Pharmacological properties : תכונות פרמקולוגיות

Pharmacodynamic Properties

5.1 Pharmacodynamic properties
Pharmacotherapeutic group: anti‐inflammatory and anti‐rheumatic products, non‐steroids, acetic acid derivatives and related substances, ATC code: M01A B08
Inhibition of prostaglandin synthesis and COX‐2 selectivity All non‐steroidal anti‐inflammatory drugs (NSAIDs) have been shown to inhibit the formation of prostaglandins. It is this action which is responsible both for their therapeutic effects and some of their side effects. The inhibition of prostaglandin synthesis observed with etodolac differs from that of other NSAIDs. In an animal model at an established anti‐inflammatory dose, cytoprotective PGE concentration in the gastric mucosa have been shown to be reduced to a lesser degree and for a shorter period than other NSAIDs. This finding is consistent with subsequent in‐vitro studies which have found etodolac to be selective for induced cyclo‐oxygenase 2 (COX‐2, associated with inflammation) over COX‐1 (cytoprotective).
Furthermore, studies in human cell models have confirmed that etodolac is selective for the inhibition of COX‐2.
The clinical benefit of preferential COX‐2 inhibition over COX‐1 has yet to be proven.
Anti‐inflammatory effects
Experiments have shown etodolac to have marked anti‐inflammatory activity, being more potent than several clinically established NSAIDs.

Pharmacokinetic Properties

5.2 Pharmacokinetic properties
In man, etodolac is well absorbed following oral administration.
Etodolac is highly bound to serum proteins.
The elimination half‐life averages seven hours in man. The primary route of excretion is in the urine, mostly in the form of metabolites.
In subjects receiving daily doses of etodolac 400 mg or 600 mg to steady state levels over a three day period, the peak plasma concentrations were 7.5 μg/ml at 7.9 hours and 11.9 μg/ml at 7.8 hours.