he hydrochloride salt of the d-isomer of the synthetic opiate propoxyphene with weak narcotic analgesic activity.
Dextropropoxyphene mimics the effects of endogenous opiates by binding to mu receptors located throughout the central nervous system. The binding results in GTP to GDP exchanges on the mu-G-protein complex, by which the effector adenylate cyclase is inactivated, decreasing intracellular cAMP. This, in turn, inhibits the release of various nociceptive neurotransmitters, such as substance P, gamma-aminobutyric acid (GABA), dopamine, acetylcholine, noradrenaline, vasopressin, and somatostatin. In addition, dextropropoxyphene closes N-type voltage-gated calcium channels and opens calcium-dependent inwardly rectifying potassium channels, which results in neuronal hyperpolarization, a reduction in neuronal excitability, and a further decrease in the perception of pain.
Dextropropoxyphene has been withdrawn in the UK, Europe, the USA, and other countries because of its relatively common use in intentional overdose and its potential fatal toxicity in accidental overdose.