Oxycodone, is a semisynthetic narcotic with multiple actions qualitatively similar to those of morphine; the most prominent of these involves the central nervous system and organs composed of smooth muscle. Oxycodone, as the hydrochloride salt, is a pure agonist opioid whose principal therapeutic action is analgesia and has been in clinical use since 1917. Like all pure opioid agonists, there is no ceiling effect to analgesia, such as is seen with partial agonists or non-opioid analgesics.


Oxycodone is an agonist of µ-opioid receptor. Compared with morphine and oxymorphone, one of its own metabolites, oxycodone has a considerably lower µ-opioid receptor-binding affinity. Oxycodone also binds to κ-opioid and δ-opioid receptors, but with a lower affinity than to µ-receptors. Interestingly, there is some evidence that the effects of oxycodone might be mediated by not only µ-receptors but partly also by κ-opioid receptors. If this were true, it would give a nice explanation for the good efficacy of oxycodone in experimental visceral and neuropathic pain in which κ-opioid receptors play an important role in the mediation of pain.
The relationship between the plasma level of Oxycodone and the analgesic response depend on the patient's age, state of health, medical condition and extent of previous opioid treatment.