The codein was reduced by hydrogen in the presence catalyst Pt (or Pd, or Ni)
and 7,8-dihydrocodein was obtained.
To the 7,8-dihydrocodein tartaric acid was added and mixed, in the result 7,8-
dihydrocodein bitartrate was obtained.
Antitussive, Narcotic analgesic
Potentially hazardous interactions with other drugs
Angiotensin-II antagonists: concentration increased
by telmisartan.
Anti-arrhythmics: concentration increased by
amiodarone, dronedarone and propafenone (half
maintenance dose of digoxin).
Antidepressants: concentration reduced by St John’s
wort - avoid.
Antifungals: increased toxicity if hypokalaemia
occurs with amphotericin; concentration increased
by itraconazole.
Antimalarials: concentration possibly increased
by quinine, hydroxychloroquine and chloroquine;
increased risk of bradycardia with mefloquine
Antivirals: concentration increased by daclatasvir.
Calcium-channel blockers: concentration increased
by diltiazem, lercanidipine, nicardipine, verapamil
and possibly nifedipine; increased risk of AV block
and bradycardia with verapamil.
Ciclosporin: concentration increased by ciclosporin.
Colchicine: possibly increased risk of myopathy
Diuretics: increased toxicity if hypokalaemia occurs;
concentration increased by spironolactone and
possibly potassium canrenoate.
Ticagrelor: concentration of digoxin increased.
Dihydrocodeine is metabolised in the liver via
the cytochrome P450 isoenzyme CYP2D6, to
dihydromorphine, which has potent analgesic activity,
although the analgesic effect of dihydrocodeine appears
to be mainly due to the parent compound; some is also
converted via CYP3A4 to nordihydrocodeine.
Dihydrocodeine is excreted in urine as unchanged drug
and metabolites, including glucuronide conjugates.
