Comparative Pharmacology
Head-to-head clinical analysis: SOLARAZE versus VOLTAREN.
Peer-Reviewed Evidence
Head-to-head clinical analysis: SOLARAZE versus VOLTAREN.
SOLARAZE vs VOLTAREN
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Solaraze (diclofenac sodium) is a nonsteroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenase (COX-1 and COX-2) enzymes, reducing prostaglandin synthesis, which mediates inflammation and pain. In actinic keratosis, it may also induce apoptosis and decrease keratinocyte proliferation.
Diclofenac inhibits cyclooxygenase (COX-1 and COX-2) enzymes, reducing prostaglandin synthesis, thereby providing anti-inflammatory, analgesic, and antipyretic effects.
Apply 0.5 mL (1 unit dose) topically to actinic keratoses twice daily for 2 to 4 weeks, then 1 week off, repeat for a total of 3 treatment cycles.
Oral: 50-100 mg every 8-12 hours; maximum 150 mg/day. IM: 75 mg once daily for up to 2 days. Topical gel: apply 2-4 g to affected area 4 times daily.
None Documented
None Documented
Following topical application, the terminal elimination half-life of diclofenac from plasma is approximately 12 hours (range 8-15 hours). This reflects the slow absorption and distribution from the skin depot, with clinical relevance for twice-daily dosing.
Terminal elimination half-life is approximately 2 hours (range 1.2–2.5 hours) for diclofenac; this short half-life supports multiple daily dosing. The half-life is not significantly altered in renal impairment but may be prolonged in hepatic disease.
Solaraze (diclofenac sodium 3% gel) is primarily eliminated via hepatic metabolism followed by renal excretion of metabolites. Approximately 65% of a dose is excreted in urine as conjugated metabolites, with less than 1% as unchanged drug. About 35% is eliminated in feces via biliary excretion of metabolites.
Approximately 65% of a dose is excreted renally as unchanged drug and glucuronide conjugates, with about 35% eliminated via biliary/fecal routes as metabolites.
Category C
Category C
NSAID
NSAID