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Mechanism of action

Dihydrocodeine is metabolized to dihydromorphine -- a highly active metabolite with a high affinity for mu opioid receptors. [3]

Pharmacodynamics

Possible opioid related side effects include, but are not limited to, drowsiness, nausea, headache, dry mouth, constipation, difficulty passing urine, and mild euphoria.

Pharmacokinetics

Half-life

4h

Absorption

Bioavailability is low (approximately 20%) if administered orally. This may be due to poor gastrointestinal absorption. It is also likely due to pre-systemic metabolism by the liver and intestinal wall. [2] The AUCs after oral and intravenous administration are similar (3203ug/l/h and 3401ug/l/h, respectively). [2] Time to peak values are 1.6 and 1.8hours for a 30mg and 60mg dose, respectively. The concentrations achieved were 71.8 ug/1 and 146 ug/1, respectively. [2]
Renal elimination and urinary excretion. [1]
The disposition of dihydrocodeine is described as a two compartment model. [2]
Plasma clearance is approximately 300ml/min. [2] The pharmacokinetics of dihydrocodeine and active metabolite dihydromorphine have been reported to be linear. [1] The decline in plasma dihydrocodeine concentrations after intravenous administration has been described as bi-exponential, with a sleep decline in the initial 2h following administration, followed by a mono-exponential decline thereafter. Clearance was not dose dependent. [2]

Metabolism

Metabolized in the liver by CYP 2D6 into an active metabolite, dihydromorphine, and by CYP 3A4 into secondary primary metabolite, nordihydrocodeine. A third primary metabolite is dihydrocodeine-6-glucuronide. [1] The time for mean peak concentration in acid metabolites is 1.76h and 1.98h for a 30 and 60mg dose, respectively. The concentrations achieved were 563 ug/1 and 1476 ug/1, respectively. [2]
Dihydrocodeine has known human metabolites that include Desmethyl dihydrocodeine and Paramorfan.

Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.