Bromfenac Sodium

Bromfenac (bromfenac sodium) by the oral route at pretreatment times of 10 min, 20 min and 300 min is respectively 3.7, 6.5 and 2.9 times more potent than zomepirac and 3.4, 6.6, and 44.2 times more potent than suprofen in the acetylcholine abdominal constriction assay in mice. Bromfenac when given orally is 5.8 times more potent than zomepirac in blocking the nociceptive response to bradykinin in dogs. Bromfenac is 6.1 to 32.8 times more potent than indometacin in inhibiting the formation of prostaglandin E2 and F2 alpha from microsomes of bovine seminal vesicles, rabbit uteri, and rabbit renal medullae. Bromfenac, given orally, is more potent than indometacin in suppressing acute (7.5-20 times) and chronic (3.8 times) inflammation in mice. ^[1] Bromfenac (1 mg/kg, i.v.) is metabolited into an unusual conjugate, bromfenac N-glucoside, in rats bile. ^[2] Bromfenac shows a rapid onset of activity (20 min) that persisted for at least 4 hours in a mouse model of pain (acetylcholine abdominal constriction). Bromfenac (0.316 mg/kg) produces significant anti-inflammatory activity up to 24 hours after dosing in a rat model of inflammation (carrageenan foot edema). Bromfenac is readily absorbed after oral administration, peak plasma levels being achieved at the earliest time tested: 20 min in the mouse and 30 min in the rat. ^[3]