Oxymorphone
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Oxymorphone (14-hydroxydihydromorphinone) is a semi-synthetic opioid of the morphinan class. It is structurally derived from morphine, distinguished by higher potency and exceptional receptor selectivity. Oxymorphone is a full agonist at µ-opioid receptors, producing its effects by suppressing pain signaling and amplifying reward circuitry.[1]
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First synthesized in Germany in 1914,[2] oxymorphone entered US clinical use in 1959 as the injectable formulation Numorphan. Oral formulations introduced in 2006 expanded its clinical footprint, but a 2012 crush-resistant reformulation drove injection abuse that caused 181 HIV cases in Scott County, Indiana — the largest rural HIV outbreak in US history.[3] The FDA requested market withdrawal in 2017; generic extended-release formulations remain available.[4]
Subjective effects include profound analgesia, euphoria, sedation, anxiolysis, and cognitive slowing. The experience centers on deep, enveloping physical comfort and emotional insulation — a warm dissolution of pain and distress that narrows awareness to a quiet, weighted calm. Nausea, constipation, respiratory slowing, and a pronounced compulsive redosing urge are characteristic unsought effects.
Oxymorphone produces rapid physical dependence and carries high acute toxicity with a narrow therapeutic index.[5] Tolerance to analgesia develops faster than tolerance to respiratory depression, meaning dose escalation progressively increases overdose risk — a dynamic amplified by low oral bioavailability, which drives some users toward more dangerous routes of administration. Decades of clinical use and post-market surveillance provide a substantial evidence base, though isolated oxymorphone-only fatality data remain sparse.
History[edit]
Discovery
Oxymorphone was first synthesized in Germany in 1914[2] as part of early efforts to produce semi-synthetic derivatives from thebaine, a minor alkaloid of Papaver somniferum. The compound entered US clinical use in 1959 under the trade name Numorphan, available only in injectable and suppository form. For nearly five decades it remained a niche analgesic, overshadowed by morphine and later oxycodone.
Clinical expansion
In 2006, the FDA approved oral immediate-release and extended-release formulations (Opana, Opana ER) for moderate-to-severe pain,[4] with Phase III trials confirming efficacy in postsurgical pain[6] and osteoarthritis.[7][8] After OxyContin was reformulated with abuse-deterrent properties in 2010, oxymorphone ER abuse rose sharply — surveillance documented a relative risk increase of 2.91 compared with the pre-reformulation period.[9]
Public health crisis
In 2012, Endo Pharmaceuticals added a crush-resistant matrix to Opana ER to deter snorting and injection. The reformulation did not reduce abuse — it shifted the primary route to intravenous injection.[10] Between 2014 and 2015, Scott County, Indiana experienced 181 confirmed HIV cases from injection of dissolved tablets, the largest rural HIV outbreak in US history.[3][11] Hepatitis C co-infection was identified in 92.3% of cases.[12]
Market withdrawal
In June 2017, an FDA advisory committee voted 18–8 that reformulated Opana ER's risks outweighed its benefits — the first time the FDA requested removal of an opioid due to abuse-related public health consequences.[4] Endo Pharmaceuticals withdrew the product in July 2017, with formal NDA withdrawal published in December 2020.[13] Generic extended-release oxymorphone formulations remain available in the United States as of 2026.
The name oxymorphone derives from its structural relationship to morphine: the oxy- prefix indicates the 14-hydroxy and C-6 keto modifications, while -morphone truncates morphinone, the ketone structural analog of morphine. The trade name Numorphan — a compression of "new morphine analog" — was used for the original 1959 injectable formulation. Opana, the oral brand introduced in 2006, became more widely recognized in the context of the opioid crisis.
Chemistry[edit]
Structural class
Oxymorphone belongs to the morphinan class — specifically the substituted morphinans, pentacyclic derivatives sharing the 4,5-epoxymorphinan core scaffold. It is derived from thebaine, a minor alkaloid of Papaver somniferum, through semi-synthetic modification. Its systematic name, 14-hydroxydihydromorphinone, reflects the two changes that distinguish it from morphine: a hydroxyl group at carbon-14 and a ketone at carbon-6, with saturation of the C-7,8 double bond. The C-6 carbonyl enhances mu opioid receptor affinity and potency relative to morphine.[15]
Oxymorphone is structurally related to several clinical opioids. Oxycodone differs by a methoxy group at C-3 rather than a free phenol; oxymorphone is in fact a metabolite of oxycodone, produced via CYP2D6-mediated O-demethylation.[16] Hydromorphone shares the C-6 ketone but lacks the 14-hydroxy group.
Molecular properties
| Molecular formula | C₁₇H₁₉NO₄ |
| Molecular weight | 301.34 g/mol |
The morphinan scaffold contains five fused rings: a benzene ring, two partially saturated cyclohexane rings, a piperidine ring, and a dihydrofuran ring forming the 4,5-epoxy bridge. The phenolic hydroxyl at C-3 and the ketone at C-6 are the principal functional groups, with an additional hydroxyl at C-14. The N-methyl group on the piperidine nitrogen is characteristic of morphinan agonists.
Stereochemistry
Oxymorphone possesses four defined stereocenters, conferring the natural (−)-morphinan configuration essential for opioid receptor activity.[17] The (+)-enantiomer is inactive at opioid receptors. Only the (−)-isomer is used therapeutically.
Physical properties
Oxymorphone hydrochloride, the pharmaceutical salt form, is a white to off-white crystalline powder. It is more lipid-soluble than morphine, facilitating rapid penetration into the central nervous system.[18] Detailed solubility and melting point data for the free base have not been published.citation needed
Pharmacology[edit]
Mechanism of action
Oxymorphone is a full agonist at the mu opioid receptor (μ-opioid), binding with exceptionally high affinity — among the strongest of any clinical opioid, alongside sufentanil and buprenorphine.[19] Modeling studies confirm 40–60-fold higher MOR affinity than its parent compound oxycodone.[16]
MOR activation triggers a signaling cascade that hyperpolarizes neurons and reduces neurotransmitter release, suppressing pain signals at both spinal and brain level.[20] In the brain's reward circuitry, this activation releases dopamine in the nucleus accumbens, producing euphoria and reinforcement.
Comprehensive pharmacological screening identifies oxymorphone as the most MOR-selective clinical opioid tested, with no significant activity at other opioid receptor types, sigma receptors, or monoamine transporters.[1] This selectivity distinguishes it from mixed-action opioids and means its effects are mediated almost entirely through a single receptor system.
Pharmacokinetics
Oral bioavailability is approximately 10% — substantially lower than most clinical opioids — due to extensive first-pass liver metabolism.[18] Immediate-release formulations reach peak blood levels in about 30 minutes; extended-release formulations peak at 2–3 hours.[18] The half-life ranges from 7 to 10 hours depending on formulation.[18]
Low plasma protein binding (10–12%) combined with high lipid solubility allows rapid entry into the central nervous system.[18] The primary metabolic pathway is glucuronidation to an inactive metabolite, with minor pathways producing small amounts of active 6-OH-oxymorphone.[21][22]
Critically, oxymorphone bypasses the CYP450 enzyme system used by nearly all other opioids,[23] resulting in fewer metabolic drug interactions than oxycodone, methadone, or fentanyl.
Neuroscience[edit]
Where it acts
Oxymorphone's pain-relieving effects originate in the periaqueductal gray and rostral ventromedial medulla, where mu receptor activation engages the brain's descending pain-suppression pathway, reducing pain signals at the spinal cord.[20] Oxymorphone also acts directly on mu receptors in the spinal dorsal horn, providing dual-level analgesia.
Its rewarding effects arise in the ventral tegmental area, where mu receptor activation releases a surge of dopamine into the nucleus accumbens — the neural substrate of opioid euphoria and the reinforcement that drives compulsive use.[20] Because oxymorphone acts almost exclusively through mu receptors,[1] its reward signal lacks the dysphoric modulation seen in mixed-action opioids.
Why it matters
The distinction between wanting (dopamine-driven craving) and liking (hedonic pleasure) is central to understanding oxymorphone dependence. With chronic use, wanting intensifies as the brain sensitizes to drug cues, while liking diminishes as tolerance erodes hedonic effects — a dissociation that drives compulsive use without proportional pleasure. The extreme dose-escalation patterns seen in the Scott County outbreak[3] illustrate this dynamic.
At the molecular level, repeated mu receptor activation triggers compensatory changes: receptor internalization, reduced signaling efficiency, and upregulation of opposing cellular pathways.[20] These adaptations define opioid tolerance and reset the brain's baseline state, producing withdrawal when the drug is removed.
Whether oxymorphone preferentially activates certain intracellular signaling pathways (G-protein versus β-arrestin) at the mu receptor remains unknown — an answer would clarify its respiratory depression and tolerance profiles. The active metabolite 6-OH-oxymorphone has never been characterized for receptor binding, leaving its contribution to overall effects uncertain.
Subjective Effects[edit]
The experience of oxymorphone centers on warm, enveloping analgesia accompanied by anxiolysis and deepening sedation. Physical comfort and emotional insulation define the gestalt — pain and distress dissolve into a weighted calm that narrows awareness. At lower doses the effect is primarily analgesic with subtle mood elevation; at higher doses euphoria intensifies and cognitive activity slows to a quiet drift. Route of administration profoundly shapes the experience: oral dosing produces gradual onset with attenuated euphoria, while parenteral routes compress onset and amplify reinforcement.
Compared with oxycodone, oxymorphone produces comparable drug liking and euphoria at equivalent analgesic doses.[24] Compared with morphine, its greater lipid solubility produces a subjectively sharper onset and higher ceiling of mu-receptor-mediated effects.[18] Set and setting modulate the anxiolytic dimension, with pain states and psychological distress amplifying the subjective relief.
Effect Grid
Full therapeutic analgesia dominates the experience. Clear euphoria emerges as warm emotional satisfaction and bodily comfort. Pronounced sedation and anxiety suppression produce a state of deep physical and psychological ease. This is the standard clinical dose range (10–20 mg IR).
Constipation, nausea, and pupil constriction (miosis) are expected. A pervasive body high — warmth and tactile euphoria — settles across the body. Respiratory depression is present but typically subclinical at these doses in opioid-naive individuals without co-intoxicants.
Thought deceleration and cognitive impairment become noticeable — focus suppression and reduced information processing. Compulsive redosing urge may emerge. Duration is 4–6 hours. Ethanol co-ingestion increases peak concentration by 14–80% and must be avoided.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Vestibular distortion · Visual haze / noise · Visual processing suppression · Internal hallucinations
Sedation · Body high · Spontaneous body sensations · Bodily heaviness · Muscle relaxation · Tactile euphoria · Nausea · Physical fatigue · Sexual arousal suppression · Dizziness · Dry mouth · Tingling / electric sensations · Appetite suppression · Excessive sweating · Insomnia · Nasal congestion · Temperature dysregulation · Vomiting · Yawning · Nystagmus (eye wobbles) · Pain enhancement · Bodily dissociation
Bodily heaviness · Muscle relaxation · Tactile euphoria · Nausea · Physical fatigue · Sexual arousal suppression · Dizziness · Dry mouth · Tingling / electric sensations · Appetite suppression · Excessive sweating · Insomnia · Nasal congestion · Vomiting · Yawning · Nystagmus (eye wobbles) · Pain enhancement · Bodily dissociation
Analysis suppression · Focus suppression · Information processing suppression · Thought deceleration · Memory suppression · Motivation suppression · Aesthetic enhancement · Confusion · Language suppression · Memory fragmentation · Thought disorganization · Amnesia
Thought deceleration · Memory suppression · Motivation suppression · Aesthetic enhancement · Confusion · Language suppression · Memory fragmentation · Thought disorganization
Anxiety · Dysphoria · Empathy enhancement · Irritability
Social disconnection · Social connection · Trust enhancement · Sociability enhancement · Depersonalization · Derealization · Cognitive disconnection
Depersonalization · Derealization · Cognitive disconnection
Timeline
Initial warmth spreads through the trunk as subtle analgesia begins. Effects are faint — a quiet shift in baseline comfort rather than a clear drug onset.
Analgesia deepens noticeably. Euphoria emerges as warm emotional satisfaction. Sedation begins settling over the body.
Full analgesia, maximum euphoria, pronounced sedation, and cognitive slowing. Miosis is established. Body high is at its warmest and most enveloping.
Effects gradually diminish. Residual sedation and analgesia persist but euphoria fades. Nausea typically resolves.
Mild residual sedation and possible constipation. Baseline affect gradually returns. Subclinical impairment may persist well beyond subjective resolution due to the 7–10 hour elimination half-life.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- High
- Withdrawal
- Severe
- Tolerance buildup
- moderate
- Tolerance reset
- 28 days
- Physical
- High
- Psychological
- High
- Compulsive redosing
- High
- Dose escalation
- High
- Cross-tol.
- morphine · oxycodone · hydromorphone
Toxicity
Acute toxicity
Oxymorphone carries high acute toxicity with a narrow therapeutic index. The primary cause of fatal overdose is respiratory depression progressing to oxygen deprivation and cardiac arrest.[25]
Published postmortem data document fatalities at blood concentrations as low as 0.13 mg/L in combination with other drugs.[5][26] No isolated oxymorphone-only fatalities with postmortem toxicology have been published, consistent with the broader pattern that most opioid overdose deaths involve co-intoxicants. No human LD₅₀ has been established.safety citation needed
Respiratory depression
Oxymorphone produces dose-dependent suppression of breathing via mu receptor activation in brainstem respiratory centers.[25] Controlled human data show that intravenous oxymorphone at clinical doses reduces breathing volume by approximately 40%.[27] THC co-administration additively worsens this effect.[27]
Thrombotic microangiopathy
A unique and severe complication — blood vessel damage with kidney injury (thrombotic microangiopathy) — was documented in patients who injected the reformulated crush-resistant Opana ER tablets.[28][29][30]
The cause is not oxymorphone itself but the polyethylene oxide (PEO) excipient added in the 2012 reformulation.[31] Symptoms include destruction of red blood cells, low platelet counts, and acute kidney failure.[28][30] Additional complications include retinal detachments.[32] Kidney recovery is often incomplete.[28][33]
This complication was a significant factor in the FDA's 2017 market withdrawal request.[4]
Chronic toxicity
No substance-specific chronic organ damage has been documented beyond the class effects of long-term opioid use: hormonal disruption, immune suppression, and increased pain sensitivity. Chronic toxicity is rated high based on the dependence and withdrawal profile inherent to potent mu opioid receptor agonists.
Psychological risks
The primary psychological risks are dependence-associated: compulsive drug-seeking, narrowing of behavioral repertoire, and withdrawal-mediated distress including anxiety, low mood, and insomnia. Cognitive impairment at therapeutic doses includes reduced attention, slowed processing, and decision impairment.[24]
Oxymorphone does not produce psychosis, hallucinations, or psychedelic-type psychological crises at standard doses. At very high doses, confusion and delirium may occur as manifestations of severe central nervous system depression rather than psychoactive effects.
Tolerance & dependence
Tolerance
Effects diminish with repeated use, requiring dose escalation to maintain pain suppression and subjective effects. Tolerance develops to analgesia, euphoria, sedation, and partially to respiratory depression, while tolerance to constipation and pupil constriction develops more slowly.[34] Cross-tolerance with all other mu opioid agonists is a class effect.[20]
Physical dependence
Physical dependence develops with repeated use. Withdrawal symptoms include anxiety, restlessness, muscle aches, sweating, diarrhea, nausea, vomiting, and insomnia. Based on the 7–10 hour half-life, withdrawal onset is expected within 12–24 hours of the last dose, peaking at 36–72 hours and resolving over 5–10 days.citation needed
Severe opioid withdrawal can in rare cases cause muscle breakdown, contradicting the common clinical assertion that opioid withdrawal is never life-threatening.[35]
Dependence liability
Oxymorphone has high dependence liability. At equianalgesic doses, it produces drug liking and euphoria comparable to oxycodone.[24] Post-OxyContin reformulation surveillance documented a 2.91-fold relative risk increase in oxymorphone ER abuse.[9] The Scott County outbreak demonstrated extreme compulsive injection patterns in a community context.[3]
People who cannot convert oxycodone to oxymorphone (CYP2D6 poor metabolizers) are significantly underrepresented among opioid-dependent individuals, suggesting oxymorphone formation contributes to the abuse liability of oxycodone itself.[36]
Drug interactions
The most dangerous interactions involve additive respiratory and central nervous system depression. Oxymorphone's unusual bypass of CYP450 metabolism reduces metabolic drug interactions relative to other opioids, but pharmacodynamic interactions remain severe.
CNS depressant synergy
Alcohol, benzodiazepines, GHB/GBL, and other opioids produce additive to synergistic respiratory depression when combined with oxymorphone. Alcohol co-ingestion increases peak blood levels by 14–80%[37] while independently suppressing breathing. Published fatalities have consistently involved co-intoxicants.[5][26]
Cannabis interaction
Controlled human data demonstrate that THC additively worsens oxymorphone-induced respiratory depression.[27]
Metabolic interactions
Oxymorphone does not inhibit or induce major CYP450 enzymes,[38][23] making it less susceptible to metabolic drug interactions than oxycodone, methadone, or fentanyl. However, when oxymorphone is generated as a metabolite of oxycodone, CYP3A4 inhibitors increase oxymorphone exposure by redirecting oxycodone through the CYP2D6 pathway.[16]
Serotonergic interactions
No significant SERT activity has been detected for oxymorphone.[1] Serotonin syndrome risk is therefore lower than for tramadol, tapentadol, or meperidine, though formal interaction studies have not been published.
Contraindications
Absolute contraindications from FDA-approved labeling[39]:
- Significant respiratory depression in unmonitored settings
- Acute or severe asthma in unmonitored settings
- Known or suspected gastrointestinal obstruction, including paralytic ileus
- Hypersensitivity to oxymorphone hydrochloride or any formulation component
Relative contraindications:
- Concurrent alcohol use — peak blood level increase of 14–80% plus additive respiratory depression[37]
- Concurrent benzodiazepine or CNS depressant use — additive respiratory depression; documented in fatal cases[5]
- Liver impairment — oxymorphone is metabolized in the liver; impaired function may increase exposurecitation needed
- Kidney impairment — reduced clearance of metabolites; dose adjustment likely requiredcitation needed
- History of substance use disorder — high abuse liability confirmed in human and surveillance data[24][9]
Harm Reduction[edit]
Forms & Identification
Oxymorphone is encountered as pharmaceutical tablets in immediate-release and extended-release formulations. Because it is a pharmaceutical product rather than a clandestine preparation, the primary identification concern is confirming tablet identity and dose — counterfeit pharmaceutical tablets containing fentanyl or fentanyl analogs circulate across opioid markets. Fentanyl test strips can detect contamination in dissolved tablet material and should be used on any tablet of uncertain provenance.
Extended-release tablets that use a crush-resistant polyethylene oxide matrix pose a specific, severe risk when injected: the excipient causes blood vessel damage and kidney failure independent of the opioid itself.[28] Identifying the specific formulation — brand, generic manufacturer, matrix type — matters for harm reduction in ways unique to this compound.
Guidelines
- Test any tablet of uncertain provenance with fentanyl test strips before use
- Start with the lowest available dose, especially with a new source or after any period of reduced use — tolerance drops rapidly during abstinence, and oxymorphone's low oral bioavailability (approximately 10%) means parenteral doses are dramatically more potent than oral doses
- Take oral doses on an empty stomach or with consistent food intake — food increases peak blood levels by approximately 38%[39]
- Do not consume alcohol before, during, or after use — alcohol increases oxymorphone blood levels by 14–80%[37] and independently suppresses breathing
- Never use alone — respiratory depression can progress without warning
- Keep naloxone accessible and ensure anyone present knows how to administer it
- Do not crush, break, or dissolve extended-release tablets — this defeats the controlled-release mechanism and delivers a potentially fatal bolus dose
Set & Setting
Oxymorphone should never be used alone. Respiratory depression can progress from breathing to not breathing without the person's awareness, and the presence of a sober observer who knows how to recognize overdose and administer naloxone is the single most important environmental safeguard. A calm, comfortable environment reduces the likelihood of anxiety-driven redosing.
Aftercare & integration. Opioid use — particularly at doses producing euphoria — creates a neurochemical aftermath. In the hours and days following use, mood may drop below baseline as the brain's reward system recalibrates. Adequate hydration, nutrition, and sleep support physical recovery. Constipation may persist for 24–48 hours after the last dose.
For people using oxymorphone for pain management, honest assessment of whether the analgesic benefit justifies escalating dose requirements is a recurring decision point. If the dose needed for pain suppression is climbing steadily, consultation with a pain specialist about opioid rotation or multimodal pain strategies is warranted.
Recovery & Support
Oxymorphone dependence responds to the same evidence-based treatments as other opioid use disorders. Medication-assisted treatment with buprenorphine or methadone reduces mortality, suppresses withdrawal, and stabilizes daily functioning. Naltrexone (oral or extended-release injectable) is an option after complete detoxification.
Abrupt cessation after prolonged use produces withdrawal that, while rarely life-threatening, is intensely uncomfortable and a primary driver of relapse. Medically supervised tapering or transition to buprenorphine reduces withdrawal severity. Peer support programs including SMART Recovery and mutual aid groups provide ongoing structure. Anyone experiencing difficulty reducing or stopping use should seek professional support — opioid use disorder is a medical condition, not a moral failure.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Breathing becomes slow (fewer than 8 breaths per minute), shallow, or stops
- Lips, fingernails, or skin turn blue or gray
- Person is unresponsive to voice or sternal rub (knuckles pressed firmly on breastbone)
- Gurgling, choking, or snoring sounds in an unconscious person
Immediate steps:
- 1. Call emergency services immediately
- 2. Administer naloxone if available — intranasal (one spray in one nostril) or intramuscular injection; repeat after 2–3 minutes if no response
- 3. Place the person in the recovery position (on their side) to prevent choking
- 4. Begin rescue breathing if the person is not breathing: tilt head back, lift chin, give one breath every 5 seconds
- 5. Stay with the person — naloxone wears off in 30–90 minutes, and respiratory depression may return
- 6. Do NOT induce vomiting
What to tell the dispatcher: State that the person is not breathing or breathing very slowly, that an opioid is suspected, whether naloxone has been given, the approximate time of last use, and any other substances involved. Good Samaritan laws in many jurisdictions protect people who call for help during an overdose.
Reversal agent: Naloxone (Narcan) reverses opioid respiratory depression within 1–3 minutes. Because oxymorphone's half-life (7–10 hours) exceeds naloxone's duration of action (30–90 minutes), repeated doses or continuous monitoring may be necessary. Naloxone will precipitate withdrawal in opioid-dependent individuals — this is uncomfortable but not life-threatening.
Legal Status[edit]
Oxymorphone is internationally controlled as a narcotic substance, reflecting its high abuse potential and accepted medical use under supervised prescribing conditions.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule II (Controlled Substances Act) | High abuse potential with accepted medical use; prescription required. Brand Opana ER withdrawn July 2017; generic ER formulations remain available[2][4] |
| United Kingdom | Class A, Schedule 2 (Misuse of Drugs Act 1971) | Most restrictive classification for therapeutic controlled drugs; placed alongside morphine and diamorphine[40] |
| Australia | Schedule 8 (Controlled Drug) | Restricted to medical use with specific prescribing requirementscitation needed |
| Canada | Schedule I (CDSA — Narcotic) | Listed under the Controlled Drugs and Substances Actcitation needed |
| International | Schedule I (UN Single Convention on Narcotic Drugs, 1961) | Subject to international narcotics controlscitation needed |
The formal NDA withdrawal for Opana ER was published in the Federal Register in December 2020.[13] This was unprecedented — the first time the FDA requested withdrawal of an approved opioid product due to abuse-related public health consequences rather than intrinsic safety defects of the active ingredient.
references
- [1] ^abcdOlson KM, Duron DI, Womer D, Fell R, Streicher JM (2019) Comprehensive molecular pharmacology screening reveals potential new receptor interactions for clinically relevant opioids — PLoS ONE doi:10.1371/journal.pone.0217371
- [2]
- [3] ^abcdPeters PJ, Pontones P, Hoover KW, et al. (2016) HIV Infection Linked to Injection Use of Oxymorphone in Indiana, 2014-2015 — New England Journal of Medicine doi:10.1056/nejmoa1515195
- [4]
- [5] ^abcdVorce SP, Levine B, McDonough PC, Past MR (2010) An overdose death involving the insufflation of extended-release oxymorphone tablets. — Journal of analytical toxicology PMID:21819798
- [6] ^Gimbel J, Ahdieh H (2004) The efficacy and safety of oral immediate-release oxymorphone for postsurgical pain — Anesthesia and Analgesia doi:10.1213/01.ane.0000132548.91622.b3