Glimepiride Tablets, USP 2 mg

DESCRIPTION

id: 0221f981-b3dc-43b3-a9a2-449e617ad49f
displayName: DESCRIPTION SECTION
FDA Article Code: 34089-3

Glimepiride Tablets, USP are an oral blood-glucose-lowering drug of the sulfonylurea class. Glimepiride, USP is a white to yellowish-white, crystalline, odorless to practically odorless powder formulated into tablets of 1-mg, 2-mg, and 4-mg strengths for oral administration. Glimepiride Tablets, USP contain the active ingredient glimepiride, USP and the following inactive ingredients: lactose monohydrate, magnesium stearate, povidone, and sodium starch glycolate. In addition, Glimepiride 1-mg tablets contain Ferric Oxide (Iron Oxide Red), Glimepiride 2-mg tablets contain Ferric Oxide (Iron Oxide Yellow), and FD and C Blue #2 Aluminum Lake, and Glimepiride 4-mg tablets contain FD and C Blue #2 Aluminum Lake.

Chemically, glimepiride is identified as 1-[[p-[2-(3-ethyl-4-methyl-2-oxo-3-pyrroline-1-carboxamido)ethyl]phenyl]sulfonyl]-3-(trans-4-methylcyclohexyl)urea.

The CAS Registry Number is 93479-97-1

The structural formula is:

Molecular Formula: C24H34N4O5S

Molecular Weight: 490.62

Glimepiride is practically insoluble in water.

Pharmacodynamics

id: 57658070-5aed-4d99-8f4c-c148f650bfa7
displayName: PHARMACODYNAMICS SECTION
FDA Article Code: 43681-6

A mild glucose-lowering effect first appeared following single
oral doses as low as 0.5-0.6 mg in healthy subjects. The time required to reach
the maximum effect (i.e., minimum blood glucose level [T_min]) was about 2 to 3 hours. In noninsulin-dependent (Type 2)
diabetes mellitus (NIDDM) patients, both fasting and 2-hour postprandial glucose
levels were significantly lower with glimepiride (1, 2, 4, and 8 mg once daily)
than with placebo after 14 days of oral dosing. The glucose-lowering effect in
all active treatment groups was maintained over 24 hours. In larger dose-ranging studies, blood glucose and HbA_1c were found to respond in a dose-dependent manner over the
range of 1 to 4 mg/day of glimepiride. Some patients, particularly those with
higher fasting plasma glucose (FPG) levels, may benefit from doses of
glimepiride up to 8 mg once daily. No difference in response was found when
glimepiride was administered once or twice daily. In two 14-week, placebo-controlled studies in 720 subjects, the average net
reduction in HbA_1c for glimepiride tablets patients
treated with 8 mg once daily was 2.0% in absolute units compared with
placebo-treated patients. In a long-term, randomized, placebo-controlled study
of Type 2 diabetic patients unresponsive to dietary management, glimepiride
therapy improved postprandial insulin/C-peptide responses, and 75% of patients
achieved and maintained control of blood glucose and HbA_1c. Efficacy results were not affected by age, gender, weight,
or race. In long-term extension trials with previously-treated patients, no meaningful
deterioration in mean fasting blood glucose (FBG) or HbA_1c levels was seen after 2 1/2 years of glimepiride therapy. Combination therapy with glimepiride and insulin (70% NPH/30% regular) was
compared to placebo/insulin in secondary failure patients whose body weight was
>130% of their ideal body weight. Initially, 5-10 units of insulin were
administered with the main evening meal and titrated upward weekly to achieve
predefined FPG values. Both groups in this double blind study achieved similar
reductions in FPG levels but the glimepiride/insulin therapy group used
approximately 38% less insulin. Glimepiride therapy is effective in controlling blood glucose without
deleterious changes in the plasma lipoprotein profiles of patients treated for
Type 2 diabetes.

Pharmacokinetics

id: e79b6942-ed82-4c24-8567-85f6fdbb46d1
displayName: PHARMACOKINETICS SECTION
FDA Article Code: 43682-4

Absorption After oral administration, glimepiride is completely (100%)
absorbed from the GI tract. Studies with single oral doses in normal subjects
and with multiple oral doses in patients with Type 2 diabetes have shown
significant absorption of glimepiride within 1 hour after administration and
peak drug levels (C_max) at 2 to 3 hours. When glimepiride
was given with meals, the mean T_max (time to reach C_max) was slightly increased (12%) and the mean C_max and AUC (area under the curve) were slightly decreased (8%
and 9%, respectively).

Distribution After intravenous (IV) dosing in normal subjects, the volume of
distribution (Vd) was 8.8 L (113 mL/kg), and the total body clearance (CL) was
47.8 mL/min. Protein binding was greater than 99.5%.

Metabolism Glimepiride is completely metabolized by oxidative
biotransformation after either an IV or oral dose. The major metabolites are the
cyclohexyl hydroxy methyl derivative (M1) and the carboxyl derivative (M2).
Cytochrome P450 2C9 has been shown to be involved in the biotransformation of
glimepiride to M1. M1 is further metabolized to M2 by one or several cytosolic
enzymes. M1, but not M2, possesses about 1/3 of the pharmacological activity as
compared to its parent in an animal model; however, whether the glucose-lowering
effect of M1 is clinically meaningful is not clear.

Excretion
When¹⁴C-glimepiride was given orally,
approximately 60% of the total radioactivity was recovered in the urine in 7
days and M1 (predominant) and M2 accounted for 80-90% of that recovered in the
urine. Approximately 40% of the total radioactivity was recovered in feces and
M1 and M2 (predominant) accounted for about 70% of that recovered in feces. No
parent drug was recovered from urine or feces. After IV dosing in patients, no
significant biliary excretion of glimepiride or its M1 metabolite has been
observed.

Pharmacokinetic Parameters The pharmacokinetic parameters of glimepiride obtained from a
single-dose, crossover, dose-proportionality (1, 2, 4, and 8 mg) study in normal
subjects and from a single- and multiple-dose, parallel, dose-proportionality (4
and 8 mg) study in patients with Type 2 diabetes are summarized below: These data indicate that glimepiride did not accumulate in serum, and the
pharmacokinetics of glimepiride were not different in healthy volunteers and in
Type 2 diabetic patients. Oral clearance of glimepiride did not change over the
1-8-mg dose range, indicating linear pharmacokinetics.

Variability In normal healthy volunteers, the intra-individual variabilities
of C_max, AUC, and CL/f for glimepiride were 23%, 17%, and
15%, respectively, and the inter-individual variabilities were 25%, 29%, and
24%, respectively.

INDICATIONS AND USAGE

id: 09a469ac-b622-4cdf-b77f-ae4aa73c20c1
displayName: INDICATIONS & USAGE SECTION
FDA Article Code: 34067-9

Glimepiride Tablets, USP are indicated as an adjunct to diet and
exercise to improve glycemic control in adults with type 2 diabetes mellitus
(See DOSAGE
AND ADMINISTRATION section).

CONTRAINDICATIONS

id: 1bb29375-f66c-4c9f-a9b7-0eacae837511
displayName: CONTRAINDICATIONS SECTION
FDA Article Code: 34070-3

Glimepiride Tablets, USP are contraindicated in patients with 1. Known hypersensitivity to the drug. 2. Diabetic ketoacidosis, with or without coma. This condition should be
treated with insulin.

WARNINGS

id: 56e96985-7e7a-40cd-ace9-519285b623fb
displayName: WARNINGS SECTION
FDA Article Code: 34071-1

SPECIAL WARNING ON INCREASED RISK OF CARDIOVASCULAR
MORTALITY The administration of oral hypoglycemic drugs has been
reported to be associated with increased cardiovascular mortality as compared to
treatment with diet alone or diet plus insulin. This warning is based on the
study conducted by the University Group Diabetes Program (UGDP), a long-term,
prospective clinical trial designed to evaluate the effectiveness of
glucose-lowering drugs in preventing or delaying vascular complications in
patients with non-insulin-dependent diabetes. The study involved 823 patients
who were randomly assigned to one of four treatment groups (Diabetes, 19 supp.
2: 747-830, 1970). UGDP reported that patients treated for 5 to 8 years with
diet plus a fixed dose of tolbutamide (1.5 grams per day) had a rate of
cardiovascular mortality approximately 2-1/2 times that of patients treated with
diet alone. A significant increase in total mortality was not observed, but the
use of tolbutamide was discontinued based on the increase in cardiovascular
mortality, thus limiting the opportunity for the study to show an increase in
overall mortality. Despite controversy regarding the interpretation of these
results, the findings of the UGDP study provide an adequate basis for this
warning. The patient should be informed of the potential risks and advantages of
glimepiride tablets and of alternative modes of therapy. Although only one drug in the sulfonylurea class
(tolbutamide) was included in this study, it is prudent from a safety standpoint
to consider that this warning may also apply to other oral hypoglycemic drugs in
this class, in view of their close similarities in mode of action and chemical
structure. Persons allergic to other sulfonamide derivatives may develop an allergic
reaction to glimepiride as well.

PRECAUTIONS

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displayName: PRECAUTIONS SECTION
FDA Article Code: 42232-9

General

Macrovascular Outcomes: There have been
no clinical studies establishing conclusive evidence of macrovascular risk
reduction with glimepiride or any other anti-diabetic drug. Hypoglycemia: All sulfonylurea drugs are capable of
producing severe hypoglycemia. Proper patient selection, dosage, and
instructions are important to avoid hypoglycemic episodes. Patients with
impaired renal function may be more sensitive to the glucose-lowering effect of
glimepiride. A starting dose of 1 mg once daily followed by appropriate dose
titration is recommended in those patients. Debilitated or malnourished
patients, and those with adrenal, pituitary, or hepatic insufficiency are
particularly susceptible to the hypoglycemic action of glucoselowering drugs.
Hypoglycemia may be difficult to recognize in patients with autonomic
neuropathy, the elderly and in people who are taking beta-adrenergic blocking
drugs or other sympatholytic agents. Hypoglycemia is more likely to occur when
caloric intake is deficient, after severe or prolonged exercise, when alcohol is
ingested, or when more than one glucose-lowering drug is used. Combined use of
glimepiride with insulin or metformin may increase the potential for
hypoglycemia. Loss of control of blood glucose: When a patient
stabilized on any diabetic regimen is exposed to stress such as fever, trauma,
infection, or surgery, a loss of control may occur. At such times, it may be
necessary to add insulin in combination with glimepiride or even use insulin
monotherapy. The effectiveness of any oral hypoglycemic drug, including
glimepiride, in lowering blood glucose to a desired level decreases in many
patients over a period of time, which may be due to progression of the severity
of the diabetes or to diminished responsiveness to the drug. This phenomenon is
known as secondary failure, to distinguish it from primary failure in which the
drug is ineffective in an individual patient when first given. Should secondary
failure occur with glimepiride or metformin monotherapy, combined therapy with
glimepiride and metformin or glimepiride and insulin may result in a response.
Should secondary failure occur with combined glimepiride/metformin therapy, it
may be necessary to initiate insulin therapy. Hemolytic anemia: Treatment of patients with glucose
6-phosphate dehydrogenase (G6DP) deficiency with sulfonylurea agents can lead to
hemolytic anemia. Because glimepiride belongs to the class of sulfonylurea
agents, caution should be used in patients with G6PD deficiency and a
non-sulfonylurea alternative should be considered. In postmarketing reports,
hemolytic anemia has also been reported in patients who did not have known G6PD
deficiency.

Pregnancy

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displayName: PREGNANCY SECTION
FDA Article Code: 42228-7

Teratogenic Effects

Pregnancy Category CGlimepiride did not produce teratogenic effects in rats exposed
orally up to 4000 mg/ kg body weight (approximately 4,000 times the maximum
recommended human dose based on surface area) or in rabbits exposed up to 32
mg/kg body weight (approximately 60 times the maximum recommended human dose
based on surface area). Glimepiride has been shown to be associated with
intrauterine fetal death in rats when given in doses as low as 50 times the
human dose based on surface area and in rabbits when given in doses as low as
0.1 times the human dose based on surface area. This fetotoxicity, observed only
at doses inducing maternal hypoglycemia, has been similarly noted with other
sulfonylureas, and is believed to be directly related to the pharmacologic
(hypoglycemic) action of glimepiride. There are no adequate and well-controlled studies in pregnant women. On the
basis of results from animal studies, glimepiride tablets should not be used
during pregnancy. Because recent information suggests that abnormal blood
glucose levels during pregnancy are associated with a higher incidence of
congenital abnormalities, many experts recommend that insulin be used during
pregnancy to maintain glucose levels as close to normal as
possible.




Nonteratogenic Effects In some studies in rats, offspring of dams exposed to high levels
of glimepiride during pregnancy and lactation developed skeletal deformities
consisting of shortening, thickening, and bending of the humerus during the
postnatal period. Significant concentrations of glimepiride were observed in the
serum and breast milk of the dams as well as in the serum of the pups. These
skeletal deformations were determined to be the result of nursing from mothers
exposed to glimepiride. Prolonged severe hypoglycemia (4 to 10 days) has been reported in neonates
born to mothers who were receiving a sulfonylurea drug at the time of delivery.
This has been reported more frequently with the use of agents with prolonged
half-lives. Patients who are planning a pregnancy should consult their
physician, and it is recommended that they change over to insulin for the entire
course of pregnancy and lactation.

Pediatric Use

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displayName: PEDIATRIC USE SECTION
FDA Article Code: 34081-0

The safety and efficacy of glimepiride were evaluated in an
active-controlled, single-blind (patients only), 24-week trial involving 272
pediatric patients, ranging from 8 to 17 years of age, with Type 2 diabetes.
Glimepiride (n=135) was administered at 1 mg initially, and then titrated up to
2, 4 or 8 mg (mean last dose 4 mg) until the therapeutic goal of self-monitored
fasting blood glucose less than  7.0 mmol/L (less than 126 mg/dL) was achieved. The active
comparator metformin (n=137) was administered at 500 mg twice daily initially
and titrated up to 1000 mg twice daily (mean last dose 1365 mg). The profile of adverse reactions in pediatric patients treated with
glimepiride was similar to that observed in adults. Hypoglycemic events, as documented by blood glucose values less than 36 mg/dL, were
observed in 4% of patients treated with glimepiride and in 1% of patients
treated with metformin.

ADVERSE REACTIONS

id: 24a49375-95cd-4136-a16e-babde8817e98
displayName: ADVERSE REACTIONS SECTION
FDA Article Code: 34084-4

Adult Patients The incidence of hypoglycemia with glimepiride, as documented by blood
glucose values less than 60 mg/dL, ranged from 0.9-1.7% in two large, well-controlled,
1-year studies. (See WARNINGS and PRECAUTIONS.) Glimepiride has been evaluated for safety in 2,013 patients in US controlled
trials, and in 1,551 patients in foreign controlled trials. More than 1,650 of
these patients were treated for at least 1 year. Adverse events, other than hypoglycemia, considered to be possibly or
probably related to study drug that occurred in US placebo-controlled trials in
more than 1% of patients treated with glimepiride are shown below.
Gastrointestinal
Reactions
Vomiting, gastrointestinal pain, and diarrhea have been reported, but the
incidence in placebo-controlled trials was less than 1%. In rare cases, there
may be an elevation of liver enzyme levels. In isolated instances, impairment of
liver function (e.g. with cholestasis and jaundice), as well as hepatitis, which
may also lead to liver failure have been reported with sulfonylureas, including
glimepiride.
Dermatologic
Reactions
Allergic skin reactions, e.g., pruritus, erythema, urticaria, and
morbilliform or maculopapular eruptions, occur in less than 1% of treated
patients. These may be transient and may disappear despite continued use of
glimepiride. If those hypersensitivity reactions persist or worsen (e.g.,
dyspnea, fall in blood pressure, shock), the drug should be discontinued. Porphyria cutanea tarda, photosensitivity reactions, and allergic vasculitis
have been reported with sulfonylureas, including glimepiride.
Hematologic
Reactions
Leukopenia, agranulocytosis, thrombocytopenia, hemolytic anemia, aplastic
anemia, and pancytopenia have been reported with sulfonylureas, including
glimepiride.
Metabolic Reactions
Hepatic porphyria reactions and disulfiram-like reactions have been reported
with sulfonylureas, including glimepiride. Cases of hyponatremia have been
reported with glimepiride and all other sulfonylureas, most often in patients
who are on other medications or have medical conditions known to cause
hyponatremia or increase release of antidiuretic hormone. The syndrome of
inappropriate antidiuretic hormone (SIADH) secretion has been reported with
sulfonylureas, including, glimepiride and it has been suggested that certain
sulfonylureas may augment the peripheral (antidiuretic) action of ADH and/or
increase release of ADH.
Other Reactions
Changes in accommodation and/or blurred vision may occur with the use of
glimepiride. This is thought to be due to changes in blood glucose, and may be
more pronounced when treatment is initiated. This condition is also seen in
untreated diabetic patients, and may actually be reduced by treatment. In
placebo-controlled trials of glimepiride, the incidence of blurred vision was
placebo, 0.7%, and glimepiride, 0.4%.
Pediatric Patients
In a clinical trial, 135 pediatric patients with Type 2 diabetes were treated
with glimepiride. The profile of adverse reactions in these patients was similar
to that observed in adults

OVERDOSAGE

id: 057ccb52-e363-4dc5-85f7-35aae016cb55
displayName: OVERDOSAGE SECTION
FDA Article Code: 34088-5

Overdosage of sulfonylureas, including glimepiride, can produce
hypoglycemia. Mild hypoglycemic symptoms without loss of consciousness or
neurologic findings should be treated aggressively with oral glucose and
adjustments in drug dosage and/or meal patterns. Close monitoring should
continue until the physician is assured that the patient is out of danger.
Severe hypoglycemic reactions with coma, seizure, or other neurological
impairment occur infrequently, but constitute medical emergencies requiring
immediate hospitalization. If hypoglycemic coma is diagnosed or suspected, the
patient should be given a rapid intravenous injection of concentrated (50%)
glucose solution. This should be followed by a continuous infusion of a more
dilute (10%) glucose solution at a rate that will maintain the blood glucose at
a level above 100 mg/dL. Patients should be closely monitored for a minimum of
24 to 48 hours, because hypoglycemia may recur after apparent clinical
recovery.

DOSAGE AND ADMINISTRATION

id: 0f7dd194-568c-4cb2-870d-94e0e891d256
displayName: DOSAGE & ADMINISTRATION SECTION
FDA Article Code: 34068-7

There is no fixed dosage regimen for the management of diabetes
mellitus with glimepiride or any other hypoglycemic agent. The patient’s fasting
blood glucose and HbA_1c must be measured periodically to
determine the minimum effective dose for the patient; to detect primary failure,
i.e., inadequate lowering of blood glucose at the maximum recommended dose of
medication; and to detect secondary failure, i.e., loss of adequate blood
glucose lowering response after an initial period of effectiveness. Glycosylated
hemoglobin levels should be performed to monitor the patient’s response to
therapy. Short-term administration of glimepiride may be sufficient during periods of
transient loss of control in patients usually controlled well on diet and
exercise.

Usual Starting Dose The usual starting dose of glimepiride as initial therapy is 1-2
mg once daily, administered with breakfast or the first main meal. Those
patients who may be more sensitive to hypoglycemic drugs should be started at 1
mg once daily, and should be titrated carefully. (See PRECAUTIONS Section for patients at increased risk.) No exact dosage relationship exists between glimepiride and the other oral
hypoglycemic agents. The maximum starting dose of glimepiride should be no more
than 2 mg. Failure to follow an appropriate dosage regimen may precipitate hypoglycemia.
Patients who do not adhere to their prescribed dietary and drug regimen are more
prone to exhibit unsatisfactory response to therapy.

Usual Maintenance Dose The usual maintenance dose is 1 to 4 mg once daily. The maximum
recommended dose is 8 mg once daily. After reaching a dose of 2 mg, dosage
increases should be made in increments of no more than 2 mg at 1-2 week
intervals based upon the patient’s blood glucose response. Long-term efficacy
should be monitored by measurement of HbA_1c levels, for
example, every 3 to 6 months.

Glimepiride-Metformin Combination Therapy If patients do not respond adequately to the maximal dose of
glimepiride monotherapy, addition of metformin may be considered. Published
clinical information exists for the use of other sulfonylureas including
glyburide, glipizide, chlorpropamide, and tolbutamide in combination with
metformin. With concomitant glimepiride and metformin therapy, the desired control of
blood glucose may be obtained by adjusting the dose of each drug. However,
attempts should be made to identify the minimum effective dose of each drug to
achieve this goal. With concomitant glimepiride and metformin therapy, the risk
of hypoglycemia associated with glimepiride therapy continues and may be
increased. Appropriate precautions should be taken.

Glimepiride-Insulin Combination Therapy Combination therapy with glimepiride and insulin may also be used
in secondary failure patients. The fasting glucose level for instituting
combination therapy is in the range of >150 mg/dL in plasma or serum
depending on the patient. The recommended glimepiride dose is 8 mg once daily
administered with the first main meal. After starting with low-dose insulin,
upward adjustments of insulin can be done approximately weekly as guided by
frequent measurements of fasting blood glucose. Once stable, combination-therapy
patients should monitor their capillary blood glucose on an ongoing basis,
preferably daily. Periodic adjustments of insulin may also be necessary during
maintenance as guided by glucose and HbA_1c
levels.

Specific Patient Populations Glimepiride tablets are not recommended for use in pregnancy or
nursing mothers. Data are insufficient to recommend pediatric use of
glimepiride. In elderly, debilitated, or malnourished patients, or in patients
with renal or hepatic insufficiency, the initial dosing, dose increments, and
maintenance dosage should be conservative to avoid hypoglycemic reactions (See CLINICAL
PHARMACOLOGY, Special
Populations and PRECAUTIONS, General).

Patients Receiving Other Oral Hypoglycemic
Agents As with other sulfonylurea hypoglycemic agents, no transition
period is necessary when transferring patients to glimepiride. Patients should
be observed carefully (1-2 weeks) for hypoglycemia when being transferred from
longer half-life sulfonylureas (e.g., chlorpropamide) to glimepiride due to
potential overlapping of drug effect.

HOW SUPPLIED

id: 4c1973f0-3a2a-42fe-abe7-09bd404a61d0
displayName: HOW SUPPLIED SECTION
FDA Article Code: 34069-5

Glimepiride Tablets, USP are available in the following strengths
and package sizes: 2 mg (green, round, flat faced, beveled edge tablets de-bossed with I on the
left side of bisect and G on right side of bisect on one side and “204” on the
other). Bottles of 30 –  NDC 42549-499-30 Relabeling and Repackaging by:

STAT Rx USA LLC
Gainesville, GA  30501

ANIMAL TOXICOLOGY

id: 4ec189b1-7e66-4ccd-a181-dd2c6cbc5fbd
displayName: ANIMAL PHARMACOLOGY & OR TOXICOLOGY SECTION
FDA Article Code: 34091-9

Reduced serum glucose values and degranulation of the pancreatic
beta cells were observed in beagle dogs exposed to 320 mg glimepiride/kg/day for
12 months (approximately 1,000 times the recommended human dose based on surface
area). No evidence of tumor formation was observed in any organ. One female and
one male dog developed bilateral subcapsular cataracts. Non-GLP studies
indicated that glimepiride was unlikely to exacerbate cataract formation.
Evaluation of the cocataractogenic potential of glimepiride in several diabetic
and cataract rat models was negative and there was no adverse effect of
glimepiride on bovine ocular lens metabolism in organ culture.

HUMAN OPHTHALMOLOGY DATA

id: 46193468-4a0f-4aad-88de-1d30c8eb6dad
displayName: SPL UNCLASSIFIED SECTION
FDA Article Code: 42229-5

Ophthalmic examinations were carried out in over 500 subjects
during long-term studies using the methodology of Taylor and West and Laties et
al. No significant differences were seen between glimepiride and glyburide in
the number of subjects with clinically important changes in visual acuity,
intra-ocular tension, or in any of the five lens-related variables examined. Ophthalmic examinations were carried out during long-term studies using the
method of Chylack et al. No significant or clinically meaningful differences
were seen between glimepiride and glipizide with respect to cataract progression
by subjective LOCS II grading and objective image analysis systems, visual
acuity, intraocular pressure, and general ophthalmic examination. Manufactured by:   InvaGen Pharmaceuticals, Inc.   Hauppauge, NY 11788   DISTRIBUTED BY   PERRIGO®   ALLEGAN, MI 49010   OH700 RC J4   Rev: 08/10 Relabeling and Repackaging by:
STAT Rx USA LLC
Gainesville, GA  30501

GLIMEPIRIDE 2 MG TABLETS

id: 8f77cab1-121f-4c64-ae03-a51098e35c19
displayName: PACKAGE LABEL.PRINCIPAL DISPLAY PANEL
FDA Article Code: 51945-4

Once a Day Rx Only