Nepafenac - How It Works
Clinical pharmacology details from the US FDA-approved label: how Nepafenac works in your body, how it's absorbed, how long it stays active, and how it's eliminated.
Mechanism of Action
12.1 Mechanism of Action After topical ocular dosing, nepafenac penetrates the cornea and is converted by ocular tissue hydrolases to amfenac, a NSAID. Nepafenac and amfenac are thought to inhibit the action of prostaglandin H synthase (cyclooxygenase), an enzyme required for prostaglandin production.
12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action After topical ocular dosing, nepafenac penetrates the cornea and is converted by ocular tissue hydrolases to amfenac, a NSAID.
Nepafenac and amfenac are thought to inhibit the action of prostaglandin H synthase (cyclooxygenase), an enzyme required for prostaglandin production.
12.3 Pharmacokinetics Following bilateral topical ocular once-daily dosing of ILEVRO ® 0.3%, the concentrations of nepafenac and amfenac peaked at a median time of 0.5 hour and 0.75 hour, respectively on both Day 1 and Day 4.
The mean steady-state C max for nepafenac and for amfenac were 0.847 ± 0.269 ng/mL and 1.13 ± 0.491 ng/mL, respectively.
Nepafenac at concentrations up to 3000 ng/mL and amfenac at concentrations up to 1000 ng/mL did not inhibit the in vitro metabolism of six specific marker substrates of cytochrome P450 (CYP) isozymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4).
Therefore, drug-drug interactions involving CYP mediated metabolism of concomitantly administered drugs are unlikely.
Pharmacokinetics
12.3 Pharmacokinetics Following bilateral topical ocular once-daily dosing of ILEVRO ® 0.3%, the concentrations of nepafenac and amfenac peaked at a median time of 0.5 hour and 0.75 hour, respectively on both Day 1 and Day 4. The mean steady-state C max for nepafenac and for amfenac were 0.847 ± 0.269 ng/mL and 1.13 ± 0.491 ng/mL, respectively. Nepafenac at concentrations up to 3000 ng/mL and amfenac at concentrations up to 1000 ng/mL did not inhibit the in vitro metabolism of six specific marker substrates of cytochrome P450 (CYP) isozymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4). Therefore, drug-drug interactions involving CYP mediated metabolism of concomitantly administered drugs are unlikely.