Enkephalins are endogenous peptides that bind to opioid receptors and have a particularly high affinity for the δ-subtype. Activation of the δ-receptors inhibits the enzyme adenylyl cyclase, resulting in a decrease in intracellular levels of the neurotransmitter cAMP. This reduces diarrhea-induced hypersecretion in the small intestine. Enkephalinase enzymes normally rapidly degrade enkephalin. In particular, the active metabolite of the drug, thiorphan, but also racecadotril itself, inhibit enkephalinase in the intestinal epithelium and protect enkephalins from degradation by these enzymes. This significantly prolongs the action of enkephalins and reduces diarrhea symptoms.
Inhibition of enkephalinases begins about 30 minutes after administration, reaches its maximum about two hours after administration, and persists for eight hours.
Racecadotril is rapidly absorbed after oral administration and reaches maximum plasma concentration within 60 minutes. Food ingestion delays the time to this maximum by 60 to 90 minutes, but has no effect on overall bioavailability. Racecadotril is rapidly and effectively metabolized in the liver to the major active metabolite, thiorphan. 90% of the substance is bound to blood plasma proteins. The elimination half-life, as measured by enkephalinase inhibition, is three hours. Thiorphan is then further metabolized to inactive metabolites. Both active and inactive metabolites are excreted largely by the kidneys (81.4%) and to a lesser extent by the feces (8%).
The drug has a very low potential for interaction with other drugs. The combination of racecadotril with an ACE inhibitor may theoretically increase the risk of angioedema.