Full Prescribing Information
Rx only
DESCRIPTION
For oral administration, reglan� tablets (metoclopramide tablets, USP) 10 mg are white, scored, capsuleshaped
tablets engraved REGLAN on one side and SP 10 on the opposite side.
Each tablet contains:
Metoclopramide base ...............................................................................................................10 mg
(as the monohydrochloride monohydrate)
Inactive Ingredients
Magnesium Stearate, Mannitol, Microcrystalline Cellulose, Stearic Acid.
reglan� tablets (metoclopramide tablets, USP) 5 mg are green, elliptical-shaped tablets engraved REGLAN
5 on one side and SP on the opposite side.
Each tablet contains:
Metoclopramide base .................................................................................................................5 mg
(as the monohydrochloride monohydrate)
Inactive Ingredients
Corn starch, D&C Yellow 10 Aluminum Lake, FD&C Blue 1 Aluminum Lake, Lactose, Microcrystalline
Cellulose, Silicon Dioxide, Stearic Acid.
Metoclopramide hydrochloride is a white crystalline, odorless substance, freely soluble in water.
Chemically, it is 4-amino-5chloro-N-[2-(diethylamino)ethyl]-2-methoxy benzamide monohydrochloride
monohydrate. Its molecular formula is C14H22CIN3O2�HCl�H2O. Its molecular weight is 354.3.
CLINICAL PHARMACOLOGY
Metoclopramide stimulates motility of the upper gastrointestinal tract without stimulating gastric, biliary, or
pancreatic secretions. Its mode of action is unclear. It seems to sensitize tissues to the action of
acetylcholine. The effect of metoclopramide on motility is not dependent on intact vagal innervation, but it
can be abolished by anticholinergic drugs.
Metoclopramide increases the tone and amplitude of gastric (especially antral) contractions, relaxes the
pyloric sphincter and the duodenal bulb, and increases peristalsis of the duodenum and jejunum resulting in
accelerated gastric emptying and intestinal transit. It increases the resting tone of the lower esophageal
sphincter. It has little, if any, effect on the motility of the colon or gallbladder.
In patients with gastroesophageal reflux and low LESP (lower esophageal sphincter pressure), single oral
doses of metoclopramide produce dose-related increases in LESP. Effects begin at about 5 mg and increase
through 20 mg (the largest dose tested). The increase in LESP from a 5 mg dose lasts about 45 minutes and
that of 20 mg lasts between 2 and 3 hours. Increased rate of stomach emptying has been observed with
single oral doses of 10 mg.
The antiemetic properties of metoclopramide appear to be a result of its antagonism of central and
peripheral dopamine receptors. Dopamine produces nausea and vomiting by stimulation of the medullary
chemoreceptor trigger zone (CTZ), and metoclopramide blocks stimulation of the CTZ by agents like ldopa
or apomorphine which are known to increase dopamine levels or to possess dopamine-like effects.
Metoclopramide also abolishes the slowing of gastric emptying caused by apomorphine.
Like the phenothiazines and related drugs, which are also dopamine antagonists, metoclopramide produces
sedation and may produce extrapyramidal reactions, although these are comparatively rare (see
WARNINGS). Metoclopramide inhibits the central and peripheral effects of apomorphine, induces release
of prolactin and causes a transient increase in circulating aldosterone levels, which may be associated with
transient fluid retention.
The onset of pharmacological action of metoclopramide is 1 to 3 minutes following an intravenous dose, 10
to 15 minutes following intramuscular administration, and 30 to 60 minutes following an oral dose;
pharmacological effects persist for 1 to 2 hours.
Pharmacokinetics
Metoclopramide is rapidly and well absorbed. Relative to an intravenous dose of 20 mg, the absolute oral
bioavailability of metoclopramide is 80% � 15.5% as demonstrated in a crossover study of 18 subjects.
Peak plasma concentrations occur at about 1 to 2 hr after a single oral dose. Similar time to peak is
observed after individual doses at steady state.
In a single dose study of 12 subjects, the area under the drug concentration-time curve increases linearly
with doses from 20 to 100 mg. Peak concentrations increase linearly with dose; time to peak concentrations
remains the same; whole body clearance is unchanged; and the elimination rate remains the same. The
average elimination half-life in individuals with normal renal function is 5 to 6 hr. Linear kinetic processes
adequately describe the absorption and elimination of metoclopramide.
Approximately 85% of the radioactivity of an orally administered dose appears in the urine within 72 hr. Of
the 85% eliminated in the urine, about half is present as free or conjugated metoclopramide.
The drug is not extensively bound to plasma proteins (about 30%). The whole body volume of distribution
is high (about 3.5 L/kg) which suggests extensive distribution of drug to the tissues.
Renal impairment affects the clearance of metoclopramide. In a study with patients with varying degrees of
renal impairment, a reduction in creatinine clearance was correlated with a reduction in plasma clearance,
renal clearance, non-renal clearance, and increase in elimination half-life. The kinetics of metoclopramide
in the presence of renal impairment remained linear however. The reduction in clearance as a result of renal
impairment suggests that adjustment downward of maintenance dosage should be done to avoid drug
accumulation.
Oral Bioavailability 80%+115.5%
In pediatric patients, the pharmacodynamics of metoclopramide following oral and intravenous
administration are highly variable and a concentration-effect relationship has not been established.
There are insufficient reliable data to conclude whether the pharmacokinetics of metoclopramide in adults
and the pediatric population are similar. Although there are insufficient data to support the efficacy of
metoclopramide in pediatric patients with symptomatic gastroesophageal reflux (GER) or cancer
chemotherapy-related nausea and vomiting, its pharmacokinetics have been studied in these patient
populations.
In an open-label study, six pediatric patients (age range, 3.5 weeks to 5.4 months) with GER received
metoclopramide 0.15 mg/kg oral solution every 6 hours for 10 doses. The mean peak plasma concentration
of metoclopramide after the tenth dose was 2-fold (56.8 �g/L) higher compared to that observed after the
first dose (29 �g/L) indicating drug accumulation with repeated dosing. After the tenth dose, the mean time
to reach peak concentrations (2.2 hr), half-life (4.1 hr), clearance (0.67 L/h/kg), and volume of distribution
(4.4 L/kg) of metoclopramide were similar to those observed after the first dose. In the youngest patient
(age, 3.5 weeks), metoclopramide half-life after the first and the tenth dose (23.1 and 10.3 hr, respectively)
was significantly longer compared to other infants due to reduced clearance. This may be attributed to
immature hepatic and renal systems at birth.
Single intravenous doses of metoclopramide 0.22 to 0.46 mg/kg (mean, 0.35 mg/kg) were administered
over 5 minutes to 9 pediatric cancer patients receiving chemotherapy (mean age, 11.7 years; range, 7 to 14
yr) for prophylaxis of cytotoxic-induced vomiting. The metoclopramide plasma concentrations extrapolated
to time zero ranged from 65 to 395 �g/L (mean, 152 �g/L). The mean elimination half-life, clearance, and
volume of distribution of metoclopramide were 4.4 hr (range, 1.7 to 8.3 hr), 0.56 L/h/kg (range, 0.12 to 1.20
L/h/kg), and 3.0 L/kg (range, 1.0 to 4.8 L/kg), respectively.
In another study, nine pediatric cancer patients (age range, 1 to 9 yr) received 4 to 5 intravenous infusions
(over 30 minutes) of metoclopramide at a dose of 2 mg/kg to control emesis. After the last dose, the peak
serum concentrations of metoclopramide ranged from 1060 to 5680 �g/L. The mean elimination half-life,
clearance, and volume of distribution of metoclopramide were 4.5 hr (range, 2.0 to 12.5 hr), 0.37 L/h/kg
(range, 0.10 to 1.24 L/h/kg), and 1.93 L/kg (range, 0.95 to 5.50 L/kg), respectively.
INDICATIONS AND USAGE
The use of reglan� tablets is recommended for adults only. Therapy should not exceed 12 weeks in
duration.
Symptomatic Gastroesophageal Reflux
Reglan tablets are indicated as short-term (4 to 12 weeks) therapy for adults with symptomatic,
documented gastroesophageal reflux who fail to respond to conventional therapy.
The principal effect of metoclopramide is on symptoms of postprandial and daytime heartburn with less
observed effect on nocturnal symptoms. If symptoms are confined to particular situations, such as
following the evening meal, use of metoclopramide as single doses prior to the provocative situation should
be considered, rather than using the drug throughout the day. Healing of esophageal ulcers and erosions has
been endoscopically demonstrated at the end of a 12-week trial using doses of 15 mg q.i.d. As there is no
documented correlation between symptoms and healing of esophageal lesions, patients with documented
lesions should be monitored endoscopically.
Diabetic Gastroparesis (Diabetic Gastric Stasis)
Reglan tablets (metoclopramide tablets, USP) is indicated for the relief of symptoms associated with acute
and recurrent diabetic gastric stasis. The usual manifestations of delayed gastric emptying (e.g., nausea,
vomiting, heartburn, persistent fullness after meals, and anorexia) appear to respond to reglan� within
different time intervals. Significant relief of nausea occurs early and continues to improve over a threeweek
period. Relief of vomiting and anorexia may precede the relief of abdominal fullness by one week or
more.
CONTRAINDICATIONS
Metoclopramide should not be used whenever stimulation of gastrointestinal motility might be dangerous,
e.g., in the presence of gastrointestinal hemorrhage, mechanical obstruction, or perforation.
Metoclopramide is contraindicated in patients with pheochromocytoma because the drug may cause a
hypertensive crisis, probably due to release of catecholamines from the tumor. Such hypertensive crises
may be controlled by phentolamine.
Metoclopramide is contraindicated in patients with known sensitivity or intolerance to the drug.
Metoclopramide should not be used in epileptics or patients receiving other drugs which are likely to cause
extrapyramidal reactions, since the frequency and severity of seizures or extrapyramidal reactions may be
increased.
WARNINGS
Mental depression has occurred in patients with and without prior history of depression. Symptoms have
ranged from mild to severe and have included suicidal ideation and suicide. Metoclopramide should be
given to patients with a prior history of depression only if the expected benefits outweigh the potential
risks.
Extrapyramidal symptoms, manifested primarily as acute dystonic reactions, occur in approximately 1 in
500 patients treated with the usual adult dosages of 30 to 40 mg/day of metoclopramide. These usually are
seen during the first 24 to 48 hours of treatment with metoclopramide, occur more frequently in pediatric
patients and adult patients less than 30 years of age and are even more frequent at higher doses. These
symptoms may include involuntary movements of limbs and facial grimacing, torticollis, oculogyric crisis,
rhythmic protrusion of tongue, bulbar type of speech, trismus, or dystonic reactions resembling tetanus.
Rarely, dystonic reactions may present as stridor and dyspnea, possibly due to laryngospasm. If these
symptoms should occur, inject 50 mg diphenhydramine hydrochloride intramuscularly, and they usually
will subside. Benztropine mesylate, 1 to 2 mg intramuscularly, may also be used to reverse these reactions.
Parkinsonian-like symptoms have occurred, more commonly within the first 6 months after beginning
treatment with metoclopramide, but occasionally after longer periods. These symptoms generally subside
within 2 to 3 months following discontinuance of metoclopramide. Patients with preexisting Parkinson�s
disease should be given metoclopramide cautiously, if at all, since such patients may experience
exacerbation of parkinsonian symptoms when taking metoclopramide.
Tardive Dyskinesia
Tardive dyskinesia, a syndrome consisting of potentially irreversible, involuntary, dyskinetic movements
may develop in patients treated with metoclopramide. Although the prevalence of the syndrome appears to
be highest among the elderly, especially elderly women, it is impossible to predict which patients are likely
to develop the syndrome. Both the risk of developing the syndrome and the likelihood that it will become
irreversible are believed to increase with the duration of treatment and the total cumulative dose.
Less commonly, the syndrome can develop after relatively brief treatment periods at low doses; in these
cases, symptoms appear more likely to be reversible.
There is no known treatment for established cases of tardive dyskinesia although the syndrome may remit,
partially or completely, within several weeks-to-months after metoclopramide is withdrawn.
Metoclopramide itself, however, may suppress (or partially suppress) the signs of tardive dyskinesia,
thereby masking the underlying disease process. The effect of this symptomatic suppression upon the longterm
course of the syndrome is unknown. Therefore, the use of metoclopramide for the symptomatic
control of tardive dyskinesia is not recommended.
Neuroleptic Malignant Syndrome (NMS)
There have been rare reports of an uncommon but potentially fatal symptom complex sometimes referred to
as Neuroleptic Malignant Syndrome (NMS) associated with metoclopramide. Clinical manifestations of
NMS include hyperthermia, muscle rigidity, altered consciousness, and evidence of autonomic instability
(irregular pulse or blood pressure, tachycardia, diaphoresis and cardiac arrhythmias).
The diagnostic evaluation of patients with this syndrome is complicated. In arriving at a diagnosis, it is
important to identify cases where the clinical presentation includes both serious medical illness (e.g.,
pneumonia, systemic infection, etc.) and untreated or inadequately treated extrapyramidal signs and
symptoms (EPS). Other important considerations in the differential diagnosis include central
anticholinergic toxicity, heat stroke, malignant hyperthermia, drug fever and primary central nervous
system (CNS) pathology.
The management of NMS should include 1) immediate discontinuation of metoclopramide and other drugs
not essential to concurrent therapy, 2) intensive symptomatic treatment and medical monitoring, and 3)
treatment of any concomitant serious medical problems for which specific treatments are available.
Bromocriptine and dantrolene sodium have been used in treatment of NMS, but their effectiveness have not
been established (see ADVERSE REACTIONS).
PRECAUTIONS
General
In one study in hypertensive patients, intravenously administered metoclopramide was shown to release
catecholamines; hence, caution should be exercised when metoclopramide is used in patients with
hypertension.
Because metoclopramide produces a transient increase in plasma aldosterone, certain patients, especially
those with cirrhosis or congestive heart failure, may be at risk of developing fluid retention and volume
overload. If these side effects occur at any time during metoclopramide therapy, the drug should be
discontinued.
Adverse reactions, especially those involving the nervous system, may occur after stopping the use of
Reglan. A small number of patients may experience a withdrawal period after stopping reglan� that could
include dizziness, nervousness, and/or headaches.
Information for Patients
The use of Reglan is recommended for adults only. Metoclopramide may impair the mental and/or
physical abilities required for the performance of hazardous tasks such as operating machinery or driving a
motor vehicle. The ambulatory patient should be cautioned accordingly.
DRUG INTERACTIONS
The effects of metoclopramide on gastrointestinal motility are antagonized by anticholinergic drugs and
narcotic analgesics. Additive sedative effects can occur when metoclopramide is given with alcohol,
sedatives, hypnotics, narcotics, or tranquilizers.
The finding that metoclopramide releases catecholamines in patients with essential hypertension suggests
that it should be used cautiously, if at all, in patients receiving monoamine oxidase inhibitors.
Absorption of drugs from the stomach may be diminished (e.g., digoxin) by metoclopramide, whereas the
rate and/or extent of absorption of drugs from the small bowel may be increased (e.g., acetaminophen,
tetracycline, levodopa, ethanol, cyclosporine).
Gastroparesis (gastric stasis) may be responsible for poor diabetic control in some patients. Exogenously
administered insulin may begin to act before food has left the stomach and lead to hypoglycemia. Because
the action of metoclopramide will influence the delivery of food to the intestines and thus the rate of
absorption, insulin dosage or timing of dosage may require adjustment.
Carcinogenesis, Mutagenesis, Impairment of Fertility
A 77-week study was conducted in rats with oral doses up to about 40 times the maximum recommended
human daily dose. Metoclopramide elevates prolactin levels and the elevation persists during chronic
administration. Tissue culture experiments indicate that approximately one-third of human breast cancers
are prolactin-dependent in vitro, a factor of potential importance if the prescription of metoclopramide is
contemplated in a patient with previously detected breast cancer. Although disturbances such as
galactorrhea, amenorrhea, gynecomastia, and impotence have been reported with prolactin-elevating drugs,
the clinical significance of elevated serum prolactin levels is unknown for most patients. An increase in
mammary neoplasms has been found in rodents after chronic administration of prolactin-stimulating
neuroleptic drugs and metoclopramide. Neither clinical studies nor epidemiologic studies conducted to
date, however, have shown an association between chronic administration of these drugs and mammary
tumorigenesis; the available evidence is too limited to be conclusive at this time.
An Ames mutagenicity test performed on metoclopramide was negative.
SPECIAL POPULATIONS
Pregnancy: Pregnancy Category B
Reproduction studies performed in rats, mice and rabbits by the I.V., I.M., S.C., and oral routes at
maximum levels ranging from 12 to 250 times the human dose have demonstrated no impairment of
fertility or significant harm to the fetus due to metoclopramide. There are, however, no adequate and wellcontrolled
studies in pregnant women. Because animal reproduction studies are not always predictive of
human response, this drug should be used during pregnancy only if clearly needed.
Nursing Mothers
Metoclopramide is excreted in human milk. Caution should be exercised when metoclopramide is
administered to a nursing mother.
Pediatric Use
Care should be exercised in administering metoclopramide to neonates since prolonged clearance may
produce excessive serum concentrations (see CLINICAL PHARMACOLOGY� Pharmacokinetics).
In addition, neonates have reduced levels of NADH-cytochrome b5 reductase which, in combination with
the aforementioned pharmacokinetic factors, make neonates more susceptible to methemoglobinemia (see
OVERDOSAGE).
The safety profile of metoclopramide in adults cannot be extrapolated to pediatric patients. Dystonias and
other extrapyramidal reactions associated with metoclopramide are more common in the pediatric
population than in adults. (See WARNINGS and ADVERSE REACTIONS�Extrapyramidal
Reactions.)
Geriatric Use
Clinical studies of reglan� did not include sufficient numbers of subjects aged 65 and over to determine
whether elderly subjects respond differently from younger subjects.
The risk of developing parkinsonian-like side effects increases with ascending dose. Geriatric patients
should receive the lowest dose of reglan� that is effective. If parkinsonian-like symptoms develop in a
geriatric patient receiving reglan�, reglan� should generally be discontinued before initiating any specific
anti-parkinsonian agents (see WARNINGS and DOSAGE AND ADMINISTRATION � For the Relief
of Symptomatic Gastroesophageal Reflux).
The elderly may be at greater risk for tardive dyskinesia (see WARNINGS � Tardive Dyskinesia).
Sedation has been reported in reglan� users. Sedation may cause confusion and manifest as over-sedation
in the elderly (see CLINICAL PHARMACOLOGY, PRECAUTIONS � Information for Patients and
ADVERSE REACTIONS � CNS Effects).
Reglan is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may
be greater in patients with impaired renal function (see DOSAGE AND ADMINISTRATION � USE IN
PATIENTS WITH RENAL OR HEPATIC IMPAIRMENT).
For these reasons, 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 renal function, concomitant
disease, or other drug therapy in the elderly (see DOSAGE AND ADMINISTRATION � For the
Relief of Symptomatic Gastroesophageal Reflux and USE IN PATIENTS WITH RENAL OR
HEPATIC IMPAIRMENT).
Other Special Populations
Patients with NADH-cytochrome b5 reductase deficiency are at an increased risk of developing
methemoglobinemia and/or sulfhemoglobinemia when metoclopramide is administered. In patients with
G6PD deficiency who experience metoclopramide-induced methemoglobinemia, methylene blue treatment
is not recommended (see OVERDOSAGE).
ADVERSE REACTIONS
In general, the incidence of adverse reactions correlates with the dose and duration of metoclopramide
administration. The following reactions have been reported, although in most instances, data do not permit
an estimate of frequency:
CNS Effects
Restlessness, drowsiness, fatigue, and lassitude occur in approximately 10% of patients receiving the most
commonly prescribed dosage of 10 mg q.i.d. (see PRECAUTIONS). Insomnia, headache, confusion,
dizziness, or mental depression with suicidal ideation (see WARNINGS) occur less frequently. The
incidence of drowsiness is greater at higher doses. There are isolated reports of convulsive seizures without
clearcut relationship to metoclopramide. Rarely, hallucinations have been reported.
Extrapyramidal Reactions (EPS)
Acute dystonic reactions, the most common type of EPS associated with metoclopramide, occur in
approximately 0.2% of patients (1 in 500) treated with 30 to 40 mg of metoclopramide per day. Symptoms
include involuntary movements of limbs, facial grimacing, torticollis, oculogyric crisis, rhythmic protrusion
of tongue, bulbar type of speech, trismus, opisthotonus (tetanus-like reactions), and, rarely, stridor and
dyspnea possibly due to laryngospasm; ordinarily these symptoms are readily reversed by
diphenhydramine (see WARNINGS).
Parkinsonian-like symptoms may include bradykinesia, tremor, cogwheel rigidity, mask-like facies (see
WARNINGS).
Tardive dyskinesia most frequently is characterized by involuntary movements of the tongue, face, mouth,
or jaw, and sometimes by involuntary movements of the trunk and/or extremities; movements may be
choreoathetotic in appearance (see WARNINGS).
Motor restlessness (akathisia) may consist of feelings of anxiety, agitation, jitteriness, and insomnia, as well
as inability to sit still, pacing, foot tapping. These symptoms may disappear spontaneously or respond to a
reduction in dosage.
Neuroleptic Malignant Syndrome
Rare occurrences of neuroleptic malignant syndrome (NMS) have been reported. This potentially fatal
syndrome is comprised of the symptom complex of hyperthermia, altered consciousness, muscular rigidity,
and autonomic dysfunction (see WARNINGS).
Endocrine Disturbances
Galactorrhea, amenorrhea, gynecomastia, impotence secondary to hyperprolactinemia (see
PRECAUTIONS). Fluid retention secondary to transient elevation of aldosterone (see CLINICAL
PHARMACOLOGY).
Cardiovascular
Hypotension, hypertension, supraventricular tachycardia, bradycardia, fluid retention, acute congestive
heart failure and possible AV block (see CONTRAINDICATIONS and PRECAUTIONS).
Gastrointestinal
Nausea and bowel disturbances, primarily diarrhea.
Hepatic
Rarely, cases of hepatotoxicity, characterized by such findings as jaundice and altered liver function tests,
when metoclopramide was administered with other drugs with known hepatotoxic potential.
Renal
Urinary frequency and incontinence
Hematologic
A few cases of neutropenia, leukopenia, or agranulocytosis, generally without clearcut relationship to
metoclopramide. Methemoglobinemia, in adults and especially with overdosage in neonates (see
OVERDOSAGE). Sulfhemoglobinemia in adults.
Allergic Reactions
A few cases of rash, urticaria, or bronchospasm, especially in patients with a history of asthma. Rarely,
angioneurotic edema, including glossal or laryngeal edema.
Miscellaneous
Visual disturbances. Porphyria.
OVERDOSAGE
Symptoms of overdosage may include drowsiness, disorientation and extrapyramidal reactions.
Anticholinergic or antiparkinson drugs or antihistamines with anticholinergic properties may be helpful in
controlling the extrapyramidal reactions. Symptoms are self-limiting and usually disappear within 24 hours.
Hemodialysis removes relatively little metoclopramide, probably because of the small amount of the drug
in blood relative to tissues. Similarly, continuous ambulatory peritoneal dialysis does not remove
significant amounts of drug. It is unlikely that dosage would need to be adjusted to compensate for losses
through dialysis. Dialysis is not likely to be an effective method of drug removal in overdose situations.
Unintentional overdose due to misadministration has been reported in infants and children with the use
of metoclopramide oral solution. While there was no consistent pattern to the reports associated with
these overdoses, events included seizures, extrapyramidal reactions, and lethargy.
Methemoglobinemia has occurred in premature and full-term neonates who were given overdoses of
metoclopramide (1 to 4 mg/kg/day orally, intramuscularly or intravenously for 1 to 3 or more days).
Methemoglobinemia can be reversed by the intravenous administration of methylene blue. However,
methylene blue may cause hemolytic anemia in patients with G6PD deficiency, which may be fatal
(see PRECAUTIONS � Other Special Populations).
DOSAGE AND ADMINISTRATION
Therapy with Reglan tablets should not exceed 12 weeks in duration.
For the Relief of Symptomatic Gastroesophageal Reflux
Administer from 10 mg to 15 mg reglan� (metoclopramide hydrochloride, USP) orally up to q.i.d. 30
minutes before each meal and at bedtime, depending upon symptoms being treated and clinical response
(see CLINICAL PHARMACOLOGY and INDICATIONS AND USAGE). If symptoms occur only
intermittently or at specific times of the day, use of metoclopramide in single doses up to 20 mg prior to the
provoking situation may be preferred rather than continuous treatment. Occasionally, patients (such as
elderly patients) who are more sensitive to the therapeutic or adverse effects of metoclopramide will require
only 5 mg per dose.
Experience with esophageal erosions and ulcerations is limited, but healing has thus far been documented
in one controlled trial using q.i.d. therapy at 15 mg/dose, and this regimen should be used when lesions are
present, so long as it is tolerated (see ADVERSE REACTIONS). Because of the poor correlation between
symptoms and endoscopic appearance of the esophagus, therapy directed at esophageal lesions is best
guided by endoscopic evaluation.
Therapy longer than 12 weeks has not been evaluated and cannot be recommended.
For the Relief of Symptoms Associated with Diabetic Gastroparesis (Diabetic Gastric
Stasis)
Administer 10 mg of metoclopramide 30 minutes before each meal and at bedtime for two to eight weeks,
depending upon response and the likelihood of continued well-being upon drug discontinuation.
The initial route of administration should be determined by the severity of the presenting symptoms. If only
the earliest manifestations of diabetic gastric stasis are present, oral administration of reglan� may be
initiated. However, if severe symptoms are present, therapy should begin with metoclopramide injection
(consult labeling of the injection prior to initiating parenteral administration).
Administration of metoclopramide injection up to 10 days may be required before symptoms subside, at
which time oral administration may be instituted. Since diabetic gastric stasis is frequently recurrent,
reglan� therapy should be reinstituted at the earliest manifestation.
USE IN PATIENTS WITH RENAL OR HEPATIC IMPAIRMENT
Since metoclopramide is excreted principally through the kidneys, in those patients whose creatinine
clearance is below 40 mL/min, therapy should be initiated at approximately one-half the recommended
dosage. Depending upon clinical efficacy and safety considerations, the dosage may be increased or
decreased as appropriate.
See OVERDOSAGE section for information regarding dialysis.
Metoclopramide undergoes minimal hepatic metabolism, except for simple conjugation. Its safe use has
been described in patients with advanced liver disease whose renal function was normal.
HOW SUPPLIED
Each white, capsule-shaped, scored Reglan tablet (metoclopramide tablets, USP) contains 10 mg
metoclopramide base (as the monohydrochloride monohydrate). Available in:
- Bottles of 100 tablets (NDC 0091-6701-63)
- Bottles of 500 tablets (NDC 0091-6701-70)
Each green, elliptical-shaped reglan� tablet (metoclopramide tablets, USP) contains 5 mg metoclopramide
base (as the monohydrochloride monohydrate). Available in:
- Bottles of 100 tablets (NDC 0091-6705-63)
Dispense tablets in tight, light-resistant container.
Tablets should be stored at controlled room temperature, between 20�C and 25�C (68�F and 77�F).
STORAGE
Store at 25o C (77o F); excursions permitted to 15-30oC (59-86o F) [see USP Controlled Room Temperature].
Marketed by:
© Schwarz Pharma.
Milwaukee, WI 53201, U.S.A.
Revised: 2004