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Loxoprofen Na Amel Actions |
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Analgesic/anti-inflammatory.
Pharmacology: Sodium Loxoprofen Na Amel, synthesized and developed by Sankyo Co. Ltd., is a new nonsteroidal analgesic and anti-inflammatory drug in the phenylpropionic acid group. It is rapidly absorbed from the gastrointestinal tract and shows excellent analgesic and anti-inflammatory effects, while this drug is characterized by its relatively lower toxicity to the gastrointestinal tract than other nonsteroidal analgesic and anti-inflammatory drugs because it is a prodrug showing effects after conversion to active compounds in the body.
Loxoprofen Na Amel has excellent analgesic and anti-inflammatory effects, and its analgesic effect is specifically powerful. Loxoprofen Na Amel has pharmacological characteristics eg, a relatively lower toxicity to the gastrointestinal tract than other nonsteroidal analgesic and anti-inflammatory drugs because it is the prodrug showing the effect after absorption from the gastrointestinal tract and conversion to active metabolites. The mode of action of Loxoprofen Na Amel is prostaglandin biosynthesis inhibition and its site of action is cyclooxygenase.
Pharmacokinetics: After oral administration, Loxoprofen Na Amel is rapidly absorbed from the digestive tract in the unchanged form causing weak irritation to the stomach mucosa, and then rapidly converted to an active metabolite, the trans-alcohol form (in SRS configuration) which potently inhibits prostaglandin biosynthesis.
Urinary excretion of Loxoprofen Na Amel is rapid, and most amount of the drug administered is excreted in the unchanged form or in the glucuronic acid conjugated trans-OH form. About 50% of the dose is excreted in the urine within 8 hrs after administration.
Should be taken with food. Take w/ or immediately after meals.
The exact mechanisms of action of Loxoprofen Na Amel is unknown. Its antiinflammatory effects are believed to be due to inhibition of both cylooxygenase-1 (COX-1) and cylooxygenase-2 (COX-2) which leads to the inhibition of prostaglandin synthesis, and results in the inhibition of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.
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Information checked by Dr. Sachin Kumar, MD Pharmacology
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