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Bromfenac volume of distribution

Bromfenac exhibits a cmax of 3.49 +/- 1.65-8.81 +/- 3.45 micrograms/ml at tmax 52 +/- 27-42 +/- 15 min. The elimination half-life was 39.8 +/- 7.3-34.2 +/- 8.0 min with a clearance (Cl/f) of 120.6 +/- 51.6-135.3 +/- 34.6 ml/min and a volume of distribution (Vd/f) 6.82 +/- 2.88-6.64 +/- 2.29 l. The results obtained show a fast absorption and rapid elimination of bromfenac when administered orally. The short plasma half-life of bromfenac apparently presents no direct relationship to its clinical effectiveness.

What is Bromfenac

Bromfenac is a nonsteroidal anti-inflammatory drug (NSAID) for ophthalmic use. Ophthalmic NSAIDs are becoming a cornerstone for the management of ocular pain and inflammation. Their well-characterized anti-inflammatory activity, analgesic property, and established safety record have also made NSAIDs an important tool to optimize surgical outcomes.

Bromfenac mechanism of action

The mechanism of its action is thought to be due to its ability to block prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2. 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.

Dosage forms of Bromfenac

Indication of Bromfenac

For the treatment of postoperative inflammation in patients who have undergone cataract extraction.

Toxicity of Bromfenac

There are no adequate and well-controlled studies of bromfenac ophthalmic solution in pregnant women. Only very small amounts, if any, are systemically absorbed, suggesting an unlikely risk of clinically significant exposure to the embryo or fetus. Treatment of rats with oral doses up to 0.9 mg/kg/day (systemic exposure 90 times the systemic exposure predicted from the recommended human ophthalmic dose assuming the human systemic concentration is detectable) and rabbits at oral doses up to 7.5 mg/kg/day (150 times predicted human systemic exposure) revealed no evidence of teratogenicity; however, embryo-fetal lethality and maternal toxicity were produced in rats and rabbits given 0.9 mg/kg/day and 7.5 mg/kg/day, respectively. Premature closure of the fetal ductus arteriosus has occurred with third trimester use of oral and injectable NSAIDs. Prostaglandin synthetase inhibitors also have the potential to prolong pregnancy and inhibit labor if taken during the third trimester.