product name Nepafenac
Description: Nepafenac (also known as AHR 9434, AL 6515) is a non-steroidal anti-inflammatory drug (NSAID), and a prodrug of amfenac that acts as an inhibitor of COX-1 and COX-2 activity, it is used in the treatment of pain and inflammation associated with cataract surgery. Nepafenac showed to significantly decrease the retinal levels of PGE2 in LPS-induced rats when administrated topically. However, nepafenac has revealed no significant effect on BRB permeability in LPS-induced rat model.
References: Inflammation. 2000 Aug;24(4):357-70; Inflammation. 2003 Oct;27(5):281-91; Invest Ophthalmol Vis Sci. 2003 Jan;44(1):409-15.
254.28
Formula
C15H14N2O2
CAS No.
78281-72-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 50 mg/mL (196.6 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
AHR 9434, AL 6515
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19406931
| In Vitro |
In vitro activity: Nepafenac is a non-steroidal anti-inflammatory drug (NSAID). The IC50 values of nepafenac for (cyclooxygenase-1) COX-1 and COX-2 are 250 nM and 150 nM, respectively Kinase Assay: Cell Assay: Nepafenac significantly reduced proliferation rate of human uveal melanoma cell lines including SP6.5, 92.1, OCM-1, MKT-BR and of human transformed uveal melanocyte cell line UW-1. Compared to rofecoxib, nepafenac might reveal a better systemic safety profile. |
|---|---|
| In Vivo | Nepafenac shows significantly greater ocular bioavailability and amfenac demonstrated greater potency at COX-2 inhibition than ketorolac or bromfenac. Nepafenac exhibits only weak COX-1 inhibitory activity with IC50 of 64.3 mM. Nepafenac inhibits prostaglandin synthesis in the iris/ciliary body (85-95%) and the retina/choroid (55%) in rabbits. Nepafenac (0.5%) produces 65% reduction in retinal edema which is correlated with 62% inhibition of blood-retinal barrier breakdown. Nepafenac (0.5%) significantly inhibits (46%) blood-retinal barrier breakdown concomitant with near total suppression of PGE2 synthesis (96%). Nepafenac significantly inhibits retinal prostaglandin E(2), superoxide, cyclooxygenase-2, and leukostasis within retinal microvessels in insulin-deficient diabetic rats, without affecting vascular endothelial growth factor (VEGF) and nitric oxide (NO). Nepafenac significantly inhibits the number of transferase-mediated dUTP nick-end labeling-positive capillary cells, acellular capillaries, and pericyte ghosts in diabetic rats. Nepafenac results in significantly less choroidal neovascularization and significant less ischemia-induced retinal neovascularization in mice compare to control. Nepafenac also blunts the increase in VEGF mRNA in the retina induced by ischemia. Nepafenac delays the progression of malignancy as well as reduces weight in an ocular and metastatic animal model of uveal melanoma. |
| Animal model | Nepafenac showed to significantly decrease the retinal levels of PGE2 in LPS-induced rats when administrated topically. However, nepafenac has revealed no significant effect on BRB permeability in LPS-induced rat model |
| Formulation & Dosage | |
| References | Inflammation. 2000 Aug;24(4):357-70; Inflammation. 2003 Oct;27(5):281-91; Invest Ophthalmol Vis Sci. 2003 Jan;44(1):409-15. |
