Actions of Ibuketa in details
Pharmacology: Ibuketa exhibits analgesic and antipyretic activity by inhibiting prostaglandin synthesis. It produces analgesia by elevating the pain threshold and antipyresis through action on the hypothalamic heat-regulating center.
In therapeutic doses, Ibuketa's analgesic and antipyretic action is comparable to that of aspirin. Ibuketa does not adversely affect platelet function and hemostasis.
Pharmacokinetics: Ibuketa is rapidly and completely absorbed after oral administration. Peak plasma concentrations occur between 15 min to 2 hrs after ingestion. The absolute oral bioavailability of Ibuketa is about 80% and is independent of dose in the range of 5-20 mg/kg.
Ibuketa is not bound to plasma proteins to any extent. The concentrations of Ibuketa in saliva are similar to those in plasma. Concentrations in whole blood are up to 20% higher and in breast milk about 20% lower than the plasma concentration. Ibuketa crosses the placenta.
Ibuketa is extensively metabolized in the liver and the total body clearance is about 5 mL/kg/min. The clearance of Ibuketa is reduced and the half-life increased following a hepatotoxic overdose. Prolongation of half-life beyond 4 hrs usually indicates impending liver damage.
Two to five percent of a therapeutic dose of Ibuketa is excreted unchanged in the urine. Its renal clearance is about 10 mL/min and is weakly dependent on urine flow rate but not on pH.
Ibuketa administration
May be taken with or without food.
Ibuketa pharmacology
The analgesic, antipyretic, and anti-inflammatory effects of aspirin are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Ibuketa directly and irreversibly inhibits the activity of both types of cyclo-oxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes aspirin different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Ibuketa's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation–inhibiting effect of aspirin specifically involves the compound's ability to act as an acetyl donor to the platelet membrane; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Ibuketa affects platelet function by inhibiting the enzyme prostaglandin cyclooxygenase in platelets, thereby preventing the formation of the aggregating agent thromboxane A2. This action is irreversible; the effects persist for the life of the platelets exposed. Ibuketa may also inhibit formation of the platelet aggregation inhibitor prostacyclin (prostaglandin I2) in blood vessels; however, this action is reversible.
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Information checked by Dr. Sachin Kumar, MD Pharmacology
