PAIN MEDICINE

Volume 10 • Number S1 • 2009

REVIEW ARTICLES

Clinical Pharmacology of Oxymorphone

Howard S. Smith, MD
Anesthesiology and Academic Director of Pain Management, Albany Medical College, Department of Anesthesiology,

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Albany, New York, USA

ABSTRACT

Oxymorphone (14-hydroxydihydromorphinone) is primarily a potent m-opioid receptor agonist

with oral immediate-release (IR) and extended-release (ER) formulations approved in the United
States in 2006. The oral oxymorphone formulations are roughly three times more potent than oral
morphine. It is more lipophilic than morphine and, thus, may more easily cross the blood-brain
barrier because it differs from morphine having a ketone-group substituent at the C-6 position.
Oxymorphone IR is indicated for the relief of moderate—to severe pain, while oxymorphone ER is
indicated for persistent pain. Initial doses (opioid-naïve) are 10–20 mg every 4–6 hours (IR) and
5 mg every 12 hours (ER).Oxymorphone was found not to have any clinically significant cyto-
chrome (CYP)3A4, CPY2C9, or CYP2D6 interactions, thus limiting its potential for causing some
of the more common drug–drug interactions via the CYP450 system.The common adverse effects
of oxymorphone are consistent with those commonly seen with other opioid, including nausea/
vomiting, constipation, pruritis, pyrexia, somnolence, and sedation.

Key Words. Opioids; Oxymorphone; Metabolism Pharmacokinetic; Pharmacodynamic Excretion;

Absorption

Introduction Oxymorphone ER is a new sustained-release

O xymorphone (14-hyroxydihydromor-
phinone) is a semisynthetic m-opioid recep-
tor agonist, which entered the United States
marketplace in 1959, available at that time in only
parenteral and rectal formulations. In June 2006,
oral oxymorphone immediate-release (IR) and
oxymorphone extended-release (ER) tablets were
approved by the Food and Drug Administration
[1,2]. Oxymorphone hydrochloride has a more
rapid onset of action and several times the analge-
sic potency of its parent compound morphine
when administered parenterally [3,4].
Reprint requests to: Howard S. Smith, MD, Anesthesiology
and Academic Director of Pain Management, Albany
Medical College, Department of Anesthesiology, 47 New
Scotland Avenue, MC-131, Albany, NY 12208, USA.
Tel: 518-262-4461; Fax: 518-262-2671; E-mail: smithh@
mail.amc.edu.
tablet formulation of oxymorphone hydrochlo-
ride developed to provide 12 hours of sustained
analgesia [5]. The ER matrix, TIMERx (Penwest
Pharmaceuticals Co., Danbury, CT), alters and
delays drug dissolution and absorption from the
gastrointestinal tract, resulting in a completely dif-
ferent pharmacokinetic profile relative to the IR
drug formulations. Drug release from the ER
matrix is controlled by the rate of penetration of
water into a hydrophilic matrix (consisting of
xanthan and locust bean gum) and the subsequent
expansion of the gel coating. Linearity of pharma-
cokinetic parameters contributes to a predictable
dose. Multiple clinical trials have been performed
evaluating the safety and/or efficacy of oxymor-
phone ER in the management of moderate—to
severe cancer and noncancer persistent pain
[6–15].
Oxymorphone is a pyridine-ring unsubstituted
pyridomorphinan (Figure 1) [16]. It differs from

© American Academy of Pain Medicine 1526-2375/09/$15.00/S3 S3–S10 doi:10.1111/j.1526-4637.2009.00594.x

S4
CH3
N CH2
HO • HCl
CH2
OH O O
Figure 1 Chemical structure of oxymorphone
hydrochloride.
morphine by having a ketone-group substituent at
the C-6 position and saturation of the 7,8 double
bond. The ketone-group substituent renders the
molecule more lipid-soluble and makes oxymor-
phone much more structurally related to hydro-
morphone. Oxymorphone is available in the freely
water-soluble hydrochloride (HCL) salt form. It
exists as a white or slightly off-white, odorless
powder. The HCL salt form is sparingly soluble in
alcohol and ether. The molecular weight of the
salt form is 337.80. The octanol/water partition
coefficient is 0.98 (at 37°C and pH 7.4) [1,2,17].
Oxymorphone is soluble in water, less soluble in
alcohol, and more lipid soluble than morphine or
oxycodone [18,19]. The increased lipophilicity is
due to the structural differences between oxymor-
phone and morphine; specifically, oxymorphone is
a 6-keto-opioid with the ketone group substituted
for a hydroxyl group at the C-6 position. Opioids
with greater lipid solubility may cross the blood-
brain barrier more readily than less lipophilic
opioids [20].
Oxymorphone is 10% to 12% plasma protein-
bound [1,2] (See Table 1). Mean oxymorphone
volume of distribution is approximately 3 L/kg
[17,21]. Oxymorphone is not extensively protein-
bound compared with other opioids [22,23], which
may be advantageous in patients who are hypoal-
buminemic and in those receiving polypharmacy
with other drugs that are highly protein bound.
Clinical trials assessing an advantage in patients
with low serum albumin have not yet been con-
ducted. Unlike morphine, oxymorphone does not
promote histamine release in human skin mast
cells [24,25].
Oral oxymorphone is more potent (per mg)
than oral oxycodone or oral morphine with esti-
mated initial oral conversion ratios for morphine
Smith
and oxycodone to oxymorphone (which do not
take into account incomplete opioid cross-
tolerance) of 3:1 and 2:1, respectively [24,26].
These conversion ratios are only estimates, neces-
sitating individualized titration with close moni-
toring of each patient until a dose providing
acceptable efficacy and tolerability is identified.
The analgesic effects of opioids are mediated
predominantly via m-opioid receptors and may be
modulated by d-opioid receptors (e.g., agonism at
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d-opioid receptors may potentiate m-mediated
analgesia and may slow the development of toler-
ance). The binding affinities of oxymorphone to
these two receptors exceed those of morphine by
2.5-fold and 3.4-fold, respectively [16,27]. Unlike
oxycodone, which has some k-opioid receptor
agonism, oxymorphone has very little binding and
no clinically significant effects at the k-opioid
receptor [28].
Oxymorphone undergoes extensive hepatic
metabolism via conjugation with glucuronic acid
to produce its primary metabolite, oxymorphone-
3-glucuronide. Uridine diphosphate glucuronyl
transferase subtype B27 catalyzes glucuronidation
at the 3 position [29]. To a lesser extent, it also
undergoes reduction of the 6 ketone group to
form 6-hydroxy (OH)-oxymorphone. Although
6-OH-oxymorphone likely has some analgesic
Table 1 Oral oxymorphone hydrochloride
pharmacokinetic data
Absolute oral
availability 10%
Tmax Oxymorphone IR—1/2 h
Oxymorphone ER—2–3 h
Time to Oxymorphone IR—after 3 days
steady state Oxymorphone ER—after 3 days
Protein binding 10–12%
Absorption Oxymorphone IR—1/2 life-7–10 h
Oxymorphone ER—1/2 life-9–12 h
Food can ↑ plasma conc. by 50%
Metabolism • 6-hydroxyoxymorphone
AUC 70% of parent compound flowing a
single dose and equivalent of steady state.
• Oxymorphone-3-glucuronide
The mean plasma AUC of oxymorphone-3-
glucuronide is 90-fold higher than is the
AUC of the parent compound after a single
dose.
• No clinically significant drug–drug
interactions.
Excretion <2% excreted unchanged in urine
<1% excreted as 6-hydroxyoxymorphone
Co-ingestion Should be avoided—oxymorphone ER serum
of Alcohol levels can ↑ unpredictably (up to 270% in
some patients)
IR = immediate release; ER = extended release; AUC = area under the
concentration-time curve.
Clinical Pharmacology of Oxymorphone
bioactivity and the pharmacologic activity of
oxymorphone-3-glucuronide has not been fully
evaluated [1,30], oxymorphone has been consid-
ered to have relatively clinically inert metabolites.
No clinically significant cytochrome (CYP)3A4,
CYP2C9, or CYP2D6 mediated drug–drug inter-
actions have been noted with oxymorphone, and,
thus, there is minimal potential for clinically sig-
nificant drug–drug interactions [31]. Less than 2%
of the parent compound is recovered in the urine
in unchanged form [32]. Upon absorption, drug
concentrations may be graphed (ordinate) against
time (abscissa). The peak drug concentration
(Cmax) is reached at Tmax and the trough concen-
tration is Cmin. The area under the concentration-
time curve (AUC) is a measure of drug exposure
that can be calculated (as the sum of trapezoids).
At steady state, the AUC for 6-OH-oxymorphone
approximates oxymorphone. For oxymorphone-3-
glucuronide, 33% to 38% is excreted in the urine
in patients with normal renal and hepatic function,
and the AUC is 90-fold higher than oxymorphone
(Endo Pharmaceuticals Inc., Chadds Ford, PA). In
an early pharmacokinetic study of oxymorphone
administered as a 10 mg IR tablet, a 10 mg oral
solution, or a 1 mg intravenous bolus, absolute
oral bioavailability was determined to be approxi-
mately 11%, a value that is in the ballpark with
that estimated for morphine and other 3-OH
opioids (Endo Pharmaceuticals Inc.). There was a
large difference in terminal elimination half-life
( t 12 ) for oral vs intravenous administration of
oxymorphone, 15.2 ⫾ 21.0 vs 2.0 ⫾ 0.6 hours
(mean ⫾ standard deviation [SD]), most likely
attributable to enterophepatic recirculation fol-
lowing oral administration. Animal studies of
6-OH-oxymorphone have shown analgesic effects
similar to oxymorphone (Endo Pharmaceuticals
Inc.). In this respect, oxymorphone may be similar
to morphine because substitution at the 6 position
appears to produce active metabolites with both
opioids. At present, it is not clear if substitution
at the 3 position also produces parallel effects.
Although the 3-glucuronide metabolite of mor-
phine is devoid of clinically meaningful analgesic
activity [33–35], the analgesic activity or inactivity
of oxymorphone-3-glucuronide has not been
established.
Pharmacokinetics
The bioavailability of oral oxymorphone is
approximately 10% [24,26] following extensive
first-pass hepatic metabolism, primarily via phase
II glucuronidation. To a lesser extent, oxymor-
S5
phone is also metabolized via hydroxylation
to 6-hydroxy-oxymorphone (OH-6-G), but this
reaction does not involve any known cytochrome
P450 system enzyme.
In pharmacokinetic studies, a high-fat meal
increased the Cmax of oxymorphone IR and ER by
38% [26] and 50% [24], respectively. The AUC
for oxymorphone IR also increased 38% but
remained relatively unchanged for oxymorphone
ER [24]. For these reasons, the package insert pru-
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dently states that oxymorphone should be taken
on an empty stomach—at least 1 hour before or 2
hours after a meal. During the clinical studies,
however, participants were not given direction on
when to take oxymorphone ER relative to meals,
and it appears that regardless of whether it is
administered preprandially vs postprandially, oxy-
morphone absorption has no clinically meaningful
differences [36]. Oxymorphone IR and ER each
provide predictable, dose-proportional plasma
concentrations across their entire dose ranges.
Gender does not appear to influence oxymor-
phone pharmacokinetics [1,2]. Patient gender does
not affect oxymorphone ER concentrations after
adjusting for body weight (gender effects with oxy-
morphone IR have not been studied).
Oxymorphone IR
In single- and multiple-dose studies of oxymor-
phone IR [37], absorption is rapid and the time of
maximum plasma concentration (tmax) was 0.5
hours following oral administration. Steady-state
concentrations (CSS) were achieved in 3 days. The
observed tmax is consistent with the rapid onset of
analgesia at 0.5–0.75 hours observed in clinical
studies with single or multiple doses of oxymor-
phone IR 20–30 mg [38,39]. The elimination half-
life (t1/2b) for a single dose of oxymorphone IR
ranges from approximately 7.2 hours for the 5-mg
dose to 9.4 hours for the 20-mg dose. The rapid
absorption and prolonged t1/2b of oxymorphone
IR compare favorably with those of morphine
and oxycodone IR formulations [40–42]. The
maximum observed concentration (Cmax) and
AUC after a single oxymorphone IR dose at CSS
increases dose proportionally with increasing
doses from 5 to -20 mg.
In a randomized crossover of oxymorphone IR
in healthy volunteers, the single-dose and steady-
state pharmacokinetic profiles of oxymorphone
were linear and dose-proportional across a dose
range of 5–20 mg [37]. Oxymorphone IR was not
associated with any clinically significant effects on
laboratory or other safety variables [37].
S6
After single-dose administration and at steady
state, the increases in mean AUC• and AUCSS,
respectively, and Cmax for oxymorphone followed a
twofold progression between doses. Mean oxy-
morphone AUCSS was 4.63, 10.19, and 21.10 fol-
lowing administration of oxymorphone IR 5, 10,
and 20 mg every 6 hours, respectively [37]. These
data provide important information for the clini-
cian in that an increase in dose in the clinical
setting will reliably produce predictable increases
in the plasma levels of oxymorphone. This may
be especially important for opioids. Individual
responses to opioids are variable, and clinicians
frequently must titrate opioids across a large mil-
ligram dose range to find a dosage that provides
adequate analgesia with acceptable opioid-related
adverse events. Formulations that provide pre-
dictable increases in drug concentrations with
increasing doses provide less uncertainty when
empirically determining a patient’s optimum dose.
Adams and Ahdieh pointed out that a limitation of
their study is that the plasma concentrations for
6-OH-oxymorphone at the 5 and 10 mg doses
were below the lower limit of quantification in
some samples, which may account for some devia-
tion in linearity that was observed with the 6-OH
metabolite [37]. In support of this interpretation,
plasma concentrations for 6-OH-oxymorphone
were higher and, therefore, more reliably ascer-
tained at steady state than during single-dose
administration. The CSS of 6-OH-oxymorphone
exhibited less deviation from a linear dose re-
sponse (approximately 10%) than during single-
dose administration (approximately 20%) [37].
An important pharmacokinetic parameter for
an IR analgesic is a short time to peak plasma
concentration. Adams and Ahdieh demonstrated
that the median time to Cmax (tmax) was 0.5 hours
across all doses of oxymorphone IR [37]. This
value compares favorably with IR tablets of mor-
phine and oxycodone, for which mean tmax has
been reported to be 1.2 and 1.5 hours, respectively
[40,41]. Although the tmax of oxymorphone pre-
dicts a more rapid onset of analgesia, the t 12 of
oxymorphone IR was measured at 7.25–9.43
hours, considerably longer than the 3- to 5.7-hour
values reported for oxycodone [41,42]. However,
active-controlled clinical trials will be required to
determine whether the shorter tmax and longer t 12
of oxymorphone IR translates into more rapid and
sustained analgesia compared with other short-
acting opioids [37].
Urinary excretion was evaluated in six healthy
volunteers after administration of a single 10-mg
Smith
oxymorphone IR oral dose. Over the subsequent
120 hours, the mean percentage of the dose
eliminated was as follows: free oxymorphone,
1.9%; conjugated oxymorphone, 44.1%; free
6 b-OH-oxymorphone, 0.3%; conjugated 6-OH-
oxymorphone, 2.6%, free 6 a-OH-oxymorphone,
none; and conjugated 6 a-OH-oxymorphone,
0.1%. Thus, 49% of the dose was eliminated in the
urine over 120 hours, with 82% of the ultimate
amount eliminated in the urine being eliminated
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during the initial 24 hours. The mean ⫾ standard
error of the mean terminal disposition half-life
of unconjugated oxymorphone, calculated using
urinary excretion data, was 8.9 ⫾ 0.4 hour
(Sigma–Minus method) and 7.6 ⫾ 2.0 hours
(urinary excretion rate plots) [32]. Oxymorphone
IR (which comes in two strengths [5 mg, 10 mg])
can be initiated in opioid-naïve patients at starting
doses of 5–10 mg every 4–6 hours depending on
the individual patient and situation.
Oxymorphone ER
The data obtained from Adams and Ahdeih in a
randomized study of oxymorphone ER in healthy
adults show that the pharmacokinetics of the ER
oral formulation and its major metabolites are also
linear and dose-proportional [43]. Furthermore,
all doses were well tolerated, with mild adverse
events typically found with opioids [43].
Single-dose and CSS data and pharmacokinetic
variables (e.g., AUC, AUCSS, Cmax, Cmin, Cavg)
reflecting drug and metabolite concentrations
showed essentially linear increases of oxymor-
phone and its metabolites (6-OH-OXM and
OXM-3-G) as the dose of oxymorphone ER was
incrementally doubled across a dose range of
5–40 mg [43]. From single dose to steady state, the
plasma concentrations of all three moieties accu-
mulate to a clinically relevant degree (oxymor-
phone 2.1- to 3.4-fold, 6-hydroxy metabolite
4.1- to 26.3-fold, and 3-glucuronide metabolite
1.8- to 2.1-fold) [1,2,17,43]. Calculated on the
basis of degree of accumulation after 40 mg every
12 hours, the mean ⫾ SD “effective” terminal dis-
position half-lives of oxymorphone, the 6-hydroxy
metabolite, and the 3-glucuronide metabolite
are 13.1 ⫾ 4.5 hours, 29.8 ⫾ 9.6 hours, and
10.6 ⫾ 2.6 hours, respectively [17,43]. The fluc-
tuation index values of less than one for all three
moieties at all oxymorphone dosage levels verify
the low degree of fluctuation of plasma concentra-
tions over the 12-hour dosing interval of oxymor-
phone ER at steady state [17,43]. The absence
Clinical Pharmacology of Oxymorphone
of statistically significant differences in dose-
normalized natural logarithm (1n)-AUC,
(1n)-AUCSS, or (1n)-Cmax confirms that the phar-
macokinetics of oxymorphone, 6-OH-OXM, and
OXM-3-G are dose-proportional after single-dose
administration and at steady state. The absence of
meaningful differences in oxymorphone clearance
across the four-dose levels is also consistent with a
linear pharmacokinetic profile [43].
Although opioid dosages typically are titrated to
provide meaningful pain relief while minimizing
adverse events, linear pharmacokinetics provide
confidence to clinicians that doubling a patient’s
dose will predictably double the plasma drug con-
centrations and the patient’s extent of exposure
[43].
Absorption is rapid, even with the ER product,
which has a time-to-peak plasma concentration
ranging from 2 to 4 hours after single- and
multiple-dose administration.
The tmax of oxymorphone ER ranges from 2.5 to
4.0 hours after a single dose [43]. CSS is achieved
following 3 days of 12-hour daily dosing. At CSS,
the tmax ranges from 1.5–3.5 hours. The 9- to
11-hour elimination t1/2b of oxymorphone ER
is longer that that observed with morphine-
controlled release or oxycodone [22,23]. As with
the IR formulation, single-dose and steady-state
Cmax and AUC increase predictability and dose
proportionally across the entire 5- to 40-mg dose
range.
The manufacturer states that oxymorphone ER
tablets, such as other ER oral opioids, should be
swallowed whole (i.e., not broken, chewed, dis-
solved, or crushed) to avoid rapid release and
absorption of a potentially fatal dose [1,2]. Patients
should also be cautioned against ingesting alcohol,
including any medication that contains alcohol,
concurrently with oxymorphone to avoid in-
creased concentrations. Oxymorphone ER (which
comes in seven strengths: 5 mg, 7.5 mg, 10 mg,
15 mg, 20 mg, 30 mg, 40 mg), can be initiated in
opioid-naïve patients at a starting dose of 5 mg
every 12 hours.
Oxymorphone and the CYP450 Systems
Oxymorphone is metabolized hepatically, princi-
pally by phase II metabolism involving conjuga-
tion with glucuronic acid, with only 1–2% of
unchanged drug excreted by the kidney. The
primary metabolites are oxymorphone-3-
glucuronide and oxymorphone-6-G. Unlike
oxycodone, fentanyl, and most other opioids, oxy-
morphone is not metabolized by the CYP pathway
S7
and does not inhibit or induce CYP enzymes
[31,44], resulting in a low interaction potential
with drugs that are CYP substrates and CYP
inhibitors or inducers.
Unpublished in vitro data suggest that oxymor-
phone is unlikely to react with any members of the
cytochrome P450 (CYP450) family of isoenzymes
at normal analgesic concentrations while produc-
ing only low levels of change (a 1.2- to 2-fold
induction) in the activity of 2 CYP450 family
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isoforms—CYP2C9 and CYP3A4—at supraphar-
macologic concentrations (plasma concentrations
300–1,000 times those expected in vivo) [45].
Adams and colleagues examined the effects of
ER oxymorphone on CYP2C9 or CYP3A4 meta-
bolic activities in healthy subjects by performing
two 14-day, randomized, open-label, parallel-
group studies [31]. On days -1, 7, and 14, subjects
received either a CYP2C9 probe (tolbutamide
500 mg) or CYP3A4 probes (midazolam and [14C
N-methyl]-erythromycin for the erythromycin
breath test) [31]. Subjects were randomized to five
groups: high-dose oxymorphone ER (3 20 mg
q12h) + naltrexone (50 mg q24h); low-dose oxy-
morphone ER (10–20 mg q12h [10 mg q12h days
1–3 and 20 mg q12h days 4–14]); rifampin
(2,300 mg q24h), an inducer of CYP2C9 and
CYP3A4 activities; naltrexone (50 mg q24h); or
CYP probes alone (controls). Probe metabolism
was significantly altered by rifampin on days 7 and
14 (P < 0.05), whereas probe metabolism was not
significantly affected by low-dose oxymorphone
ER or by high-dose oxymorphone ER plus
naltrexone. Adams et al. concluded that oxymor-
phone ER exhibits a minimal potential for causing
metabolic drug–drug interactions mediated by
CYP2C9 or CYP3A4 [31].
Oxymorphone in Special Populations
The safety and efficacy of oxymorphone in
patients less than 18 years of age have not been
established. Oxymorphone is listed as Pregnancy
Category C, as studies have not yet established
possible adverse effects on fetal development.
Additionally, it is unknown whether oxymorphone
passes into breast milk [1,2].
In the elderly (ⱖ65 years old), plasma oxymor-
phone, 3-hydroxy metabolite, and 3-glucuronide
metabolite concentrations were a mean of 40%
higher than those in younger (18–40 years old)
subjects [1,2]. On average, oxymorphone AUC
and Cmax were increased 1.4- and 1.5-fold, respec-
tively, in the elderly group. Elderly patients should
S8
receive smaller dosages initially, and dose titration
should proceed slowly with caution. Adverse
effects seen more often with oxymorphone in the
elderly include dizziness, somnolence, confusion,
and nausea [1,2].
There may be significant effects of hepatic
disease on oxymorphone pharmacokinetics. The
bioavailability of oxymorphone was increased by
means of 1.6-fold and 3.7-fold in subjects with
mild (Child-Pugh class A) and moderate (Child-
Pugh class B) hepatic impairment, respectively;
compared with healthy controls. In the one subject
with severe hepatic impairment (Child-Pugh class
C), the bioavailability was increased by 12.2-fold
[1,2,17]. No dosage adjustment is needed in mild
hepatic impairment but starting at a low dose and
titrating upwards slowly is prudent. However,
oxymorphone is relatively contraindicated in
patients with moderately severe to severe hepatic
dysfunction.
Oxymorphone bioavailability was increased by
means of 26%, 57%, and 65% in patients with
creatinine clearance values of 51–80 mL/min,
30–50 mL/min, and below 30 mL/min, respec-
tively, compared with healthy controls [1,2].
There are virtually no data regarding the dialyz-
ability of oxymorphone. A single case report has
provided pre- and posthemodialysis plasma con-
centrations obtained at the midpoint of a 4-hour
hemodialysis session. Oxymorphone appeared to
be removed by hemodialysis, with a predialysis
concentration of 4.98 ng/mL and postdialysis
concentration of 2.36 ng/mL. However, further
studies are needed before the dialyzability of
oxymorphone can be completely characterized
[17,46].
Oxymorphone in Urine Drug Testing
Oxymorphone is not metabolized to other avail-
able opioids or their metabolites; hence, confirma-
tory assays using liquid chromatography/mass
spectroscopy (the current gold standard for urine
toxicology screening) performed in oxymorphone-
treated patients will reveal almost exclusively
oxymorphone. During the manufacture of oxy-
morphone, a small fraction (1%) of oxycodone is
present as a manufacturing process contaminant,
but this would result in merely trace amounts of
oxycodone in the urine. McDonough et al. as well
as Cone et al. have detected hydromorphone in
the urine of patients who are administering signifi-
cant doses of morphine [47,48]. However, Cone
and colleagues concluded that oxymorphone is not
a metabolite of morphine or hydromorphone and
Smith
so was not detected in any urine samples analyzed
from patients who administered morphine or
hydromorphone [47]. Thus, a patient who is
taking only oxymorphone ER and/or oxymor-
phone IR for chronic pain (without any drugs)
should have a urine in which only oxymorphone is
detected.
Summary
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Oxymorphone is a semi-synthetic opioid, which,
like morphine, is predominantly a mopioid recep-
tor agonist. Oxymorphone is a World Health
Organization Step 3 opioid for moderate to severe
pain and has been utilized for cancer and noncan-
cer pain. It is more potent and more lipophilic
than morphine and, thus, may more easily cross
the blood-brain barrier because it differs from
morphine having a ketone-group substituent at
the C-6 position. It is currently available in the
United States in an oral IR formulation with every
4- to 6-hour dosing and an ER formulation with
every 12-hour dosing. Oxymorphone ER yields a
reasonably stable plateau concentration over much
of the 12-hour period.
Oxymorphone has no reported CYP450 system
interactions and so few drug–drug interactions for
patient on multiple medications. The common
adverse effects of oxymorphone are consistent
with those commonly seen with other opioids,
including nausea/vomiting, constipation, pruritis,
pyrexia, somnolence, and sedation [1,2].
Disclosure
There were no grants or other forms of support for this
project.
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