United States - English - NLM (National Library of Medicine)
ISOSORBIDE MONONITRATE- isosorbide mononitrate tablet, extended release
Unit Dose Services
Isosorbide Mononitrate Extended-release Tablets, USP Rx only
Isosorbide Mononitrate (ISMN), an organic nitrate and the major biologically active metabolite of
isosorbide dinitrate (ISDN), is a vasodilator with effects on both arteries and veins.
Each Isosorbide mononitrate extended-release tablet, USP, for oral administration contains either 30 mg
or 60 mg of ISMN.
ISMN 30 mg tablets, USP containes the following inactive ingredients: colloidal silicon dioxide,
compressible sugar, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate.
ISMN 60 mg tablets, USP contains the following inactive ingredients: colloidal silicon dioxide,
compressible sugar, hydroxypropyl methylcellulose, yellow iron oxide, lactose monohydrate,
The molecular formula of ISMN is C H NO and the molecular weight is 191.14. The chemical name
for ISMN is 1,4:3,6-dianhydro-D-glucitol 5-nitrate; the compound has the following structural formula:
ISMN is a white, crystalline, odorless compound which is stable in air and in solution, has a melting
point of about 90°C, and an optical rotation of +144° (2% in water, 20°C). ISMN is freely soluble in
water, ethanol, methanol, chloroform, ethyl acetate and dichloromethane.
Mechanism of Action
This product is an oral extended-release formulation of ISMN, the major active metabolite of
isosorbide dinitrate; most of the clinical activity of the dinitrate is attributable to the mononitrate.
The principal pharmacological action of ISMN and all organic nitrates in general is relaxation of
vascular smooth muscle, producing dilatation of peripheral arteries and veins, especially the latter.
Dilatation of the veins promotes peripheral pooling of blood, decreases venous return to the heart,
thereby reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure
(preload). Arteriolar relaxation reduces systemic vascular resistance, and systolic arterial pressure and
mean arterial pressure (afterload). Dilatation of the coronary arteries also occurs. The relative
importance of preload reduction, afterload reduction and coronary dilatation remains undefined.
Dosing regimens for most chronically used drugs are designed to provide plasma concentrations that
are continuously greater than a minimally effective concentration. This strategy is inappropriate for
organic nitrates. Several well-controlled clinical trials have used exercise testing to assess the
antianginal efficacy of continuously delivered nitrates. In the large majority of these trials, active agents
were indistinguishable from placebo after 24 hours (or less) of continuous therapy. Attempts to
overcome tolerance by dose escalation, even to doses far in excess of those used acutely, have
consistently failed. Only after nitrates have been absent from the body for several hours has their
antianginal efficacy been restored.
Isosorbide mononitrate extended-release tablets during long-term use over 42 days dosed at 120 mg
once daily continued to improve exercise performance at 4 hours and at 12 hours after dosing but their
effects (although better than placebo) are less than or at best equal to the effects of the first dose of 60
Pharmacokinetics and Metabolism:
After oral administration of ISMN as a solution or immediate-release tablets, maximum plasma
concentrations of ISMN are achieved in 30 to 60 minutes, with an absolute bioavailability of
approximately 100%. After intravenous administration, ISMN is distributed into total body water in
about 9 minutes with a volume of distribution of approximately 0.6 to 0.7 L/kg. ISMN is approximately
5% bound to human plasma proteins and is distributed into blood cells and saliva. ISMN is primarily
metabolized by the liver, but unlike oral isosorbide dinitrate, it is not subject to first-pass metabolism.
ISMN is cleared by denitration to isosorbide and glucuronidation as the mononitrate, with 96% of the
administered dose excreted in the urine within 5 days and only about 1% eliminated in the feces. At least
six different compounds have been detected in urine, with about 2% of the dose excreted as the
unchanged drug and at least five metabolites. The metabolites are not pharmacologically active. Renal
clearance accounts for only about 4% of total body clearance. The mean plasma elimination half-life of
ISMN is approximately 5 hours.
The disposition of ISMN in patients with various degrees of renal insufficiency, liver cirrhosis, or
cardiac dysfunction was evaluated and found to be similar to that observed in healthy subjects. The
elimination half-life of ISMN was not prolonged, and there was no drug accumulation in patients with
chronic renal failure after multiple oral dosing.
The pharmacokinetics and/or bioavailability of Isosorbide mononitrate extended-release tablets have
been studied in both normal volunteers and patients following single-and multiple-dose administration.
Data from these studies suggest that the pharmacokinetics of ISMN administered as Isosorbide
mononitrate extended-release tablets are similar between normal healthy volunteers and patients with
angina pectoris. In single and multiple-dose studies, the pharmacokinetics of ISMN were dose
proportional between 30 mg and 240 mg.
In a multiple - dose study, the effect of age on the pharmacokinetic profile of Isosorbide mononitrate
extended-release 60 mg and 120 mg (2 x 60 mg) tablets was evaluated in subjects ≥ 45 years. The
results of that study indicate that there are no significant differences in any of the pharmacokinetic
variables of ISMN between elderly (≥65 years) and younger individuals (45 to 64 years) for the ISMN
extended-release 60 mg dose. The administration of Isosorbide mononitrate extended-release tablets
120 mg (2 x 60 mg) tablets every 24 hours for 7 days) produced a dose-proportional increase in Cmax
and AUC, without changes in Tmax or the terminal half-life. The older group (65 to 74 years) showed
30% lower apparent oral clearance (CI/F) following the higher dose, i.e., 120 mg, compared to the
younger group (45 to 64 years); CI/F was not different between the two groups following the 60 mg
regimen. While CI/F was independent of dose in the younger group, the older group showed slightly
lower CI/F following the 120 mg regimen compared to the 60 mg regimen. Differences between the
two age groups, however, were not statistically significant. In the same study, females showed a slight
(15%) reduction in clearance when the dose was increased. Females showed higher AUCs and Cmax
compared to males, but these differences were accounted for by differences in body weight between
the two groups. When the data were analyzed using age as a variable, the results indicated that there
were no significant differences in any of the pharmacokinetic variables of ISMN between older (≥65
years) and younger individuals (45 to 64 years). The results of this study, however, should be viewed
with caution due to the small numbers of subjects in each age subgroup and consequently the lack of
sufficient statistical power.
The following table summarizes key pharmacokinetic parameters of Isosorbide Mononitrate (ISMN)
after single- and multiple-dose administration of ISMN as an oral solution or Isosorbide mononitrate
release tablets 60 mg
release tablets 60 mg
release tablets 120 mg
424 to 541
557 to 572
1151 to 1180
3.1 to 4.5
2.9 to 4.2
3.1 to 3.2
5990 to 7452
6625 to 7555
14241 to 16800
6.3 to 6.6
6.2 to 6.3
6.2 to 6.4
151 to 187
132 to 151
119 to 140
Food Effects: The influence of food on the bioavailability of ISMN after single-dose administration of
Isosorbide mononitrate extended-release tablets 60 mg was evaluated in three different studies
involving either a "light" breakfast or a high-calorie, high-fat breakfast. Results of these studies
indicate that concomitant food intake may decrease the rate (increase in Tmax) but not the extent (AUC)
of absorption of ISMN.
Controlled trials with Isosorbide mononitrate extended-release tablets have demonstrated antianginal
activity following acute and chronic dosing. Administration of Isosorbide mononitrate extended-release
tablets once daily, taken early in the morning on arising, provided at least 12 hours of antianginal
In a placebo-control parallel study, 30 mg, 60 mg, 120 mg, and 240 mg of Isosorbide mononitrate
extended-release tablets were administered once daily for up to 6 weeks. Prior to randomization, all
patients completed a 1-to 3-week single-blind placebo phase to demonstrate nitrate responsiveness and
total exercise treadmill time reproducibility. Exercise tolerance tests using the Bruce Protocol were
conducted prior to and at 4 and 12 hours after the morning dose on days 1, 7, 14, 28 and 42 of the
double-blind period. Isosorbide mononitrate extended-release tablets 30 mg and 60 mg (only doses
evaluated acutely) demonstrated a significant increase from baseline in total treadmill time relative to
placebo at 4 and 12 hours after the administration of the first dose. At day 42, the 120 mg and 240 mg
dose of Isosorbide mononitrate extended-release tablets demonstrated a significant increase in total
treadmill time at 4 and 12 hours post dosing, but by day 42 the 30 mg and 60 mg doses no longer were
differentiable from placebo. Throughout chronic dosing rebound was not observed in any Isosorbide
mononitrate extended-release tablets treatment group.
Pooled data from two other trials, comparing Isosorbide mononitrate extended-release tablets 60 mg
once daily, isosorbide dinitrate 30 mg QID, and placebo QID in patients with chronic stable angina
using a randomized, double-blind, three-way crossover design found statistically significant increases
in exercise tolerance times for Isosorbide mononitrate extended-release tablets compared to placebo at
hours 4, 8 and 12 and to isosorbide dinitrate at hour 4. The increases in exercise tolerance on day 14,
although statistically significant compared to placebo, were about half of that seen on day 1 of the trial.
INDICATIONS AND USAGE
Isosorbide mononitrate extended-release tablets, USP are indicated for the prevention of angina
pectoris due to coronary artery disease. The onset of action of oral ISMN is not sufficiently rapid for
this product to be useful in aborting an acute anginal episode.
Isosorbide mononitrate extended-release tablets are contraindicated in patients who have shown
hypersensitivity or idiosyncratic reactions to other nitrates or nitrites.
Amplification of the vasodilatory effects of Isosorbide mononitrate extended-release tablets by
sildenafil can result in severe hypotension. The time course and dose dependence of this
interaction have not been studied. Appropriate supportive care has not been studied, but it seems
reasonable to treat this as a nitrate overdose, with elevation of the extremities and with central
The benefits of ISMN in patients with acute myocardial infarction or congestive heart failure have not
been established; because the effects of ISMN are difficult to terminate rapidly, this drug is not
recommended in these settings. If ISMN is used in these conditions, careful clinical or hemodynamic
monitoring must be used to avoid the hazards of hypotension and tachycardia.
Severe hypotension, particularly with upright posture, may occur with even small doses of ISMN. This
drug should therefore be used with caution in patients who may be volume depleted or who, for
whatever reason, are already hypotensive. Hypotension induced by ISMN may be accompanied by
paradoxical bradycardia and increased angina pectoris.
Nitrate therapy may aggravate the angina caused by hypertrophic cardiomyopathy
In industrial workers who have had long term exposure to unknown (presumably high) doses of organic
nitrates, tolerance clearly occurs. Chest pain, acute myocardial infarction, and even sudden death have
occurred during temporary withdrawal of nitrates from these workers, demonstrating the existence of
true physical dependence. The importance of these observations to the routine, clinical use of oral
ISMN is not known.
Information for Patients
Patients should be told that the antianginal efficacy of Isosorbide mononitrate extended-release tablets
can be maintained by carefully following the prescribed schedule of dosing. For most patients, this can
be accomplished by taking the dose on arising.
As with other nitrates, daily headaches sometimes accompany treatment with ISMN. In patients who get
these headaches, the headaches are a marker of the activity of the drug. Patients should resist the
temptation to avoid headaches by altering the schedule of their treatment with ISMN, since loss of
headache may be associated with simultaneous loss of antianginal efficacy. Aspirin or acetaminophen
often successfully relieves ISMN induced headaches with no deleterious effect on ISMN’s antianginal
efficacy. Treatment with ISMN may be associated with light-headedness on standing, especially just
after rising from a recumbent or seated position. This effect may be more frequent in patients who have
also consumed alcohol.
The vasodilating effects of ISMN may be additive with those of other vasodilators. Alcohol, in
particular, has been found to exhibit additive effects of this variety. Marked symptomatic orthostatic
hypotension has been reported when calcium channel blockers and organic nitrates were used in
Dose adjustments of either class of agents may be necessary.
DRUG / LABORATORY TEST INTERACTIONS
Nitrates and nitrites may interfere with the Zlatkis-Zak color reaction, causing falsely low readings in
serum cholesterol determinations.
Carcinogenesis, Mutagenesis, Impairment of Fertility
No evidence of carcinogenicity was observed in rats exposed to Isosorbide Mononitrate (ISMN) in
their diets at doses of up to 900 mg/kg/day for the first 6 months and 500 mg/kg/day for the remaining
duration of a study in which males were dosed for up to 121 weeks and females were dosed for up to
137 weeks. No evidence of carcinogenicity was observed in mice exposed to isosorbide mononitrate in
their diets for up to 104 weeks at doses of up to 900 mg/kg/day.
ISMN did not produce gene mutations (Ames test, mouse lymphoma test) or chromosome aberrations
(human lymphocyte and mouse micronucleus tests) at biologically relevant concentrations. No effects
on fertility were observed in a study in which male and female rats were administered doses of up to
750 mg/kg/day beginning, in males, 9 weeks prior to mating, and in females, 2 weeks prior to mating.
Pregnancy Category B
In studies designed to detect effects of ISMN on embryo-fetal development, doses of up to 240 or 248
mg/kg/day, administered to pregnant rats and rabbits, were unassociated with evidence of such effects.
These animal doses are about 100 times the maximum recommended human dose (120 mg in a 50 kg
woman) when comparison is based on body weight; when comparison is based on body surface area, the
rat dose is about 17 times the human dose and the rabbit dose is about 38 times the human dose. There
are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction
studies are not always predictive of human response, Isosorbide mononitrate extended-release tablets
should be used during pregnancy only if clearly needed.
Neonatal survival and development and incidence of stillbirths were adversely affected when pregnant
rats were administered oral doses of 750 (but not 300) mg ISMN/kg/day during late gestation and
lactation. This dose (about 312 times the human dose when comparison is based on body weight and 54
times the human dose when comparison is based on body surface area) was associated with decreases
in maternal weight gain and motor activity and evidence of impaired lactation.
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human
milk, caution should be exercised when ISMN is administered to a nursing mother.
The safety and effectiveness of ISMN in pediatric patients have not been established.
Clinical studies of Isosorbide Mononitrate Extended-release Tablets did not include sufficient
information on patients age 65 and over to determine whether they respond differently from younger
patients. Other reported clinical experience for Isosorbide Mononitrate Extended-release Tablets has
not identified differences in response between elderly and younger patients. Clinical experience for
organic nitrates reported in the literature identified a potential for severe hypotension and increased
sensitivity to nitrates in the elderly. In general, dose selection for an elderly patient should be cautious,
usually starting at the low end of the dosing range, reflecting the greater frequency of decreased
hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
Elderly patients may have reduced baroreceptor function and may develop severe orthostatic
hypotension when vasodilators are used. Isosorbide Mononitrate Extended-release Tablets should
therefore be used with caution in elderly patients who may be volume depleted, on multiple medications
or who, for whatever reason, are already hypotensive. Hypotension induced by isosorbide mononitrate
may be accompanied by paradoxical bradycardia and increased angina pectoris.
Elderly patients may be more susceptible to hypotension and may be at greater risk of falling at
therapeutic doses of nitroglycerin.
Nitrate therapy may aggravate the angina caused by hypertrophic cardiomyopathy, particularly in the
The table below shows the frequencies of the adverse events that occurred in >5% of the subjects in
three placebo-controlled North American studies, in which patients in the active treatment arm received
30 mg, 60 mg, 120 mg or 240 mg of ISMN as Isosorbide mononitrate extended-release tablets once
daily. In parentheses, the same table shows the frequencies with which these adverse events were
associated with the discontinuation of treatment. Overall, 8% of the patients who received 30 mg, 60
mg, 120 mg or 240 mg of ISMN in the three placebo-controlled North American studies discontinued
treatment because of adverse events. Most of these discontinued because of headache. Dizziness was
rarely associated with withdrawal from these studies. Since headache appears to be a dose-related
adverse effect and tends to disappear with continued treatment, it is recommended that Isosorbide
mononitrate extended-release tablets treatment be initiated at low doses for several days before being
increased to desired levels.
FREQUENCY AND ADVERSE EVENTS (DISCONTINUED)*
Three controlled North America Studies
*Some individuals discontinued for multiple reasons
** Patients were started on 60 mg and titrated to their final dose
In addition, the three North American trials were pooled with 11 controlled trials conducted in Europe.
Among the 14 controlled trials, a total of 711 patients were randomized to Isosorbide mononitrate
extended-release tablets. When the pooled data were reviewed, headache and dizziness were the only
adverse events that were reported by >5% of patients. Other adverse events, each reported by ≤5% of
exposed patients, and in many cases of uncertain relation to drug treatment, were:
Autonomic Nervous System Disorders: Dry mouth, hot flushes
Body as a Whole: Asthenia, back pain, chest pain, edema, fatigue, fever, flu-like symptoms, malaise,
Cardiovascular Disorders, General: Cardiac failure, hypertension, hypotension.
Central and Peripheral Nervous System Disorders: Dizziness, headache, hypoesthesia, migraine, neuritis,
paresis, paresthesia, ptosis, tremor, vertigo.
Gastrointestinal System Disorders: Abdominal pain, constipation, diarrhea, dyspepsia, flatulence, gastric
ulcer, gastritis, glossitis, hemorrhagic gastric ulcer, hemorrhoids, loose stools, melena, nausea,
Hearing and Vestibular Disorders: Earache, tinnitus, tympanic membrane perforation.
Heart Rate and Rhythm Disorders: Arrhythmia, arrhythmia atrial, atrial fibrillation, bradycardia, bundle
branch block, extrasystole, palpitation, tachycardia, ventricular tachycardia.
Liver and Biliary System Disorders: SGOT increase, SGPT increase.
Metabolic and Nutritional Disorders: Hyperuricemia, hypokalemia.
Musculoskeletal System Disorders: Arthralgia, frozen shoulder, muscle weakness, musculoskeletal pain,
myalgia, myositis,tendon disorder, torticollis.
Myo-, Endo-, Pericardial and Valve Disorders: Angina pectoris aggravated, heart murmur, heart sound
abnormal, myocardial infarction, Q-Wave abnormality.
Platelet, Bleeding and Clotting Disorders: Purpura, thrombocytopenia.
Psychiatric Disorders: Anxiety, concentration impaired, confusion, decreased libido, depression,
impotence, insomnia, nervousness, paroniria, somnolenc
Red Blood Cell Disorder: Hypochromic anemiae.
Reproductive Disorders, Female: Atrophic vaginitis, breast pain.
Resistance Mechanism Disorders: Bacterial infection, moniliasis, viral infection.
Respiratory System Disorders: Bronchitis, bronchospasm, coughing, dyspnea, increased sputum, nasal
congestion, pharyngitis, pneumonia, pulmonary infiltration, rales, rhinitis, sinusitis.
Skin and Appendages Disorders: Acne, hair texture abnormal, increased sweating, pruritus, rash, skin
Urinary System Disorders: Polyuria, renal calculus, urinary tract infection.
Vascular (Extracardiac) Disorders: Flushing, intermittent claudication, leg ulcer, varicose vein.
Vision Disorders: Conjunctivitis, photophobia, vision abnormal.
In addition, the following spontaneous adverse event has been reported during the marketing of
Isosorbide Mononitrate (ISMN): syncope.
The ill effects of ISMN overdose are generally the results of ISMN’s capacity to induce
vasodilatation, venous pooling, reduced cardiac output, and hypotension. These hemodynamic changes
may have protean manifestations, including increased intracranial pressure, with any or all of persistent
throbbing headache, confusion and moderate fever; vertigo; palpitations; visual disturbances; nausea and
vomiting (possibly with colic and even bloody diarrhea); syncope (especially in the upright posture); air
hunger and dyspnea, later followed by reduced ventilatory effort; diaphoresis, with the skin either
flushed or cold and clammy; heart block and bradycardia; paralysis; coma; seizures and death.
Laboratory determinations of serum levels of ISMN and its metabolites are not widely available, and
such determinations have, in any event, no established role in the management of ISMN overdose.
There are no data suggesting what dose of ISMN is likely to be life threatening in humans. In rats and
mice, there is significant lethality at doses of 2000 mg/kg and 3000 mg/kg, respectively. No data are
mice, there is significant lethality at doses of 2000 mg/kg and 3000 mg/kg, respectively. No data are
available to suggest physiological maneuvers (e.g. maneuvers to change the pH of the urine) that might
accelerate elimination of ISMN. In particular, dialysis is known to be ineffective in removing ISMN
from the body. No specific antagonist to the vasodilator effects of ISMN is known, and no intervention
has been subject to controlled study as a therapy of ISMN overdose. Because the hypotension
associated with ISMN overdose is the result of venodilatation and arterial hypovolemia, prudent therapy
in this situation should be directed toward an increase in central fluid volume. Passive elevation of the
patient’s legs may be sufficient, but intravenous infusion of normal saline or similar fluid may also be
The use of epinephrine or other arterial vasoconstrictors in this setting is likely to do more harm than
good. In patients with renal disease or congestive heart failure, therapy resulting in central volume
expansion is not without hazard. Treatment of ISMN overdose in these patients may be subtle and
difficult, and invasive monitoring may be required.
Methemoglobinemia has been reported in patients receiving other organic nitrates, and it probably could
also occur as a side effect of ISMN. Certainly nitrate ions liberated during metabolism of ISMN can
oxidize hemoglobin into methemoglobin. Even in patients totally without cytochrome b5 reductase
activity, however, and even assuming that the nitrate moiety of ISMN is quantitatively applied to
oxidation of hemoglobin, about 2 mg/kg of ISMN should be required before any of these patients
manifest clinically significant (≥10%) methemoglobinemia. In patients with normal reductase function,
significant production of methemoglobin should require even larger doses of ISMN. In one study in
which 36 patients received 2 to 4 weeks of continuous nitroglycerin therapy at 3.1 to 4.4 mg/hr
(equivalent, in total administered dose of nitrate ions, to 7.8 - 11.1 mg of ISMN per hour), the average
methemoglobin level measured was 0.2%; this was comparable to that observed in parallel patients who
Notwithstanding these observations, there are case reports of significant methemoglobinemia in
association with moderate overdoses of organic nitrates. None of the affected patients had been thought
to be unusually susceptible.
Methemoglobin levels are available from most clinical laboratories. The diagnosis should be suspected
in patients who exhibit signs of impaired oxygen delivery despite adequate cardiac output and adequate
arterial pO2. Classically, methemoglobinemic blood is described as chocolate brown, without color
change on exposure to air.
When methemoglobinemia is diagnosed, the treatment of choice is methylene blue, 1 to 2 mg/kg
DOSAGE AND ADMINISTRATION
The recommended starting dose of Isosorbide mononitrate extended-release tablets is 30 mg (given as
1/2 of a 60 mg tablet) or 60 mg (given as a single tablet) once daily. After several days the dosage may
be increased to 120 mg (given as two 60 mg tablets) once daily. Rarely, 240 mg may be required. The
daily dose of Isosorbide mononitrate extended-release tablets should be taken in the morning on arising.
Isosorbide mononitrate extended-release tablets should not be chewed or crushed and should be
swallowed together with a half-glassful of fluid. Do not break 30 mg tablet.
NDC: 50436-3945-1 30 TABLET, EXTENDED RELEASE in a BOTTLE
NDC: 50436-3945-3 90 TABLET, EXTENDED RELEASE in a BOTTLE
ISOSORBIDE MONONITRATE TABLET, EXTENDED RELEASE
isosorbide mononitrate tablet, extended release
Product T ype
HUMAN PRESCRIPTION DRUG
Ite m Code (Source )
NDC:50 436 -39 45(NDC:23155-178 )
Route of Administration
Active Ingredient/Active Moiety
Basis of Strength
Stre ng th
ISO SO RBIDE MO NO NITRATE (UNII: LX1OH6 30 30 ) (ISOSORBIDE MONONITRATE -
UNII:LX1OH6 30 30 )
6 0 mg
Stre ng th
SILICO N DIO XIDE (UNII: ETJ7Z6 XBU4)
SUCRO SE (UNII: C151H8 M554)
HYDRO XYPRO PYL CELLULO SE ( 12 0 0 0 0 0 MW) (UNII: RFW2ET6 71P)
LACTO SE MO NO HYDRATE (UNII: EWQ57Q8 I5X)
MAGNESIUM STEARATE (UNII: 70 0 9 7M6 I30 )
S hap e
OVAL (bico nvex)
S iz e
Marketing Start Date
Marketing End Date
NDC:50 436 -39 45-1
30 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct
0 6 /0 7/20 10
Unit Dose Services
NDC:50 436 -39 45-3
9 0 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct
0 6 /0 7/20 10
Marke ting Cate gory
Application Numbe r or Monograph Citation
Marke ting Start Date
Marke ting End Date
0 6 /0 7/20 10
Unit Dose Services (831995316)
Ad d re s s
Busine ss Ope rations
Unit Do se Services
8 319 9 5316
REPACK(50 436 -39 45) , RELABEL(50 436 -39 45)