Disease relevance of Nevanac

• Nepafenac did not have a significant effect on diabetes-induced loss of cells in the ganglion cell layer or in corneal protease activity [1].
• We explored the effect of topical Nepafenac, an anti-inflammatory drug known to reach the retina when administered via eyedrops, on the development of early stages of diabetic retinopathy and on metabolic and physiologic abnormalities that contribute to the retinal disease [1].
• CONCLUSIONS: Topical nepafenac inhibits CNV and ischemia-induced retinal neovascularization by decreasing production of VEGF [2].
• Nepafenac also blunted the increase in VEGF mRNA in the retina induced by ischemia [2].
• For the nepafenac 0.03% group, the mean pain and mean photophobia scores were 2.5 and 1.6, respectively [3].

High impact information on Nevanac

• At 9 months of diabetes, a significant increase in the number of transferase-mediated dUTP nick-end labeling-positive capillary cells, acellular capillaries, and pericyte ghosts were measured in control diabetic rats versus nondiabetic controls, and topical Nepafenac significantly inhibited all of these abnormalities (all P < 0.05) [1].
• RESULTS: Nepafenac, diclofenac, and ketorolac reduced the mean frequency of the impulse response evoked by repeated CO(2) stimuli in polymodal nociceptor fibers [4].
• CONCLUSIONS: The inhibition of polymodal nociceptor activity by nepafenac, a weak inhibitor of cyclooxygenase, is most likely due to its greater lipophilicity compared with diclofenac and ketorolac, leading to a rapid saturation of the corneal epithelium where nociceptor terminals are located [4].
• In cultured mice trigeminal ganglion neurons, diclofenac significantly suppressed sodium currents, whereas nepafenac or its metabolite, amfenac, exhibited only minimal inhibitory effects [4].
• Comparative Effects of the Nonsteroidal Anti-inflammatory Drug Nepafenac on Corneal Sensory Nerve Fibers Responding to Chemical Irritation [4].

Chemical compound and disease context of Nevanac

• On day 2, the nepafenac 0.1% group had less pain at bedtime than the diclofenac group (mean score, 1.9 vs 3.1; P<0.024) and less photophobia in the morning (mean score, 1.2 vs 1.8; P<0.023) [3].

Biological context of Nevanac

• SETTING: Twenty-one ophthalmology clinics in the United States. METHODS: A randomized double-blind vehicle-controlled trial was conducted in which adult patients were randomly assigned to receive nepafenac 0.1% or vehicle beginning 1 day before surgery and continuing on the day of surgery (day 0) for 14 days [5].
• An MTT-based proliferation assay was used to compare Rb cell growth with and without amfenac, the active metabolite of nepafenac [6].

Anatomical context of Nevanac

• PURPOSE: To compare the corneal analgesic efficacy of the nonsteroidal anti-inflammatory drugs (NSAIDs) nepafenac, diclofenac, and ketorolac, and to evaluate the possibility that their inhibitory effects on corneal polymodal nociceptor fiber activity are partly mediated by a decrease in sodium currents [4].
• In a subsequent study, 0.5% nepafenac significantly inhibited (46%) blood-retinal barrier breakdown concomitant with near total suppression of PGE2 synthesis (96%) [7].
• Nepafenac may therefore have a clinical role in conditions that are caused by PG-mediated vascular leakage, such as anterior chamber inflammation and cystoid macular edema following cataract surgery [8].
• PurposeTo examine the effect of nepafenac, a selective cyclooxygenase-2 (COX-2) inhibitor, on the proliferation rate of two human retinoblastoma (Rb)cell lines.MethodsTwo human Rb cell lines (WERI-RB and Y79) were cultured [6].

Associations of Nevanac with other chemical compounds

• Topical nepafenac administration also significantly inhibits prostaglandin (PG)-mediated blood-retinal barrier breakdown and concurrent protein extravasation into the vitreous [8].

Gene context of Nevanac

• PURPOSE: Topical nepafenac readily penetrates the cornea and is metabolized to amfenac, a potent cyclooxygenase (COX)-1 and COX-2 inhibitor [2].
• RESULTS: Mice treated with 0.1% or 0.5% nepafenac had significantly less CNV and significant less ischemia-induced retinal NV than did vehicle-treated mice [2].

Analytical, diagnostic and therapeutic context of Nevanac

• Topical administration of nepafenac inhibits diabetes-induced retinal microvascular disease and underlying abnormalities of retinal metabolism and physiology [1].
• PURPOSE: To determine whether nepafenac ophthalmic suspension 0.1% decreases the incidence and severity of inflammation and pain after cataract surgery with posterior chamber intraocular lens implantation [5].
• Comparison of the analgesic efficacy and safety of nepafenac ophthalmic suspension compared with diclofenac ophthalmic solution for ocular pain and photophobia after excimer laser surgery: a phase II, randomized, double-masked trial [3].
• Short term perfusion (5 min) of the corneal surface with 0.1% nepafenac resulted in sustained flux of drug across the cornea for 6 h [9].
• SCOPE: We searched the PubMed database from 1966 to 2005 for various combinations of the search terms 'nepafenac', 'ophthalmic', 'inflammation', 'anterior segment', and 'posterior segment'. We review here the three articles identified in the search, and also include findings from three recent clinical trials [8].

References