[Rich66]

Ok...no idea if this makes it ok, but..looks like Oxycodone works on a different receptor(not mu) than morphine:

The intrinsic antinociceptive effects of oxycodone appear to be kappa-opioid receptor mediated Journal name Pain Publication date 1997 Volume number 73 Start page 151 End page 157 Abstract Our previous studies in the Sprague-Dawley rat showed that the intrinsic antinociceptive effects of oxycodone are naloxone reversible in a manner analogous to morphine but that in contrast to morphine, oxycodone's antinociceptive effects have a rapid onset of maximum effect (approximate to 5-7 min compared to 30-45 min for morphine), comprise one antinociceptive phase (compared to two phases) and are of relatively short duration (approximate to 90 min compared to approximate to 180 min). In the present study, administration of a range of selective opioid receptor antagonists has shown that the intrinsic antinociceptive effects of oxycodone (171 nmol) are not attenuated by i.c.v. administration of (i) naloxonazine, a mu(1)-selective opioid receptor antagonist, or (ii) naltrindole, a delta-selective opioid receptor antagonist, in doses that completely attenuated the intrinsic antinociceptive effects of equipotent doses of the respective mu- and delta-opioid agonists, morphine and enkephalin-[D-Pen(2,5)] (DPDPE). Although beta-funaltrexamine (beta-FNA) attenuated the antinociceptive effects of oxycodone (171 nmol i.c.v.), it also attenuated the antinociceptive effects of morphine and bremazocine (kappa-opioid agonist) indicative of non-selective antagonism. Importantly, the antinociceptive effects of oxycodone (171 nmol i.c.v.) were markedly attenuated by the prior i.c.v. administration of the selective kappa-opioid receptor antagonist, norbinaltorphimine (nor-BNI), in a dose (0.3 nmol) that did not attenuate the antinociceptive effects of an equipotent dose of i.c.v. morphine (78 nmol). Taken together, these data strongly suggest that the intrinsic antinociceptive effects of oxycodone are mediated by K-opioid receptors, in contrast to morphine which interacts primarily with mu-opioid receptors. (C) 1997 International Association for the Study of Pain. Published by Elsevier Science B.V.

But...a subset of mu?
Preclinical Studies of the Combination of Morphine Plus Oxycodone

Pharmacology

Different opioids appear to interact differently with various opioid receptor subtypes (mu, delta, kappa), and some opioids have mixed agonist/antagonist effects. Recent studies have shown that there are at least 10 mu receptor subtypes in humans, and that individual patients differ in the extent to which a drug such as morphine binds to a subset of these mu receptors. Based on results of molecular pharmacology studies, a research team headed by Maree Smith (Univ. Queensland, AUS) and others have demonstrated morphine binds to multiple mu receptors with varying potencies, whereas oxycodone binds to kappa-2 receptors, as well as a subset of mu-receptors (Nielsen et al, Pain, 2007, 132: 289-300).
This work supports the concept of opioid potentiation (see Fig 1). Isobologram analysis (Fig 2) in rodent pain models demonstrated that the concurrent administration of morphine and oxycodone in ratios of 3:1, 1:1 or 1:3, produced marked analgesic synergy in response to painful stimuli (Ross et al, Pain, 2000, 84: 421-428). Interestingly, Smith’s group observed no potentiation of side effects.
Specifically, sedation and respiratory depression were not enhanced by dual opioids. Other studies in rodents suggest that a kappa agonist (eg, oxycodone) and a mu agonist (morphine) are antagonistic in respect to respiratory depression (Dosaka-Akita, J. Pharm. Exptl. Ther., 1993, 264: 631-637). Subsequently, Pasternak’s group in U.S. similarly demonstrated in rodents that combinations of other opioid agonists commonly produced analgesic synergy compared to the doses needed of either opioid given alone (Bolan et al, J. Pharmacol. Exptl. Ther., 2002, 303: 557-562).