Infen-25 Mechanism of Action

Non-steroidal anti-inflammatory.
Pharmacology: Mechanism of Action: The mechanism of action of non-steroidal anti-inflammatory drugs is related to the reduction of prostaglandin synthesis by the inhibition of cyclooxygenase pathway. Dexketoprofen has been demonstrated to be an inhibitor of COX-1 and COX-2 activities in experimental animals and humans. Specifically, there is an inhibition of the transformation of arachidonic into cyclic endoperoxides, PGG₂ and PGH₂, which produce prostaglandins PGE₁, PGE₂, PGF_2α and PGD₂ and also prostacyclin PGI₂ and thromboxanes (TxA₂ and TxB₂). Inhibition of the synthesis of prostaglandins may also affect other inflammatory mediators like kinins which is an indirect action. Clinical studies performed on several pain models demonstrated effective analgesic activity of dexketoprofen trometamol. The onset of the analgesic activity was obtained in some studies at 30 minutes post-administration. The analgesic effect persists for 4 to 6 hours.
Pharmacokinetics: After oral administration of dexketoprofen trometamol to humans, the C_max is reached at 30 min (range 15 to 60 min). When administered concomitantly with food, the AUC does not change, however the C_max of dexketoprofen trometamol decreases and its absorption rate is delayed (increased t_max). The distribution half-life and elimination half-life values of dexketoprofen trometamol are 0.35 and 1.65 hours, respectively. As with other drugs with a high plasma protein binding (99%), its volume of distribution has a mean value below 0.25 l/kg. The main elimination route for dexketoprofen is glucuronide conjugation followed by renal excretion. There is no conversion of dexketoprofen to the R-(-) enantiomer in humans. Dexketoprofen does not accumulate after multiple-doses in humans.