Source: Medicines & Healthcare Products Regulatory Agency (GB) Revision Year: 2018 Publisher: Almirall, S.A., Ronda General Mitre 151, 08022, Barcelona, Spain
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.
Experiments have shown etodolac to have marked anti-inflammatory activity, being more potent than several clinically established NSAIDs.
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 Lodine SR 400mg or 600mg to steady state levels over a three day period, the peak plasma concentrations were 7.5µg/ml at 7.9 hours and 11.9µg/ml at 7.8 hours.
Nothing of note to the prescriber.
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