DESCRIPTION
CLINICAL PHARMACOLOGY
PHARMACOKINETICS
INDICATIONS AND USAGE
CONTRAINDICATIONS
WARNINGS
PRECAUTIONS
ADVERSE REACTIONS
OVERDOSAGE
DOSAGE AND ADMINISTRATION
HOW SUPPLIED
DESCRIPTION: SYNTHROID (Levothyroxine Sodium, USP) Tablets and Injection contain synthetic crystalline L-3, 3’, 5,
5’-tetralodothyronine sodium salt [levothyroxine (T4) sodium]. Synthetic T4 is identical to that produced in the human
thyroid gland.
Levothyroxine (T4) Sodium has an empirical formula of C15H10I4NNaO4xH20, molecular weight of 798.86 (anhydrous), and
structural formula as shown:
Inactive Ingredients (SYNTHROID Tablets): acacia, confectioner’s sugar, lactose, magnesium stearate, povidone, talc.
The following are the color additives by tablet strength:
Inactive Ingredients (SYNTHROID Injection): 10 mg mannitol, USP, sodium hydroxide, 0.7 mg tribasic sodium
phosphate, anhydrous dodecahydrate.
Levothyroxine sodium powder for reconstitution for injection is a sterile preparation.
CLINICAL PHARMACOLOGY: The synthesis and secretion of the major thyroid hormones, L-thyroxine (T4) and L-
triiodothyronine (T3), from the normally functioning thyroid gland are regulated by complex feedback mechanisms of the
hypothalamicpituitary-thyroid axis. The thyroid gland is stimulated to secrete thyroid hormones by the action of
thyrotropin (thyroid stimulating hormone, TSH), which is produced in the anterior pituitary gland. TSH secretion is in turn
controlled by thyrotropin-releasing hormone (TRH) produced in the hypothalamus, circulating thyroid hormones, and
possibly other mechanisms. Thyroid hormones circulating in the blood act as feedback inhibitors of both TSH and TRH
secretion. Thus, when serum concentrations of T3 and T4 are increased, secretion of TSH and TRH decreases.
Conversely, when serum thyroid hormone concentrations are decreased, secretion of TSH and TRH is increased.
Administration of exogenous thyroid hormones to euthyroid individuals results in suppression of endogenous thyroid
hormone secretion.
The mechanisms by which thyroid hormones exert their physiologic actions have not been completely elucidated. T4 and
T3 are transported into cells by passive and active mechanisms. T4 in cell cytoplasm and T3 generated from T4 within
the cell diffuse into the nucleus and bind to thyroid receptor proteins, which appear to be primarily attached to DNA.
Receptor binding leads to activation or repression of DNA transcription, thereby altering the amounts of mRNA and
resultant proteins. Changes in protein concentrations are responsible for the metabolic changes observed in organs and
tissues.
Thyroid hormones enhance oxygen consumption of most body tissues and increase the basal metabolic rate and
metabolism of carbohydrates, lipids, and proteins. Thus, they exert a profound influence on every organ system and are
of particular importance in the development of the central nervous system. Thyroid hormones also appear to have direct
effects on tissues, such as increased myocardial contractility and decreased systemic vascular resistance.
The physiologic effects of thyroid hormones are produced primarily by T3, a large portion of which is derived from the
deiodination of T4 in peripheral tissues. About 70 to 90 percent of peripheral T3 is produced by monodeiodinafion of T4 at
the 5′ position (outer ring). Peripheral monodeiodination of T4 at the 5 position (inner ring) results in the formation of
reverse triiodothyronine (rT3), which is calorigenically inactive.
PHARMACOKINETICS: Few clinical studies have evaluated the kinetics of orally administered thyroid hormone. In
animals, the most active sites of absorption appear to be the proximal and mid-jejunum. T4 is not absorbed from the
stomach and little, if any, drug is absorbed from the duodenum. There seems to be no absorption of T4 from the distal
colon in animals. A number of human studies have confirmed the importance of an intact jejunum and ileum for T4,
absorption and have shown some absorption from the duodenum. Studies involving radioiodinated T4 fecal tracer
excretion methods, equilibration, and AUC methods have shown that absorption varies from 48 to 80 percent of the
administered dose. The extent of absorption is increased in the fasting state and decreased in malabsorption syndromes,
such as sprue. Absorption may also decrease with age. The degree of T4 absorption is dependent on the product
formulation as well as on the character of the intestinal contents, including plasma protein and soluble dietary factors,
which bind thyroid hormone making it unavailable for diffusion. Decreased absorption may result from administration of
infant soybean formula, ferrous sulfate, sodium polystyrene sulfonate, aluminum hydroxide, sucralfate, or bile acid
sequestrants. T4 absorption following intramuscular administration is variable.
Distribution of thyroid hormones in human body tissues and fluids has not been fully elucidated. More than percent of
circulating hormones is bound to serum proteins, including thyroxIne-binding globulin (TBG), thyroxine-binding
prealburnin (TBPA), and albumin (TBA). T4 is more extensively and firmly bound to serum proteins than is T3. Only
unbound thyroid hormone is metabolically active. The higher affinity of TBG and TBPA for T4 partly explains the higher
serum levels, slower metabolic clearance, and longer serum elimination half-life of this hormone.
Certain drugs and physiologic conditions can alter the binding of thyroid hormones to serum proteins and/or the
concentrations of the serum proteins available for thyroid hormone binding. These effects must be considered when
interpreting the results of thyroid function tests. (See Drug Interactions and Laboratory Test Interactions.)
T4 is eliminated slowly from the body, with a half-life of 6 to 7 days. T3 has a half-life of 1 to 2 days. The liver is the
major site of degradation for both hormones. T4 and T33 are conjugated with glucuronic and sulfuric acids and excreted in
the bile. There is an enterohepatic circulation of thyroid hormones, as they are liberated by hydrolysis in the intestine
and reabsorbed. A portion of the conjugated material reaches the colon unchanged, is hydrolyzed there, and is
eliminated as free compounds in the feces. In man, approximately 20 to 40 percent of T4 is eliminated in the stool.
About 70 percent of the T4 secreted daily is deiodinated to yield equal amounts of T3 and rT3. Subsequent deiodination
of T3 and rT3 yields multiple forms of diiodothyronine. A number of other minor T4 metabolites have also been identified.
Although some of these metabolites have biologic activity, their overall contribution to the therapeutic effect of T4 is
minimal.
INDICATIONS AND USAGE: SYNTHROID is indicated:
1. As replacement or supplemental therapy in patients of any age or state (including pregnancy) with hypothyroidism of
any etiology except transient hypothyroidism. During the recovery phase of subacute thyroiditis: primary hypothyroidism
resulting from thyroid dysfunction, primary atrophy, or partial or total absence of the thyroid gland, or from the effects of
surgery, radiation or drugs, with or without the presence of goiter, including subclinical hypothyroidism; secondary
(pituitary) hypothyroidism; and tertiary (hypothalamic) hypothyroldism (see CONTRAINDICATIONS and
PRECAUTIONS). SYNTHROID Injection can be used intravenously when rapid repletion is required, and either
intravenously or intramuscularly when the oral route is precluded.
2. As a pituitary TSH suppressant in the treatment or prevention of various types of euthyroid goiters, including thyroid
nodules, subacute or chronic lymphocytic thyroiditis (Hashimoto’s), multinodular goiter, and in conjunction with surgery
and radioactive iodine therapy in the management of thyrotropin-dependent well-differentiated papillary or follicular
carcinoma of the thyroid.
CONTRAINDICATIONS: SYNTHROID is contraindicated in patients with untreated thyrotoxicosis of any etiology or an
apparent hypersensitivity to thyroid hormones or any of the inactive product constituents. (The 50 mcg tablet is
formulated without color additives for patients who are sensitive to dyes.) There is no well-documented evidence of true
allergic or idiosyncratic reactions to thyroid hormone. SYNTHROID is also contraindicated in the patients with
uncorrected adrenal insufficiency, as thyroid hormones increase tissue demands for adrenocortical hormones and may
thereby precipitate acute adrenal crisis (see PRECAUTIONS).
WARNINGS: Thyroid hormones, either alone or together with other therapeutic agents, should not be used for the
treatment of obesity. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for
weight reduction. Larger doses may produce serious or even life threatening manifestations of toxicity, particularly when
given in association with sympathomimetic amines such as those used for their anorectic effects.
The use of SYNTHROID in the treatment of obesity, either alone or in combination with other drugs, is unjustified. The
use of SYNTHROID is also unjustified in the treatment of male or female infertility unless this condition is associated with
hypothyroidism.
PRECAUTIONS General: SYNTHROID should be used with caution in patients with cardiovascular disorders, including
angina, coronary artery disease, and hypertension, and in the elderly who have a greater likelihood of occult cardiac
disease. Concomitant administration of thyroid hormone and sympathornimetic agents to patients with coronary artery
disease may increase the risk of coronary insufficiency.
Use of SYNTHROID in patients with concomitant diabetes mellitus, diabetes insipidus or adrenal cortical insufficiency
may aggravate the intensity of their symptoms. Appropriate adjustments of the various therapeutic measures directed at
these concomitant endocrine diseases may therefore be required. Treatment of myxedema coma may require
simultaneous administration of glucocorticoids (see DOSAGE AND ADMINISTRATION).
T4 enhances the response to anticoagulant therapy. Prothrombin time should be closely monitored in patients taking
both SYNTHROID and oral anticoagulants, and the dosage of anticoagulant adjusted accordingly.
Seizures have been reported rarely in association with the initiation of levothyroxine sodium therapy, and may be related
to the effect of thyroid hormone on seizure threshold.
Lithium blocks the TSH-mediated release of T4 and T3. Thyroid function should therefore be carefully monitored during
lithium initiation, stabilization, and maintenance. If hypothyroidism occurs during lithium treatment, a higher than usual
SYNTHROID dose may be required.
Information for the Patient:
1. SYNTHROID is intended to replace a hormone that is normally produced by your thyroid gland. It is generally taken
for life, except in cases of temporary hypothyroidism associated with an inflammation of the thyroid gland.
2. Before or at any time while using SYNTHROID you should tell your doctor if you are allergic to any foods or
medicines, are pregnant or intend to become pregnant, are breast-feeding, are taking or start taking any other
prescription or nonprescription (OTC) medications, or have any other medical problems (especially hardening of the
arteries, heart disease, high blood pressure, or history of thyroid, adrenal or pituitary gland problems).
3. Use SYNTHROID only as prescribed by your doctor. Do not discontinue SYNTHROID or change the amount you take
or how often you take it, except as directed by your doctor.
4. SYNTHROID, like all medicines obtained from your doctor, must be used only by you and for the condition
determined appropriate by your doctor.
5. It may take a few weeks for SYNTHROID to begin working. Until it begins working, you may not notice any change
in your symptoms.
6. You should notify your doctor if you experience any of the following symptoms, or if you experience any other unusual
medical event: chest pain, shortness of breath, hives or skin rash, rapid or irregular heartbeat, headache, irritability,
nervousness, sleeplessness, diarrhea, excessive sweating, heat intolerance, changes in appetite, vomiting, weight gain
or loss, changes in menstrual periods, fever, hand tremors, leg cramps.
7. You should inform your doctor or dentist that you are taking SYNTHROID before having any kind of surgery.
8. You should notify your doctor if you become pregnant while taking SYNTHROID. Your dose of this medicine will
likely have to be increased while you are pregnant.
9. If you have diabetes, your dose of insulin or oral antidiabetic agent may need to be changed after starting
SYNTHROID. You should monitor your blood or urinary glucose levels as directed by your doctor and report any
changes to your doctor immediately.
10. If you are taking an oral anticoagulant drug such as warfarin, your dose may need to be changed after starting
SYNTHROID. Your coagulation status should be checked often to determine if a change in dose is required.
11. Partial hair loss may occur rarely during the first few months of SYNTHROID therapy, but it is usually temporary.
12. SYNTHROID is the trade name for tablets containing the thyroid hormone levothyroxine, manufactured by Knoll
Pharmaceutical Company. Other manufacturers also make tablets containing levothyroxine. You should not change to
another manufacturer’s product without discussing that change with your doctor first. Repeat blood tests and a change in
the amount of levothyroxine you take may be required.
13. Keep SYNTHROID out of the reach of children. Store SYNTHROID away from heat and moisture.
Laboratory Tests: Treatment of patients with SYNTHROID requires periodic assessment of thyroid status by appropriate
laboratory tests and clinical evaluation. Selection of appropriate tests for the diagnosis and management of thyroid
disorders depends on patient variables such as presenting signs and symptoms, pregnancy, and concomitant
medications. A combination of sensitive TSH assay and free T4 estimate (free T4 index, FT4I ) are recommended to
confirm a diagnosis of thyroid disease. TSH alone or initially may be useful for thyroid disease screening and for
monitoring therapy for primary hypothyroidism as a linear inverse correlation exists between serum TSH and free T4.
Measurement of total serum T4 and T3, resin T3 uptake, and free T3 concentrations may also be useful. Antithyroid
microsomal antibodies are an indicator of autoimmune thyroid disease. The combination of an increased TSH and
positive microsomal antibodies in an euthyroid patient is a major risk factor for the future development of clinical
hypothyroidism. An elevated serum TSH in the presence of a normal T4 may indicate subclinical hypothyroidism.
Intracellular resistance to thyroid hormone is quite rare, and is suggested by clinical signs and symptoms of
hypothyroidism in the presence of high serum T4 levels. Adequacy of SYNTHROID therapy for hypothyroidism of
pituitary or hypothalamic origin should be assessed by measuring FT4I, which should be maintained in the upper half of
the normal range. Measurement of TSH is not a reliable indicator of response to therapy for this condition.
Drug Interactions: The magnitude and relative clinical importance of the effects noted below are likely to be patient-
specific and may vary by such factors as age, gender, race, intercurrent illnesses, dose of either agent, additional
concomitant medications, and timing of drug administration. Any agent that alters thyroid hormone synthesis, secretion,
distribution, effect on target tissues, metabolism, or elimination may alter the optimal therapeutic dose of SYNTHROID.
Levothyroxine sodium absorption-The following agents may bind and decrease absorption of levothyroxine sodium from
the gastrointestinal tract: aluminum hydroxide, cholestyramine resin, colestipol hydrochloride, ferrous sulfate, sodium
polystyrene sulfonate, soybean flour (e.g., infant formula), sucralfate.
Binding to serum proteins-The following agents may either inhibit levothyroxine sodium binding to serum proteins or alter
the concentrations of serum binding proteins: androgens and related anabolic hormones, asparaginase, clofibrate, estrogens and estrogen-containing compounds, 5-fluorouracil, furosemide, glucocorticoids, meclofenamic acid, mefenamic acid, methadone, perphe
nazine, phenylbutazone, phenytoin, salicylates, tamoxifen.
Thyroid physiology-The following agents may alter thyroid hormone or TSH levels, generally by effects on thyroid
hormone synthesis, secretion, distribution, metabolism, hormone action, or elimination, or altered TSH secretion:
aminoglutethimide, paminosalicylic acid, amiodarone, androgens and related anabolic hormones, complex anions
(thiocyanate, Perchlorate, pertechnetate), antithyroid drugs, Beta-adrenergic blocking agents, carbamazepine, chloral
hydrate, diazepam, dopamine and doparnine agonists, ethionamide, glucocorticoids, heparin, hepatic enzyme inducers,
insulin, iodinated cholestographic agents, iodine-containing compounds, levodopa, lovastatin, lithium, 6-mercaptopurine,
metoclopramide, mitotane, nitroprusside, phenobarbital, phenytoin, resorcinol, rifampin, somatostatin analogs,
sulfonarnides, sulfonylureas, thiazide diuretics.
Adrenocorticoids-Metabolic clearance of adrenocorticoids is decreased in hypothyroid patients and increased in
hyperthyroid patients, and may therefore change with changing thyroid status.
Amiodarone-Amiodarone therapy alone can cause hypothyroidism or hyperthyroidism.
Anticoagulants (oral)-The hypoprothrombinemic effect of anticoagulants may be potentiated, apparently by increased
catabolism of vitamin K-dependent clotting factors.
Antidiabetic agents (insulin, sulfonylureas)-Requirements for insulin or oral antidiabetic agents may be reduced in
hypothyroid patients with diabetes mellitus, and may subsequently increase with the initiation of thyroid hormone
replacement therapy.
Beta-adrenergic blocking agents-Actions of some beta-blocking agents may be impaired when hypothyroid patients become
euthyroid.
Cytokines (interferon, interleukin)-Cytokines have been reported to induce both hyperthyroidism and hypothyroidism.
Digitalis glycosides-Therapeutic effects of digitalis glycosides may be reduced. Serum digitalis levels may be decreased in hyperthyroidism or when a hypothyroid patient becomes euthyroid.
Ketamine-Marked hypertension and tachycardia have been reported in association with concomitant administration of
levothyroxine sodium and ketamine.
Maprotiline-Risk of cardiac arrhythmias may increase.
Sodium iodide (123I and 131I), sodium pertechnetateTc99m-Uptake of radiolabeled ions may be decreased.
Somatrem/Somatropin-Excessive concurrent use of thyroid hormone may accelerate epiphyseal closure. Untreated
hypothyroidism may interfere with the growth response to somatrern or somatropin.
Theophylline-Theophylline clearance may decrease in hypothyroid patients and return toward normal when a euthyroid
state is achieved.
Tricyclic antidepressants–Concurrent use may increase the therapeutic and toxic effects of both drugs, possibly due to
increased catecholamine sensitivity. Onset of action of tricyclics may be accelerated.
Sympathomimetic agents-Possible increased risk of coronary insufficiency in patients with coronary artery disease.
Laboratory Test Interactions: A number of drugs or moieties are known to alter serum levels of TSH, T4 and T3 and
may thereby influence the interpretation of laboratory tests of thyroid function (see Drug Interactions).
1. Changes in TBG concentration should be taken into consideration when interpreting T4 and T3 values. Drugs such as
estrogens and estrogen-containing oral contraceptives increase TBG concentrations. TBG concentrations may also be
increased during pregnancy and in infectious hepatitis. Decreases in TBG concentrations are observed in nephrosis,
acromegaly, and after androgen or corticosteriod therapy. Familial hyper- or hypo-thyroxine-binding-globulinemias have
been described. The incidence of TBG deficiency is approximately 1 in 9000. Certain drugs such as salicylates inhibit
the protein-binding of T4. In such cases, the unbound (free) hormone should be measured. Alternatively, an indirect
measure of free thyroxine, such as the FT4I may be used.
2. Medicinal or dietary iodine interferes with in vivo tests of radioiodine uptake, producing low uptakes which may not
indicate a true decrease in hormone synthesis.
3. Persistent clinical and laboratory evidence of hypothyroidism despite an adequate replacement dose suggests either
poor patient compliance, impaired absorption, drug interactions, or decreased potency of the preparation due to improper
storage.
Carcinogenesis, Mutagenesis, and Impairment of Fertility: Although animal studies to determine the mutagenic or
carcinogenic potential of thyroid hormones have not been performed, synthetic T4 is identical to that produced by the
human thyroid gland. A reported association between prolonged thyroid hormone therapy and breast cancer has not
been confirmed and patients receiving levothyroxine sodium for established indications should not discontinue therapy.
Pregnancy: Pregnancy Category A. Studies in pregnant women have not shown that levothyroxine sodium increases the
risk of fetal abnormalities if administered during pregnancy. If levothyroxine sodium is used during pregnancy, the
possibility of fetal harm appears remote. Because studies cannot rule out the possibility of harm, levothyroxine sodium
should be used during pregnancy only if clearly needed.
Thyroid hormones cross the placental barrier to some extent. T4 levels in the cord blood of athyroid fetuses have been
shown to be about one-third of maternal levels. Nevertheless, maternal-fetal transfer of T4 may not prevent in utero
hypothyroidism.
Hypothyroidism during pregnancy is associated with a higher rate of complications, including spontaneous abortion and
preeclampsia, and has been reported to have an adverse effect on fetal and childhood development. On the basis of
current knowledge, SYNTHROID® (Levothyroxine Sodium, USP) should therefore not be discontinued during pregnancy,
and hypothyroidism diagnosed during pregnancy should be treated. Studies have shown that during pregnancy T4
concentrations may decrease and TSH concentrations may increase to values outside normal ranges. Postpartum
values are similar to preconception values. Elevations in TSH may occur as early as 4 weeks gestation.
Pregnant women who are maintained on SYNTHROID should have their TSH measured periodically. An elevated TSH
should be corrected by an increase in SYNTHROID dose. After pregnancy, the dose can be decreased to the optimal
preconception dose.
Nursing Mothers: Minimal amounts of thyroid hormones are excreted in human milk. Thyroid hormones are not
associated with serious adverse reactions and do not have known tumorigenic potentials While caution should be
exercised when SYNTHROID is administered to a nursing woman, adequate replacement doses of levothyroxine sodium
are generally needed to maintain normal lactation.
Pediatric Use: The incidence of congenital hypothyroidism is relatively high (1 in 4,000). Routine determinations of
serum T4 and/or TSH are therefore strongly advised in neonates in view of the deleterious effects of thyroid deficiency on
growth and development.
Treatment should be initiated immediately upon diagnosis and generally maintained for life. If, however, transient
hypothyroidism is suspected, therapy may be interrupted for 30 days after the age of 3 years to reassess the condition. If
T4 is low and TSH is elevated after that time, permanent hypothyroidism is confirmed and therapy should be reinstituted.
If the T4 and TSH remain in the normal range, a preliminary diagnosis of transient hypothyroidism can be made.
Nevertheless, continued close observation with periodic thyroid function testing is warranted.
ADVERSE REACTIONS: Adverse reactions other than those indicative of thyrotoxicosis as a result of therapeutic
overdosage, either initially or during the maintenance periods, are rare (see OVERDOSAGE). Craniosynostosis has
been associated with iatrogenic hyperthyroidism in infants receiving thyroid hormone replacement therapy. Inadequate
doses of SYNTHROID may produce or fail to resolve symptoms of hypothyroidism. Hypersensitivity reactions to the
product excipients, such as rash and urticaria, may occur. Partial hair loss may occur during the initial months of
therapy, but is generally transient. The incidence of continued hair loss is unknown. Pseudotumor cerebri has been
reported in pediatric patients receiving thyroid hormone replacement therapy.
OVERDOSAGE: Signs and Symptoms: Excessive doses of SYNTHROID result in a hypermetabolic state
indistinguishable from thyrotoxicosis of endogenous origin. Signs and symptoms of thyrotoxicosis include weight loss,
increased appetite, palpitations, nervousness, diarrhea, abdominal cramps, sweating, tachycardia, increased pulse and
blood pressure, cardiac arrhythmias, tremors, insomnia, heat intolerance, fever, and menstrual irregularities. Symptoms
are not always evident or may not appear until several days after ingestion.
Treatment of Overdosage: SYNTHROID should be reduced in dose or temporarily discontinued if signs and symptoms
of overdosage appear.
In the treatment of acute massive SYNTHR0ID overdosage, symptomatic and supportive therapy should be instituted
immediately. Treatment is aimed at reducing gastrointestinal absorption and counteracting central and peripheral
effects, mainly those of increased sympathetic activity. The stomach should be emptied immediately by emesis or
gastric lavage if not otherwise contraindicated (e.g., by coma, convulsions or loss of gag reflex). Cholestyramine and
activated charcoal have also been used to decrease levothyroxine sodium absorption. Oxygen should be administered
and ventilation maintained as necessary. Preceptor antagonists, particularly propranolol, are useful in counteracting
many of the effects of increased sympathetic activity. Propranolol may be administered intravenously at a dosage of 1 to
3 mg over a 10 minute period or orally, 80 to 160 mg/day, especially when no contraindications exist for its use. Cardiac
glycosides, may be administered if congestive heart failure develops. Measures to control fever, hypoglycemia, or fluid
loss should be initiated as necessary. Glucocorticoids may be administered to inhabit the conversion of T4 to T3.
Since T4 is extensively protein bound, very little drug will be removed by dialysis.
The average initial oral dose of SYNTHROID at the start of treatment is 10 to 15 mcg/kg/day. Infants with very low (less
than 5 mU/L) or undetectable serum T4 levels should be started at 50 mcg daily. A lower dose (e.g., 25 mcg daily)
should be considered for premature neonates weighing less than 2 kg and neonates at risk of cardiac failure, increasing
to 37.5 or 50 mcg daily after 4 to 6 weeks.
Recommended Pediatric Dosage
For Congenital Hypothyroidism*
*To be adjusted on the basis of clinical response and laboratory tests (see Laboratory Tests).
Evaluation of the infant’s response to SYNTHROID by determination of the serum T4 and TSH should be performed 2 to
4 weeks after initiation of therapy and after any change in dosage. Additional evaluations should be performed every 1
to 2 months in the first year, every 2 to 3 months between ages 1 and 3, and every 3 to 12 months thereafter until growth
is complete. More frequent intervals are indicated when compliance is questioned or abnormal laboratory values are
obtained. SYNTHROID may be given to infants and children who cannot swallow intact tablets by crushing the tablet and
suspending the freshly crushed tablet in a small amount of water (5 to 10 mL), breast milk or non-soybean based
formula. The suspension can be given by spoon or dropper. DO NOT STORE THE SUSPENSION FOR ANY PERIOD
OF TIME. The crushed tablet may also be sprinkled over a small amount of food, such as cooked cereal or apple sauce.
HOW SUPPLIED: SYNTHROID® (Levothyroxine Sodium, USP) Tablets: round, color coded, scored tablet debossed with ‘FLINT’ and potency.
25 mcg, orange
Bottles of 100, Code 3P1023 NDC 0048-1020-03
Bottles of 1000, Code 3P1025 NDC 0048-1020-05
50 mcg, white
Bottles of 100, Code 3P1043 NDC 0048-1040-03
Bottles of 1000, Code 3P1045 NDC 0048-1040-05
Unit Dose Cartons of 100, Code 3P1033 NDC 0048-1040-13
75 mcg, violet
Bottles of 100, Code 3P1053 NDC 0048-1050-03
Bottles of 1000, Code 3P1055 NDC 0048-1050-05
Unit Dose Cartons of 100, Code 3P1003 NDC 0048-1050-13
88 mcg, olive
Bottles of 100, Code 3P0883 NDC 0048-1060-03
100 mcg, yellow
Bottles of 100, Code 3P1073 NDC 0048-1070-03
Bottles of 1000, Code 3P1075 NDC 0048-1070-05
Unit Dose Cartons of 100, Code 3P1063 NDC 0048-1070-13
112 mcg, rose
Bottles of 100, Code 3P1183 NDC 0048-1080-03
Bottles of 1000, Code 3P1185 NDC 0048-1080-05
125 mcg, brown
Bottles of 100, Code 3P1103 NDC 0048-1130-03
Bottles of 1000, Code 3P1105 NDC 0048-1130-05
Unit Dose Cartons of 100 Code 3P1113 NDC 0048-1130-13
150 mcg, blue
Bottles of 100, Code 3P1093 NDC 0048-1090-03
Bottles of 1000, Code 3P1095 NDC 0048-1090-05
Unit Dose Cartons of 100, Code 3P1083 NDC 0048-1090-13
175 mcg, lilac
Bottles of 100, Code 3P1153 NDC 0048-1100-03
200 mcg, pink
Bottles of 100, Code 3P1143 NDC 0048-1140-03
Bottles of 1000, Code 3P1145 NDC 0048-1140-05
Unit Dose Cartons of 100, Code 3P1133 NDC 0048-1140-13
300 mcg, green
Bottles of 100, Code 3P1173 NDC 0048-1170-03
Bottles of 1000, Code 3P1175 NDC 0048-1170-05
Store at controlled room temperature 15o-30oC (59o-86oF). SYNTHROID Tablets should be protected from light and moisture.
SYNTHROID® (Levothyroxine Sodium, USP)Injection is a lyophilized powder. It is supplied in color coded vials as
follows:
200 mcg, gray
10 mL Single Dose Vial, Code 3P1312 NDC 0048-1014-99
500 mcg, yellow
10 mL Single Dose Vial, Code 3P1302 NDC 0048-1012-99
Store at controlled room temperature 15o-30oC (59o– 86oF).
DIRECTIONS FOR RECONSTITUTION: Reconstitute the lyophilized levothyroxine sodium by aseptically adding 5 mL
of 0.9% Sodium Chloride Injection, USP or Bacteriostatic Sodium Chloride Injection, USP with Benzyl Alcohol (final
volume approximately 5mL). Shake vial to insure complete mixing. Do not add to other intravenous fluids. Discard any
unused portion.
CAUTION: Federal (USA) law prohibits dispensing without a prescription.
Tablets Manufactured by
BASF Pharmaceuticals
A Unit of BASF
Jayuya, Puerto Rico 00664
Injection Manufactured by
Ben Venue Laboratories, Inc.
Bedford, Ohio 44146 USA
