Disease relevance of amfenac sodium

• Analgesic efficacy of amfenac, aspirin and placebo after extraction of impacted teeth [1].
• Amfenac Na is a new non-steroidal analgesic anti-inflammatory drug which is clinically used for ailments such as rheumatoid arthritis and pain and/or inflamation after surgery [2].

High impact information on amfenac sodium

• In cultured mice trigeminal ganglion neurons, diclofenac significantly suppressed sodium currents, whereas nepafenac or its metabolite, amfenac, exhibited only minimal inhibitory effects [3].
• A series of potential prodrugs of 2-amino-3-benzoylbenzeneacetic acid (amfenac) and 2-amino-3-(4-chlorobenzoyl)benzeneacetic acid were synthesized and evaluated for their cyclooxygenase inhibiting properties, antiinflammatory potency, and gastrointestinal irritation liability [4].
• QSAR and conformational analysis of the antiinflammatory agent amfenac and analogues [5].
• Simultaneous determination of amfenac sodium and its metabolite (7-benzoyl-2-oxindole) in human plasma by high-performance liquid chromatography [6].
• The two Rb cell lines were positive for COX-2 only in the Western blot, indicating that they probably express low levels of COX-2, which was undetectable by immucytochemical analysis.ConclusionThe selective, anti-COX-2 molecule amfenac inhibited proliferation of both tested Rb cell lines [7].

Biological context of amfenac sodium

• However, amfenac was a potent inhibitor of both COX-1 (IC50 = 0.25 microM) and COX-2 activity (IC50 = 0.15 microM) [8].

Anatomical context of amfenac sodium

• Nepafenac's clinical effectiveness in the posterior segment may be explained by its superior corneal permeation, biodistribution, and bioactivation to amfenac by the target tissues (i.e., iris, ciliary body, retina, and choroid) known to generate PGs [9].
• When amfenac was added to both of the cell lines, a statistically significant reduction in proliferation was observed in both cell lines [7].
• The enhanced permeability of nepafenac, combined with rapid bioactivation to amfenac by the iris/ciliary body and retina/choroid, make it a target specific NSAID for inhibiting prostaglandin formation in the anterior and posterior segments of the eye [10].
• It is concluded that amfenac sodium and the other drugs are able to inhibit granulocyte O2- production by blocking the activation of NADPH-oxidase [11].
• Effect of a non-steroidal anti-inflammatory drug (amfenac sodium) on polymorphonuclear leukocytes [12].

Gene context of amfenac sodium

• A series of substituted derivatives of 2-amino-3-benzoylphenylacetic acid (amfenac) has been synthesized and evaluated for antiinflammatory, analgesic, and cyclooxygenase inhibiting activity [13].
• Nepafenac is hydrolyzed by intraocular tissues to amfenac, a potent cyclooxygenase inhibitor [9].

Analytical, diagnostic and therapeutic context of amfenac sodium

• Compared with aspirin 600 mg, amfenac 100 mg provided greater and faster analgesia, lasting at least for 4 hours [1].

References