inflammatory effects of bromfenac occurs as a result of decreased prostaglandin synthesis.

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References

  1. Botting, R., & Botting, J. (2004). Cyclooxygenases. In S. Offermanns, & W. Rosenthal (Eds.). Encyclopedic reference of molecular pharmacology (pp. 279-283). Berlin, Germany: Springer.
  2. Breyer, R.M., & Breyer, M.D. (2004). Prostanoids. In S. Offermanns, & W. Rosenthal (Eds.). Encyclopedic reference of molecular pharmacology (pp. 752-757). Berlin, Germany: Springer.
  3. Geisslinger, G., & Lötsch, J. (2004). Non-steroidal anti-inflammatory drugs. In S. Offermanns, & W. Rosenthal (Eds.). Encyclopedic reference of molecular pharmacology (pp. 667-671). Berlin, Germany: Springer.