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| Product NDC Code | 60846-806 | ||||
|---|---|---|---|---|---|
| Drug Name | Unithroid |
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| Type | Brand | ||||
| Pharm Class | Thyroxine [CS], l-Thyroxine [EPC] |
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| Active Ingredients |
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| Route | ORAL | ||||
| Dosage Form | TABLET | ||||
| RxCUI drug identifier | 892246, 892251, 892255, 966220, 966221, 966222, 966224, 966225, 966228, 966232, 966233, 966235, 966237, 966238, 966241, 966243, 966244, 966246, 966248, 966249, 966253, 966270, 966286, 966436 |
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| Application Number | NDA021210 | ||||
| Labeler Name | Amneal Pharmaceuticals LLC | ||||
| Packages |
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Overdosage of Unithroid
Information about signs, symptoms, and laboratory findings of acute ovedosage and the general principles of overdose treatment.10 OVERDOSAGE The signs and symptoms of overdosage are those of hyperthyroidism [see Warnings and Precautions ( 5.4 ) and Adverse Reactions ( 6 )] . In addition, confusion and disorientation may occur. Cerebral embolism, shock, coma, and death have been reported. Seizures occurred in a 3-year-old child ingesting 3.6 mg of levothyroxine. Symptoms may not necessarily be evident or may not appear until several days after ingestion of levothyroxine sodium. Reduce the UNITHROID dose or temporarily discontinued if signs or symptoms of overdosage occur. Initiate appropriate supportive treatment as dictated by the patient’s medical status. For current information on the management of poisoning or overdosage, contact the National Poison Control Center at 1‑800-222-1222 or www.poison.org.
Adverse reactions
Information about undesirable effects, reasonably associated with use of the drug, that may occur as part of the pharmacological action of the drug or may be unpredictable in its occurrence. Adverse reactions include those that occur with the drug, and if applicable, with drugs in the same pharmacologically active and chemically related class. There is considerable variation in the listing of adverse reactions. They may be categorized by organ system, by severity of reaction, by frequency, by toxicological mechanism, or by a combination of these.6 ADVERSE REACTIONS Common adverse reactions with UNITHROID therapy are primarily those of hyperthyroidism due to therapeutic overdosage [see Warnings and Precautions ( 5.4 ) and Overdosage (10) ] . They include the following: General: fatigue, increased appetite, weight loss, heat intolerance, fever, excessive sweating Central nervous system: headache, hyperactivity, nervousness, anxiety, irritability, emotional lability, insomnia Musculoskeletal: tremors, muscle weakness and cramps Cardiovascular: palpitations, tachycardia, arrhythmias, increased pulse and blood pressure, heart failure, angina, myocardial infarction, cardiac arrest Respiratory: dyspnea Gastrointestinal: diarrhea, vomiting, abdominal cramps, elevations in liver function tests Dermatologic: hair loss, flushing Endocrine: decreased bone mineral density Reproductive: menstrual irregularities, impaired fertility Seizures have been reported rarely with levothyroxine therapy. Adverse Reactions in Pediatric Patients Pseudotumor cerebri and slipped capital femoral epiphysis have been reported in pediatric patients receiving levothyroxine therapy. Overtreatment may result in craniosynostosis in infants and premature closure of the epiphyses in pediatric patients with resultant compromised adult height. Hypersensitivity Reactions Hypersensitivity reactions to inactive ingredients have occurred in patients treated with thyroid hormone products. These include urticaria, pruritus, skin rash, flushing, angioedema, various gastrointestinal symptoms (abdominal pain, nausea, vomiting and diarrhea), fever, arthralgia, serum sickness and wheezing. Hypersensitivity to levothyroxine itself is not known to occur. Common adverse reactions for UNITHROID are primarily those of hyperthyroidism due to therapeutic overdosage: arrhythmias, myocardial infarction, dyspnea, muscle spasm, headache, nervousness, irritability, insomnia, tremors, muscle weakness, increased appetite, weight loss, diarrhea, heat intolerance, menstrual irregularities, and skin rash ( 6 ) To report SUSPECTED ADVERSE REACTIONS, Amneal Pharmaceuticals Inc. at 1-877-835-5472 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
Unithroid Drug Interactions
Information about and practical guidance on preventing clinically significant drug/drug and drug/food interactions that may occur in people taking the drug.7 DRUG INTERACTIONS See full prescribing information for drugs that affect thyroid hormone pharmacokinetics and metabolism (e.g., absorption, synthesis, secretion, catabolism, protein binding, and target tissue response) and may alter the therapeutic response to UNITHROID ( 7 ) 7.1 Drugs Known to Affect Thyroid Hormone Pharmacokinetics Many drugs can exert effects on thyroid hormone pharmacokinetics (e.g. absorption, synthesis, secretion, catabolism, protein binding, and target tissue response) and may alter the therapeutic response to UNITHROID (see Tables 2 – 5). Table 2: Drugs That May Decrease T4 Absorption (Hypothyroidism) Potential impact: Concurrent use may reduce the efficacy of UNITHROID by binding and delaying or preventing absorption, potentially resulting in hypothyroidism. Drug or Drug Class Effect Calcium Carbonate Ferrous Sulfate Calcium carbonate may form an insoluble chelate with levothyroxine, and ferrous sulfate likely forms a ferric-thyroxine complex. Administer UNITHROID at least 4 hours apart from these agents. Orlistat Monitor patients treated concomitantly with orlistat and UNITHROID for changes in thyroid function. Bile Acid Sequestrants -Colesevelam -Cholestyramine -Colestipol Ion Exchange Resins -Kayexalate -Sevelamer Bile acid sequestrants and ion exchange resins are known to decrease levothyroxine absorption. Administer UNITHROID at least 4 hours prior to these drugs or monitor thyrotropin-stimulating hormone (TSH) levels. Other drugs: Proton Pump Inhibitors Sucralfate Antacids - Aluminum & Magnesium Hydroxides - Simethicone Gastric acidity is an essential requirement for adequate absorption of levothyroxine. Sucralfate, antacids and proton pump inhibitors may cause hypochlorhydria, affect intragastric pH, and reduce levothyroxine absorption. Monitor patients appropriately. Table 3: Drugs That May Alter T and Triiodothyronine (T3) Serum Transport Without Affecting Free Thyroxine (FT4) Concentration (Euthyroidism) Drug or Drug Class Effect Clofibrate Estrogen-containing oral contraceptives Estrogens (oral) Heroin / Methadone 5-Fluorouracil Mitotane Tamoxifen These drugs may increase serum thyroxine-binding globulin (TBG) concentration. Androgens / Anabolic Steroids Asparaginase Glucocorticoids Slow-Release Nicotinic Acid These drugs may decrease serum TBG concentration. Potential impact (below) : Administration of these agents with UNITHROID results in an initial transient increase in FT4. Continued administration results in a decrease in serum T4 and normal FT4 and TSH concentrations. Salicylates (>2 g/day) Salicylates inhibit binding of T4 and T3 to TBG and transthyretin. An initial increase in serum FT4 is followed by return of FT4 to normal levels with sustained therapeutic serum salicylate concentrations, although total T4 levels may decrease by as much as 30%. Other drugs: Carbamazepine Furosemide (>80 mg IV) Heparin Hydantoins Non-Steroidal Anti-inflammatory Drugs - Fenamates These drugs may cause protein-binding site displacement. Furosemide has been shown to inhibit the protein binding of T4 to TBG and albumin, causing an increased free-T4 fraction in serum. Furosemide competes for T4-binding sites on TBG, prealbumin, and albumin, so that a single high dose can acutely lower the total T4 level. Phenytoin and carbamazepine reduce serum protein binding of levothyroxine, and total and FT4 may be reduced by 20% to 40%, but most patients have normal serum TSH levels and are clinically euthyroid. Closely monitor thyroid hormone parameters. Table 4: Drugs That May Alter Hepatic Metabolism of T4 (Hypothyroidism) Potential impact: Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of levothyroxine, resulting in increased UNITHROID requirements. Drug or Drug Class Effect Phenobarbital Rifampin Phenobarbital has been shown to reduce the response to thyroxine. Phenobarbital increases L-thyroxine metabolism by inducing uridine 5'-diphospho-glucuronosyltransferase (UGT) and leads to a lower T4 serum levels. Changes in thyroid status may occur if barbiturates are added or withdrawn from patients being treated for hypothyroidism. Rifampin has been shown to accelerate the metabolism of levothyroxine. Table 5: Drugs That May Decrease Conversion of T4 to T3 Potential impact: Administration of these enzyme inhibitors decreases the peripheral conversion of T4 to T3, leading to decreased T3 levels. However, serum T4 levels are usually normal but may occasionally be slightly increased. Drug or Drug Class Effect Beta-adrenergic antagonists (e.g., Propranolol >160 mg/day) In patients treated with large doses of propranolol (>160 mg/day), T3 and T4 levels change slightly, TSH levels remain normal, and patients are clinically euthyroid. It should be noted that actions of particular beta-adrenergic antagonists may be impaired when the hypothyroid patient is converted to the euthyroid state. Glucocorticoids (e.g., Dexamethasone ≥4 mg/day) Short-term administration of large doses of glucocorticoids may decrease serum T3 concentrations by 30% with minimal change in serum T4 levels. However, long-term glucocorticoid therapy may result in slightly decreased T3 and T4 levels due to decreased TBG production (See above). Other: Amiodarone Amiodarone inhibits peripheral conversion of levothyroxine (T4) to triiodothyronine (T3) and may cause isolated biochemical changes (increase in serum free-T4, and decreased or normal free-T3) in clinically euthyroid patients. 7.2 Antidiabetic Therapy Addition of UNITHROID therapy in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent or insulin requirements. Carefully monitor glycemic control, especially when UNITHROID is started, changed, or discontinued [see Warnings and Precautions ( 5.5 )] . 7.3 Oral Anticoagulants UNITHROID increases the response to oral anticoagulant therapy. Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state or when the UNITHROID dose is increased. Closely monitor coagulation tests to permit appropriate and timely dosage adjustments. 7.4 Digitalis Glycosides UNITHROID may reduce the therapeutic effects of digitalis glycosides. Serum digitalis glycoside levels may be decreased when a hypothyroid patient becomes euthyroid, necessitating an increase in the dose of digitalis glycosides. 7.5 Antidepressant Therapy Concurrent use of tricyclic (e.g., amitriptyline) or tetracyclic (e.g., maprotiline) antidepressants and UNITHROID may increase the therapeutic and toxic effects of both drugs, possibly due to increased receptor sensitivity to catecholamines. Toxic effects may include increased risk of cardiac arrhythmias and central nervous system stimulation. UNITHROID may accelerate the onset of action of tricyclics. Administration of sertraline in patients stabilized on UNITHROID may result in increased UNITHROID requirements. 7.6 Ketamine Concurrent use of ketamine and UNITHROID may produce marked hypertension and tachycardia. Closely monitor blood pressure and heart rate in these patients. 7.7 Sympathomimetics Concurrent use of sympathomimetics and UNITHROID may increase the effects of sympathomimetics or thyroid hormone. Thyroid hormones may increase the risk of coronary insufficiency when sympathomimetic agents are administered to patients with coronary artery disease. 7.8 Tyrosine-Kinase Inhibitors Concurrent use of tyrosine-kinase inhibitors such as imatinib may cause hypothyroidism. Closely monitor TSH levels in such patients. 7.9 Drug-Food Interactions Consumption of certain foods may affect UNITHROID absorption thereby necessitating adjustments in dosing [see Dosage and Administration (2.1) ] . Soybean flour (infant formula), cotton seed meal, walnuts, and dietary fiber may bind and decrease the absorption of UNITHROID from the GI tract. Grapefruit juice may delay the absorption of levothyroxine and reduce its bioavailability. 7.10 Drug-Laboratory Test Interactions Consider changes in TBG concentration when interpreting T4 and T3 values. Measure and evaluate unbound (free) hormone and/or determine the free T4 index (FT4I) in this circumstance. Pregnancy, infectious hepatitis, estrogens, estrogen-containing oral contraceptives, and acute intermittent porphyria increase TBG concentrations. Nephrosis, severe hypoproteinemia, severe liver disease, acromegaly, androgens and corticosteroids decrease TBG concentration. Familial hyper- or hypo-thyroxine binding globulinemias have been described, with the incidence of TBG deficiency approximating 1 in 9000.
| Potential impact: Concurrent use may reduce the efficacy of UNITHROID by binding and delaying or preventing absorption, potentially resulting in hypothyroidism. | |
|---|---|
| Calcium Carbonate Ferrous Sulfate | Calcium carbonate may form an insoluble chelate with levothyroxine, and ferrous sulfate likely forms a ferric-thyroxine complex. Administer UNITHROID at least 4 hours apart from these agents. |
| Orlistat | Monitor patients treated concomitantly with orlistat and UNITHROID for changes in thyroid function. |
| Bile Acid Sequestrants -Colesevelam -Cholestyramine -Colestipol Ion Exchange Resins -Kayexalate -Sevelamer | Bile acid sequestrants and ion exchange resins are known to decrease levothyroxine absorption. Administer UNITHROID at least 4 hours prior to these drugs or monitor thyrotropin-stimulating hormone (TSH) levels. |
| Other drugs: Proton Pump Inhibitors Sucralfate Antacids - Aluminum & Magnesium Hydroxides - Simethicone | Gastric acidity is an essential requirement for adequate absorption of levothyroxine. Sucralfate, antacids and proton pump inhibitors may cause hypochlorhydria, affect intragastric pH, and reduce levothyroxine absorption. Monitor patients appropriately. |
| Clofibrate Estrogen-containing oral contraceptives Estrogens (oral) Heroin / Methadone 5-Fluorouracil Mitotane Tamoxifen | These drugs may increase serum thyroxine-binding globulin (TBG) concentration. |
| Androgens / Anabolic Steroids Asparaginase Glucocorticoids Slow-Release Nicotinic Acid | These drugs may decrease serum TBG concentration. |
| Potential impact (below) | |
| Salicylates (>2 g/day) | Salicylates inhibit binding of T4 and T3 to TBG and transthyretin. An initial increase in serum FT4 is followed by return of FT4 to normal levels with sustained therapeutic serum salicylate concentrations, although total T4 levels may decrease by as much as 30%. |
| Other drugs: Carbamazepine Furosemide (>80 mg IV) Heparin Hydantoins Non-Steroidal Anti-inflammatory Drugs - Fenamates | These drugs may cause protein-binding site displacement. Furosemide has been shown to inhibit the protein binding of T4 to TBG and albumin, causing an increased free-T4 fraction in serum. Furosemide competes for T4-binding sites on TBG, prealbumin, and albumin, so that a single high dose can acutely lower the total T4 level. Phenytoin and carbamazepine reduce serum protein binding of levothyroxine, and total and FT4 may be reduced by 20% to 40%, but most patients have normal serum TSH levels and are clinically euthyroid. Closely monitor thyroid hormone parameters. |
| Potential impact: Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of levothyroxine, resulting in increased UNITHROID requirements. | |
|---|---|
| Phenobarbital Rifampin | Phenobarbital has been shown to reduce the response to thyroxine. Phenobarbital increases L-thyroxine metabolism by inducing uridine 5'-diphospho-glucuronosyltransferase (UGT) and leads to a lower T4 serum levels. Changes in thyroid status may occur if barbiturates are added or withdrawn from patients being treated for hypothyroidism. Rifampin has been shown to accelerate the metabolism of levothyroxine. |
| Potential impact: Administration of these enzyme inhibitors decreases the peripheral conversion of T4 to T3, leading to decreased T3 levels. However, serum T4 levels are usually normal but may occasionally be slightly increased. | |
| Beta-adrenergic antagonists (e.g., Propranolol >160 mg/day) | In patients treated with large doses of propranolol (>160 mg/day), T3 and T4 levels change slightly, TSH levels remain normal, and patients are clinically euthyroid. It should be noted that actions of particular beta-adrenergic antagonists may be impaired when the hypothyroid patient is converted to the euthyroid state. |
| Glucocorticoids (e.g., Dexamethasone ≥4 mg/day) | Short-term administration of large doses of glucocorticoids may decrease serum T3 concentrations by 30% with minimal change in serum T4 levels. However, long-term glucocorticoid therapy may result in slightly decreased T3 and T4 levels due to decreased TBG production (See above). |
| Other: Amiodarone | Amiodarone inhibits peripheral conversion of levothyroxine (T4) to triiodothyronine (T3) and may cause isolated biochemical changes (increase in serum free-T4, and decreased or normal free-T3) in clinically euthyroid patients. |
Clinical pharmacology
Information about the clinical pharmacology and actions of the drug in humans.12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action Thyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis. Triiodothyronine (T3) and L-thyroxine (T4) diffuse into the cell nucleus and bind to thyroid receptor proteins attached to DNA. This hormone nuclear receptor complex activates gene transcription and synthesis of messenger RNA and cytoplasmic proteins. The physiological actions of thyroid hormones are produced predominantly by T3, the majority of which (approximately 80%) is derived from T4 by deiodination in peripheral tissues. 12.2 Pharmacodynamics Oral levothyroxine sodium is a synthetic T4 hormone that exerts the same physiologic effect as endogenous T4, thereby maintaining normal T4 levels when a deficiency is present. 12.3 Pharmacokinetics Absorption Absorption of orally administered T4 from the gastrointestinal tract ranges from 40% to 80%. The majority of the levothyroxine dose is absorbed from the jejunum and upper ileum. The relative bioavailability of UNITHROID tablets, compared to an equal nominal dose of oral levothyroxine sodium solution, is approximately 97 to 99%. T4 absorption is increased by fasting, and decreased in malabsorption syndromes and by certain foods such as soybeans. Dietary fiber decreases bioavailability of T4. Absorption may also decrease with age. In addition, many drugs and foods affect T4 absorption [see Drug Interactions (7) ] . Distribution Circulating thyroid hormones are greater than 99% bound to plasma proteins, including thyroxine-binding globulin (TBG), thyroxine‑binding prealbumin (TBPA), and thyroxine-binding albumin (TBA), whose capacities and affinities vary for each hormone. The higher affinity of both TBG and TBPA for T4 partially explains the higher serum levels, slower metabolic clearance, and longer half‑life of T4 compared to T3. Protein-bound thyroid hormones exist in reverse equilibrium with small amounts of free hormone. Only unbound hormone is metabolically active. Many drugs and physiologic conditions affect the binding of thyroid hormones to serum proteins [see Drug Interactions (7) ] . Thyroid hormones do not readily cross the placental barrier [see Use in Specific Populations (8.1) ] . Elimination Metabolism T4 is slowly eliminated (Table 6). The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately 80 % of circulating T3 is derived from peripheral T4 by monodeiodination. The liver is the major site of degradation for both T4 and T3, with T4 deiodination also occurring at a number of additional sites, including the kidney and other tissues. Approximately 80% of the daily dose of T4 is deiodinated to yield equal amonts of T3 and reverse T3 (r T3). T3 and rT3 are further deiodinated to diiodothyronine. Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation. Excretion Thyroid hormones are primarily eliminated by the kidneys. A portion of the conjugated hormone reaches the colon unchanged and is eliminated in the feces. Approximately 20% of T4 is eliminated in the stool. Urinary excretion of T4 decreases with age. Table 6: Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients Hormone Ratio in Thyroglobulin Biologic Potency t½ (days) Protein Binding (%) 2 Levothyroxine (T4) 10–20 1 6–7 1 99.96 Liothyronine (T3) 1 4 ≤ 2 99.5 1 3 to 4 days in hyperthyroidism, 9 to 10 days in hypothyroidism 2 Includes TBG, TBPA, and TBA
| Hormone | Ratio in Thyroglobulin | Biologic Potency | t½ (days) | Protein Binding (%)2 |
|---|---|---|---|---|
| Levothyroxine (T4) | 10–20 | 1 | 6–71 | 99.96 |
| Liothyronine (T3) | 1 | 4 | ≤ 2 | 99.5 |
Mechanism of action
Information about the established mechanism(s) of the drugÕs action in humans at various levels (for example receptor, membrane, tissue, organ, whole body). If the mechanism of action is not known, this field contains a statement about the lack of information.12.1 Mechanism of Action Thyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis. Triiodothyronine (T3) and L-thyroxine (T4) diffuse into the cell nucleus and bind to thyroid receptor proteins attached to DNA. This hormone nuclear receptor complex activates gene transcription and synthesis of messenger RNA and cytoplasmic proteins. The physiological actions of thyroid hormones are produced predominantly by T3, the majority of which (approximately 80%) is derived from T4 by deiodination in peripheral tissues.
Pharmacodynamics
Information about any biochemical or physiologic pharmacologic effects of the drug or active metabolites related to the drugÕs clinical effect in preventing, diagnosing, mitigating, curing, or treating disease, or those related to adverse effects or toxicity.12.2 Pharmacodynamics Oral levothyroxine sodium is a synthetic T4 hormone that exerts the same physiologic effect as endogenous T4, thereby maintaining normal T4 levels when a deficiency is present.
Pharmacokinetics
Information about the clinically significant pharmacokinetics of a drug or active metabolites, for instance pertinent absorption, distribution, metabolism, and excretion parameters.12.3 Pharmacokinetics Absorption Absorption of orally administered T4 from the gastrointestinal tract ranges from 40% to 80%. The majority of the levothyroxine dose is absorbed from the jejunum and upper ileum. The relative bioavailability of UNITHROID tablets, compared to an equal nominal dose of oral levothyroxine sodium solution, is approximately 97 to 99%. T4 absorption is increased by fasting, and decreased in malabsorption syndromes and by certain foods such as soybeans. Dietary fiber decreases bioavailability of T4. Absorption may also decrease with age. In addition, many drugs and foods affect T4 absorption [see Drug Interactions (7) ] . Distribution Circulating thyroid hormones are greater than 99% bound to plasma proteins, including thyroxine-binding globulin (TBG), thyroxine‑binding prealbumin (TBPA), and thyroxine-binding albumin (TBA), whose capacities and affinities vary for each hormone. The higher affinity of both TBG and TBPA for T4 partially explains the higher serum levels, slower metabolic clearance, and longer half‑life of T4 compared to T3. Protein-bound thyroid hormones exist in reverse equilibrium with small amounts of free hormone. Only unbound hormone is metabolically active. Many drugs and physiologic conditions affect the binding of thyroid hormones to serum proteins [see Drug Interactions (7) ] . Thyroid hormones do not readily cross the placental barrier [see Use in Specific Populations (8.1) ] . Elimination Metabolism T4 is slowly eliminated (Table 6). The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately 80 % of circulating T3 is derived from peripheral T4 by monodeiodination. The liver is the major site of degradation for both T4 and T3, with T4 deiodination also occurring at a number of additional sites, including the kidney and other tissues. Approximately 80% of the daily dose of T4 is deiodinated to yield equal amonts of T3 and reverse T3 (r T3). T3 and rT3 are further deiodinated to diiodothyronine. Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation. Excretion Thyroid hormones are primarily eliminated by the kidneys. A portion of the conjugated hormone reaches the colon unchanged and is eliminated in the feces. Approximately 20% of T4 is eliminated in the stool. Urinary excretion of T4 decreases with age. Table 6: Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients Hormone Ratio in Thyroglobulin Biologic Potency t½ (days) Protein Binding (%) 2 Levothyroxine (T4) 10–20 1 6–7 1 99.96 Liothyronine (T3) 1 4 ≤ 2 99.5 1 3 to 4 days in hyperthyroidism, 9 to 10 days in hypothyroidism 2 Includes TBG, TBPA, and TBA
| Hormone | Ratio in Thyroglobulin | Biologic Potency | t½ (days) | Protein Binding (%)2 |
|---|---|---|---|---|
| Levothyroxine (T4) | 10–20 | 1 | 6–71 | 99.96 |
| Liothyronine (T3) | 1 | 4 | ≤ 2 | 99.5 |
Contraindications
Information about situations in which the drug product is contraindicated or should not be used because the risk of use clearly outweighs any possible benefit, including the type and nature of reactions that have been reported.4 CONTRAINDICATIONS UNITHROID is contraindicated in patients with uncorrected adrenal insufficiency [see Warnings and Precautions ( 5.3 )] . Uncorrected adrenal insufficiency ( 4 )
Description
General information about the drug product, including the proprietary and established name of the drug, the type of dosage form and route of administration to which the label applies, qualitative and quantitative ingredient information, the pharmacologic or therapeutic class of the drug, and the chemical name and structural formula of the drug.11 DESCRIPTION UNITHROID contains the active ingredient, levothyroxine, a synthetic crystalline levothyroxine (T4) in sodium salt form. It is chemically designated as L-3,3’,5,5’-tetraiodothyronine monosodium hydrate. Synthetic T4 is identical in chemical structure to the T4 produced in the human thyroid gland. Levothyroxine sodium has an empirical formula of C 15 H 10 I 4 N NaO 4 • H 2 O, molecular weight of 798.85 g/mol (anhydrous), and structural formula as shown: UNITHROID tablets for oral administration are supplied in the following strengths: 25 mcg, 50 mcg, 75 mcg, 88 mcg, 100 mcg, 112 mcg, 125 mcg, 137 mcg, 150 mcg, 175 mcg, 200 mcg and 300 mcg. Inactive Ingredients Acacia, colloidal silicon dioxide, corn starch, lactose, magnesium stearate, microcrystalline cellulose, and sodium starch glycolate. The following are the coloring additives per tablet strength: Strength (mcg) Color additive(s) 25 FD&C Yellow No. 6 Aluminum Lake 50 None 75 FD&C Red No. 40 Aluminum Lake, FD&C Blue No. 2 Aluminum Lake 88 D&C Yellow No. 10 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake 100 D&C Yellow No. 10 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake 112 D&C Red No. 27 Aluminum Lake 125 FD&C Yellow No. 6 Aluminum Lake, FD&C Red No. 40 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake 137 FD&C Blue No. 1 Aluminum Lake 150 FD&C Blue No. 2 Aluminum Lake 175 FD&C Blue No. 1 Aluminum Lake, D&C Red No. 27 Aluminum Lake 200 FD&C Red No. 40 Aluminum Lake 300 D&C Yellow No. 10 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake UNITHROID_structural_formula
| Strength (mcg) | Color additive(s) |
|---|---|
| 25 | FD&C Yellow No. 6 Aluminum Lake |
| 50 | None |
| 75 | FD&C Red No. 40 Aluminum Lake, FD&C Blue No. 2 Aluminum Lake |
| 88 | D&C Yellow No. 10 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake |
| 100 | D&C Yellow No. 10 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake |
| 112 | D&C Red No. 27 Aluminum Lake |
| 125 | FD&C Yellow No. 6 Aluminum Lake, FD&C Red No. 40 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake |
| 137 | FD&C Blue No. 1 Aluminum Lake |
| 150 | FD&C Blue No. 2 Aluminum Lake |
| 175 | FD&C Blue No. 1 Aluminum Lake, D&C Red No. 27 Aluminum Lake |
| 200 | FD&C Red No. 40 Aluminum Lake |
| 300 | D&C Yellow No. 10 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake |
Dosage and administration
Information about the drug product’s dosage and administration recommendations, including starting dose, dose range, titration regimens, and any other clinically sigificant information that affects dosing recommendations.2 DOSAGE AND ADMINISTRATION Administer once daily, on an empty stomach, one-half to one hour before breakfast with a full glass of water. ( 2.1 ) Administer at least 4 hours before or after drugs that are known to interfere with absorption ( 2.1 ) Evaluate the need for dose adjustments when regularly administering within one hour of certain foods that may affect absorption. ( 2.1 ) Starting dose depends on a variety of factors, including age, body weight, cardiovascular status, concomitant medical conditions (including pregnancy), concomitant medications, co-administered food, and the specific nature of the condition being treated. Peak therapeutic effect may not be attained for 4 to 6 weeks. ( 2.2 ) See full prescribing information for dosing in specific patient populations. ( 2.3 ) Adequacy of therapy determined with periodic monitoring of TSH and/or T4 as well as clinical status. ( 2.4 ) 2.1 General Administration Information Administer UNITHROID tablets orally as a single daily dose, on an empty stomach, one-half to one hour before breakfast. Administer UNITHROID at least 4 hours before or after drugs that are known to interfere with UNITHROID absorption [see Drug Interactions ( 7.1 )] . Evaluate the need for dose adjustments when regularly administering within one hour of certain foods that may affect UNITHROID absorption [see Drug Interactions ( 7.9 ), Clinical Pharmacology ( 12.3 )] . Administer UNITHROID to infants and children who cannot swallow intact tablets by crushing the tablet, suspending the freshly crushed tablet in a small amount (5 mL to 10 mL or 1 teaspoon to 2 teaspoons) of water and immediately administering the suspension by spoon or dropper. Do not store the suspension. Do not administer in foods that decrease absorption of UNITHROID, such as soybean-based infant formula [see Drug Interactions ( 7.9 )] . 2.2 General Principles of Dosing The dose of UNITHROID for hypothyroidism or pituitary TSH suppression depends on a variety of factors including: the patient's age, body weight, cardiovascular status, concomitant medical conditions (including pregnancy), concomitant medications, co-administered food and the specific nature of the condition being treated [see Dosage and Administration ( 2.3 ), Warnings and Precautions ( 5 ), Drug Interactions ( 7 )] . Dosing must be individualized to account for these factors and dose adjustments made based on periodic assessment of the patient's clinical response and laboratory parameters [see Dosage and Administration ( 2.4 )] . The peak therapeutic effect of a given dose of UNITHROID may not be attained for 4 to 6 weeks. 2.3 Dosing in Specific Populations Primary Hypothyroidism in Adults and in Adolescents in Whom Growth and Puberty Are Complete Start UNITHROID at the full replacement dose in otherwise healthy, non-elderly individuals who have been hypothyroid for only a short time (such as a few months). The average full replacement dose of UNITHROID is approximately 1.6 mcg per kg per day (for example: 100 mcg per day to 125 mcg per day for a 70 kg adult). Adjust the dose by 12.5 mcg to 25 mcg increments every 4 to 6 weeks until the patient is clinically euthyroid and the serum TSH returns to normal. Doses greater than 200 mcg per day are seldom required. An inadequate response to daily doses of greater than 300 mcg per day is rare and may indicate poor compliance, malabsorption, drug interactions, or a combination of these factors. For elderly patients or patients with underlying cardiac disease, start with a dose of 12.5 mcg to 25 mcg per day. Increase the dose every 6 to 8 weeks, as needed until the patient is clinically euthyroid and the serum TSH returns to normal. The full replacement dose of UNITHROID may be less than 1 mcg per kg per day in elderly patients. In patients with severe longstanding hypothyroidism, start with a dose of 12.5 mcg to 25 mcg per day. Adjust the dose in 12.5 mcg to 25 mcg increments every 2 to 4 weeks until the patient is clinically euthyroid and the serum TSH level is normalized. Secondary or Tertiary Hypothyroidism Start UNITHROID at the full replacement dose in otherwise healthy, non-elderly individuals. Start with a lower dose in elderly patients, patients with underlying cardiovascular disease or patients with severe longstanding hypothyroidism as described above. Serum TSH is not a reliable measure of UNITHROID dose adequacy in patients with secondary or tertiary hypothyroidism and should not be used to monitor therapy. Use the serum free-T4 level to monitor adequacy of therapy in this patient population. Titrate UNITHROID dosing per above instructions until the patient is clinically euthyroid and the serum free-T4 level is restored to the upper half of the normal range. Pediatric Dosage - Congenital or Acquired Hypothyroidism The recommended daily dose of UNITHROID in pediatric patients with hypothyroidism is based on body weight and changes with age as described in Table 1. Start UNITHROID at the full daily dose in most pediatric patients. Start at a lower starting dose in newborns (0 to 3 months) at risk for cardiac failure and in children at risk for hyperactivity (see below). Monitor for clinical and laboratory response [see Dosage and Administration ( 2.4 )] . Table 1: UNITHROID Dosing Guidelines for Pediatric Hypothyroidism Age Daily Dose Per Kg Body Weight a 0 to 3 months 10 mcg/kg daily to 15 mcg/kg daily 3 to 6 months 8 mcg/kg daily to 10 mcg/kg daily 6 to 12 months 6 mcg/kg daily to 8 mcg/kg daily 1 to 5 years 5 mcg/kg to 6 mcg/kg daily 6 to 12 years 4 mcg/kg to 5 mcg/kg daily Greater than 12 years but growth and puberty incomplete 2 mcg/kg to 3 mcg/kg daily Growth and puberty complete 1.6 mcg/kg daily a - The dose should be adjusted based on clinical response and laboratory parameters [see Warnings and Precautions ( 5.4 ), Drug Interactions ( 7.10 ), and Use In Specific Populations ( 8.4 )] . Newborns (0 to 3 months) at Risk for Cardiac Failure: Consider a lower starting dose in newborns at risk for cardiac failure. Increase the dose every 4 to 6 weeks as needed based on clinical and laboratory response. Pediatric Patients at Risk for Hyperactivity: To minimize the risk of hyperactivity in pediatric patients, start at one-fourth the recommended full replacement dose, and increase on a weekly basis by one-fourth the full recommended replacement dose until the full recommended replacement dose is reached. Pregnancy Pre-existing Hypothyroidism: UNITHROID dose requirements may increase during pregnancy. Measure serum TSH and free-T4 as soon as pregnancy is confirmed and, at minimum, during each trimester of pregnancy. In patients with primary hypothyroidism, maintain serum TSH in the trimester-specific reference range. For patients with serum TSH above the normal trimester-specific range, increase the dose of UNITHROID by 12.5 mcg daily to 25 mcg daily and measure TSH every 4 weeks until a stable UNITHROID dose is reached and serum TSH is within the normal trimester-specific range. Reduce UNITHROID dosage to pre-pregnancy levels immediately after delivery and measure serum TSH levels 4 to 8 weeks postpartum to ensure UNITHROID dose is appropriate. New Onset Hypothyroidism: Normalize thyroid function as rapidly as possible. In patients with moderate to severe signs and symptoms of hypothyroidism, start UNITHROID at the full replacement dose (1.6 mcg per kg body weight per day). In patients with mild hypothyroidism (TSH less than 10 mIU per liter) start UNITHROID at 1 mcg per kg body weight per day. Evaluate serum TSH every 4 weeks and adjust UNITHROID dosage until a serum TSH is within the normal trimester specific range [see Use in Specific Populations ( 8.1 )] . TSH Suppression in Well-Differentiated Thyroid Cancer The dose of UNITHROID should target TSH levels within the desired therapeutic range. This may require a UNITHROID dose of greater than 2 mcg per kg per day, depending on the target level for TSH suppression. 2.4 Monitoring TSH and/or Thyroxine (T4) Levels Assess the adequacy of therapy by periodic assessment of laboratory tests and clinical evaluation. Persistent clinical and laboratory evidence of hypothyroidism despite an apparent adequate replacement dose of UNITHROID may be evidence of inadequate absorption, poor compliance, drug interactions, or a combination of these factors. Adults In adult patients with primary hypothyroidism, monitor serum TSH levels after an interval of 6 to 8 weeks after any change in dose. In patients on a stable and appropriate replacement dose, evaluate clinical and biochemical response every 6 to 12 months and whenever there is a change in the patient’s clinical status. Pediatrics In patients with congenital hypothyroidism, assess the adequacy of replacement therapy by measuring both serum TSH and total or free-T. Monitor TSH and total or free-T4 in children as follows: 2 and 4 weeks after the initiation of treatment, 2 weeks after any change in dosage, and then every 3 to 12 months thereafter following dose stabilization until growth is completed. Poor compliance or abnormal values may necessitate more frequent monitoring. Perform routine clinical examination, including assessment of development, mental and physical growth, and bone maturation, at regular intervals. While the general aim of therapy is to normalize the serum TSH level, TSH may not normalize in some patients due to in utero hypothyroidism causing a resetting of pituitary-thyroid feedback. Failure of the serum T4 to increase into the upper half of the normal range within 2 weeks of initiation of UNITHROID therapy and/or of the serum TSH to decrease below 20 mIU per liter within 4 weeks may indicate the child is not receiving adequate therapy. Assess compliance, dose of medication administered, and method of administration prior to increasing the dose of UNITHROID [see Warnings and Precautions ( 5.1 ) and Use in Specific Populations ( 8.4 )] )]. Secondary and Tertiary Hypothyroidism Monitor serum free-T4 levels and maintain in the upper half of the normal range in these patients.
| 0 to 3 months | 10 mcg/kg daily to 15 mcg/kg daily |
| 3 to 6 months | 8 mcg/kg daily to 10 mcg/kg daily |
| 6 to 12 months | 6 mcg/kg daily to 8 mcg/kg daily |
| 1 to 5 years | 5 mcg/kg to 6 mcg/kg daily |
| 6 to 12 years | 4 mcg/kg to 5 mcg/kg daily |
| Greater than 12 years but growth and puberty incomplete | 2 mcg/kg to 3 mcg/kg daily |
| Growth and puberty complete | 1.6 mcg/kg daily |
Dosage forms and strengths
Information about all available dosage forms and strengths for the drug product to which the labeling applies. This field may contain descriptions of product appearance.3 DOSAGE FORMS AND STRENGTHS UNITHROID tablets are round and color-coded available as follows: Strength (mcg) Color Tablet Markings 25 Peach JSP / 513 50 White JSP / 514 75 Purple JSP / 515 88 Olive JSP / 561 100 Yellow JSP / 516 112 Rose JSP / 562 125 Tan JSP / 519 137 Blue JSP / 564 150 Light Blue JSP / 520 175 Lilac JSP / 563 200 Pink JSP / 522 300 Green JSP / 523 Tablets: 25 mcg, 50 mcg, 75 mcg, 88 mcg, 100 mcg, 112 mcg, 125 mcg, 137 mcg, 150 mcg, 175 mcg, 200mcg, 300 mcg ( 3 )
| 25 | Peach | JSP / 513 |
| 50 | White | JSP / 514 |
| 75 | Purple | JSP / 515 |
| 88 | Olive | JSP / 561 |
| 100 | Yellow | JSP / 516 |
| 112 | Rose | JSP / 562 |
| 125 | Tan | JSP / 519 |
| 137 | Blue | JSP / 564 |
| 150 | Light Blue | JSP / 520 |
| 175 | Lilac | JSP / 563 |
| 200 | Pink | JSP / 522 |
| 300 | Green | JSP / 523 |
Indications and usage
A statement of each of the drug products indications for use, such as for the treatment, prevention, mitigation, cure, or diagnosis of a disease or condition, or of a manifestation of a recognized disease or condition, or for the relief of symptoms associated with a recognized disease or condition. This field may also describe any relevant limitations of use.1 INDICATIONS AND USAGE Hypothyroidism UNITHROID is indicated in pediatric and adult patients as a replacement therapy in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism. Pituitary Thyrotropin (Thyroid-Stimulating Hormone, TSH) Suppression UNITHROID is indicated in pediatric and adult patients as an adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer. Limitations of Use: UNITHROID is not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients as there are no clinical benefits and overtreatment with UNITHROID may induce hyperthyroidism [see Warnings and Precautions ( 5.4 )] . UNITHROID is not indicated for treatment of hypothyroidism during the recovery phase of subacute thyroiditis. UNITHROID is L-thyroxine (T4) indicated in pediatric and adult patients for: Hypothyroidism: As replacement in primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism. ( 1 ) Pituitary Thyrotropin (Thyroid-Stimulating Hormone, TSH) Suppression: As an adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer. ( 1 ) Limitations of Use: Not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients. ( 1 ) Not indicated for treatment of hypothyroidism during the recovery phase of subacute thyroiditis. ( 1 )
Spl product data elements
Usually a list of ingredients in a drug product.Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato FD&C Yellow No. 6 Peach JSP;513 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato FD&C Blue No. 1 D&C Red No. 27 Lilac JSP;563 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato FD&C Red No. 40 PINK JSP;522 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato D&C Yellow No. 10 FD&C Yellow No. 6 fd&c blue no. 1 GREEN JSP;523 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato WHITE JSP;514 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato FD&C Red No. 40 FD&C Blue No. 2 PURPLE JSP;515 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato D&C Yellow No. 10 FD&C Yellow No. 6 FD&C Blue No. 1 Olive JSP;561 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato D&C Yellow No. 10 FD&C Yellow No. 6 YELLOW JSP;516 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato D&C Red No. 27 Rose JSP;562 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato FD&C Yellow No. 6 FD&C Red No. 40 FD&C Blue No. 1 Tan JSP;519 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato FD&C Blue No. 1 BLUE JSP;564 ROUND Unithroid levothyroxine sodium levothyroxine sodium levothyroxine levothyroxine sodium anhydrous silicon dioxide Lactose, Unspecified Form magnesium stearate cellulose, microcrystalline starch, corn acacia sodium starch glycolate type a potato FD&C Blue No. 2 Light Blue JSP;520 ROUND
Carcinogenesis and mutagenesis and impairment of fertility
Information about carcinogenic, mutagenic, or fertility impairment potential revealed by studies in animals. Information from human data about such potential is part of the warnings field.13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of levothyroxine sodium.
Nonclinical toxicology
Information about toxicology in non-human subjects.13 NONCLINICAL TOXICOLOGY 13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of levothyroxine sodium.
Package label principal display panel
The content of the principal display panel of the product package, usually including the product’s name, dosage forms, and other key information about the drug product.PRINCIPAL DISPLAY PANEL - 25 mcg (0.025 mg) jsp NDC 60846-801-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 25 mcg (0.025 mg) Rx ONLY 100 TABLETS 25
PRINCIPAL DISPLAY PANEL - 50 mcg (0.05 mg) jsp NDC 60846-802-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 50 mcg (0.05 mg) Rx ONLY 100 TABLETS 50
PRINCIPAL DISPLAY PANEL - 75 mcg (0.075 mg) jsp NDC 60846-803-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 75 mcg (0.075 mg) Rx ONLY 100 TABLETS 75
PRINCIPAL DISPLAY PANEL - 88 mcg (0.088 mg) jsp NDC 60846-804-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 88 mcg (0.088 mg) Rx ONLY 100 TABLETS 88
PRINCIPAL DISPLAY PANEL - 100 mcg (0.1 mg) jsp NDC 60846-805-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 100 mcg (0.1 mg) Rx ONLY 100 TABLETS 100
PRINCIPAL DISPLAY PANEL - 112 mcg (0.112 mg) jsp NDC 60846-806-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 112 mcg (0.112 mg) Rx ONLY 100 TABLETS 112
PRINCIPAL DISPLAY PANEL - 125 mcg (0.125 mg) jsp NDC 60846-807-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 125 mcg (0.125 mg) Rx ONLY 100 TABLETS 125
PRINCIPAL DISPLAY PANEL - 137 mcg (0.137 mg) jsp NDC 60846-808-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 137 mcg (0.137 mg) Rx ONLY 100 TABLETS 137
PRINCIPAL DISPLAY PANEL - 150 mcg (0.15 mg) jsp NDC 60846-809-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 150 mcg (0.15 mg) Rx ONLY 100 TABLETS 150
PRINCIPAL DISPLAY PANEL - 175 mcg (0.175 mg) jsp NDC 60846-810-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 175 mcg (0.175 mg) Rx ONLY 100 TABLETS 175
PRINCIPAL DISPLAY PANEL - 200 mcg (0.2 mg) jsp NDC 60846-811-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 200 mcg (0.200 mg) Rx ONLY 100 TABLETS 200
PRINCIPAL DISPLAY PANEL - 300 mcg (0.3 mg) jsp NDC 60846-812-01 UNITHROID® (Levothyroxine Sodium Tablets, USP) 300 mcg (0.300 mg) Rx ONLY 100 TABLETS 300
Unithroid: Information for patients
Information necessary for patients to use the drug safely and effectively, such as precautions concerning driving or the concomitant use of other substances that may have harmful additive effects.17 PATIENT COUNSELING INFORMATION Dosing and Administration Instruct patients to take UNITHROID only as directed by their healthcare provider. Instruct patients to take UNITHROID as a single dose, preferably on an empty stomach, one-half to one hour before breakfast with a full glass of water to avoid choking or gagging. Inform patients that agents such as iron and calcium supplements and antacids can decrease the absorption of levothyroxine. Instruct patients not to take UNITHROID tablets within 4 hours of these agents. Instruct patients to notify their healthcare provider should they become pregnant or breastfeeding or are thinking of becoming pregnant, while taking UNITHROID. Important Information Inform patients that it may take several weeks before they notice an improvement in symptoms. Inform patients that the levothyroxine in UNITHROID is intended to replace a hormone that is normally produced by the thyroid gland. Generally, replacement therapy is to be taken for life. Inform patients that UNITHROID should not be used as a primary or adjunctive therapy in a weight control program. Instruct patients to notify their healthcare provider if they are taking any other medications, including prescription and over‑the-counter preparations. Instruct patients to notify their healthcare provider of any other medical conditions you may have, particularly heart disease, diabetes, clotting disorders, and adrenal or pituitary gland problems as the dose of medications used to control these other conditions may need to be adjusted while taking UNITHROID. If they have diabetes, instruct patients to monitor their blood and/or urinary glucose levels as directed by their physician and immediately report any changes to their physician. If patients are taking anticoagulants, their clotting status should be checked frequently. Instruct patients to notify their physician or dentist if they are taking UNITHROID prior to any surgery. Adverse Reactions Instruct patients to notify their healthcare provider if they experience any of the following symptoms: rapid or irregular heartbeat, chest pain, shortness of breath, leg cramps, headache, nervousness, irritability, sleeplessness, tremors, change in appetite, weight gain or loss, vomiting, diarrhea, excessive sweating, heat intolerance, fever, changes in menstrual periods, hives or skin rash, or any other unusual medical event Inform patients that partial hair loss may occur rarely during the first few months of UNITHROID therapy; this is usually temporary. Manufactured by: Jerome Stevens Pharmaceuticals, Inc. Bohemia, NY 11716 Distributed by: Amneal Specialty, a division of Amneal Pharmaceuticals LLC Bridgewater, NJ 08807 Revised: 06/2019
Geriatric use
Information about any limitations on any geriatric indications, needs for specific monitoring, hazards associated with use of the drug in the geriatric population.8.5 Geriatric Use Because of the increased prevalence of cardiovascular disease among the elderly, initiate UNITHROID at less than the full replacement dose [see Dosage and Administration ( 2.3 ) and Warnings and Precautions ( 5.1 )] . Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with levothyroxine overtreatment in the elderly.
Labor and delivery
Information about the drug’s use during labor or delivery, whether or not the use is stated in the indications section of the labeling, including the effect of the drug on the mother and fetus, on the duration of labor or delivery, on the possibility of delivery-related interventions, and the effect of the drug on the later growth, development, and functional maturation of the child.8.2 Lactation Risk Summary Limited published studies report that levothyroxine is present in human milk. However, there is insufficient information to determine the effects of levothyroxine on the breastfed infant and no available information on the effects of levothyroxine on milk production. Adequate levothyroxine treatment during lactation may normalize milk production in hypothyroid lactating mothers. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for UNITHROID and any potential adverse effects on the breastfed infant from UNITHROID or from the underlying maternal condition.
Pediatric use
Information about any limitations on any pediatric indications, needs for specific monitoring, hazards associated with use of the drug in any subsets of the pediatric population (such as neonates, infants, children, or adolescents), differences between pediatric and adult responses to the drug, and other information related to the safe and effective pediatric use of the drug.8.4 Pediatric Use The initial dose of UNITHROID varies with age and body weight. Dosing adjustments are based on an assessment of the individual patient’s clinical and laboratory parameters [see Dosage and Administration ( 2.3 , 2.4 )] . In children in whom a diagnosis of permanent hypothyroidism has not been established, discontinue UNITHROID for a trial period, but only after the child is at least 3 years of age. Obtain serum T4 and TSH levels at the end of the trial period, and use laboratory test results and clinical assessments to guide diagnosis and treatment, if warranted. Congenital Hypothyroidism [see Dosage and Administration ( 2.3 , 2.4 )] Rapid restoration of normal serum T4 concentrations is essential for preventing the adverse effects of congenital hypothyroidism on intellectual development as well as on overall physical growth and maturation. Therefore, initiate UNITHROID therapy immediately upon diagnosis. Levothyroxine is generally continued for life in these patients. Closely monitor infants during the first 2 weeks of UNITHROID therapy for cardiac overload, arrhythmias, and aspiration from avid suckling. Closely monitor patients to avoid undertreatment or overtreatment. Undertreatment may have deleterious effects on intellectual development and linear growth. Overtreatment is associated with craniosynostosis in infants, may adversely affect the tempo of brain maturation, and may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature. Acquired Hypothyroidism in Pediatric Patients Closely monitor patients to avoid undertreatment and overtreatment. Undertreatment may result in poor school performance due to impaired concentration and slowed mentation and in reduced adult height. Overtreatment may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature. Treated children may manifest a period of catch-up growth, which may be adequate in some cases to normalize adult height. In children with severe or prolonged hypothyroidism, catch-up growth may not be adequate to normalize adult height.
Pregnancy
Information about effects the drug may have on pregnant women or on a fetus. This field may be ommitted if the drug is not absorbed systemically and the drug is not known to have a potential for indirect harm to the fetus. It may contain information about the established pregnancy category classification for the drug. (That information is nominally listed in the teratogenic_effects field, but may be listed here instead.)8.1 Pregnancy Risk Summary Experience with levothyroxine use in pregnant women, including data from post-marketing studies, have not reported increased rates of major birth defects or miscarriages (see Data) . There are risks to the mother and fetus associated with untreated hypothyroidism in pregnancy. Since thyroid-stimulating hormone (TSH) levels may increase during pregnancy, TSH should be monitored and UNITHROID dosage adjusted during pregnancy (see Clinical Considerations) . There are no animal studies conducted with levothyroxine during pregnancy. UNITHROID should not be discontinued during pregnancy and hypothyroidism diagnosed during pregnancy should be promptly treated. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. Clinical Considerations Disease-Associated Maternal and/or Embryo/Fetal Risk Maternal hypothyroidism during pregnancy is associated with a higher rate of complications, including spontaneous abortion, gestational hypertension, pre-eclampsia, stillbirth, and premature delivery. Untreated maternal hypothyroidism may have an adverse effect on fetal neurocognitive development. Dose Adjustments During Pregnancy and the Postpartum Period Pregnancy may increase UNITHROID requirements. Serum TSH level should be monitored and the UNITHROID dosage adjusted during pregnancy. Since postpartum TSH levels are similar to preconception values, the UNITHROID dosage should return to the pre-pregnancy dose immediately after delivery [see Dosage and Administration ( 2.3 )] . Data Human Data Levothyroxine is approved for use as a replacement therapy for hypothyroidism. There is a long experience of levothyroxine use in pregnant women, including data from post-marketing studies that have not reported increased rates of fetal malformations, miscarriages or other adverse maternal or fetal outcomes associated with levothyroxine use in pregnant women.
Use in specific populations
Information about use of the drug by patients in specific populations, including pregnant women and nursing mothers, pediatric patients, and geriatric patients.8 USE IN SPECIFIC POPULATIONS Pregnancy may require the use of higher doses of levothyroxine ( 2.3 , 8.1 ) 8.1 Pregnancy Risk Summary Experience with levothyroxine use in pregnant women, including data from post-marketing studies, have not reported increased rates of major birth defects or miscarriages (see Data) . There are risks to the mother and fetus associated with untreated hypothyroidism in pregnancy. Since thyroid-stimulating hormone (TSH) levels may increase during pregnancy, TSH should be monitored and UNITHROID dosage adjusted during pregnancy (see Clinical Considerations) . There are no animal studies conducted with levothyroxine during pregnancy. UNITHROID should not be discontinued during pregnancy and hypothyroidism diagnosed during pregnancy should be promptly treated. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. Clinical Considerations Disease-Associated Maternal and/or Embryo/Fetal Risk Maternal hypothyroidism during pregnancy is associated with a higher rate of complications, including spontaneous abortion, gestational hypertension, pre-eclampsia, stillbirth, and premature delivery. Untreated maternal hypothyroidism may have an adverse effect on fetal neurocognitive development. Dose Adjustments During Pregnancy and the Postpartum Period Pregnancy may increase UNITHROID requirements. Serum TSH level should be monitored and the UNITHROID dosage adjusted during pregnancy. Since postpartum TSH levels are similar to preconception values, the UNITHROID dosage should return to the pre-pregnancy dose immediately after delivery [see Dosage and Administration ( 2.3 )] . Data Human Data Levothyroxine is approved for use as a replacement therapy for hypothyroidism. There is a long experience of levothyroxine use in pregnant women, including data from post-marketing studies that have not reported increased rates of fetal malformations, miscarriages or other adverse maternal or fetal outcomes associated with levothyroxine use in pregnant women. 8.2 Lactation Risk Summary Limited published studies report that levothyroxine is present in human milk. However, there is insufficient information to determine the effects of levothyroxine on the breastfed infant and no available information on the effects of levothyroxine on milk production. Adequate levothyroxine treatment during lactation may normalize milk production in hypothyroid lactating mothers. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for UNITHROID and any potential adverse effects on the breastfed infant from UNITHROID or from the underlying maternal condition. 8.4 Pediatric Use The initial dose of UNITHROID varies with age and body weight. Dosing adjustments are based on an assessment of the individual patient’s clinical and laboratory parameters [see Dosage and Administration ( 2.3 , 2.4 )] . In children in whom a diagnosis of permanent hypothyroidism has not been established, discontinue UNITHROID for a trial period, but only after the child is at least 3 years of age. Obtain serum T4 and TSH levels at the end of the trial period, and use laboratory test results and clinical assessments to guide diagnosis and treatment, if warranted. Congenital Hypothyroidism [see Dosage and Administration ( 2.3 , 2.4 )] Rapid restoration of normal serum T4 concentrations is essential for preventing the adverse effects of congenital hypothyroidism on intellectual development as well as on overall physical growth and maturation. Therefore, initiate UNITHROID therapy immediately upon diagnosis. Levothyroxine is generally continued for life in these patients. Closely monitor infants during the first 2 weeks of UNITHROID therapy for cardiac overload, arrhythmias, and aspiration from avid suckling. Closely monitor patients to avoid undertreatment or overtreatment. Undertreatment may have deleterious effects on intellectual development and linear growth. Overtreatment is associated with craniosynostosis in infants, may adversely affect the tempo of brain maturation, and may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature. Acquired Hypothyroidism in Pediatric Patients Closely monitor patients to avoid undertreatment and overtreatment. Undertreatment may result in poor school performance due to impaired concentration and slowed mentation and in reduced adult height. Overtreatment may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature. Treated children may manifest a period of catch-up growth, which may be adequate in some cases to normalize adult height. In children with severe or prolonged hypothyroidism, catch-up growth may not be adequate to normalize adult height. 8.5 Geriatric Use Because of the increased prevalence of cardiovascular disease among the elderly, initiate UNITHROID at less than the full replacement dose [see Dosage and Administration ( 2.3 ) and Warnings and Precautions ( 5.1 )] . Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with levothyroxine overtreatment in the elderly.
How supplied
Information about the available dosage forms to which the labeling applies, and for which the manufacturer or distributor is responsible. This field ordinarily includes the strength of the dosage form (in metric units), the units in which the dosage form is available for prescribing, appropriate information to facilitate identification of the dosage forms (such as shape, color, coating, scoring, and National Drug Code), and special handling and storage condition information.16 HOW SUPPLIED/STORAGE AND HANDLING UNITHROID (levothyroxine sodium) tablets are round and color-coded available as follows: Strength (mcg) Color Tablet Markings NDC - bottles of 100 25 Peach JSP / 513 NDC 60846-801-01 50 White JSP / 514 NDC 60846-802-01 75 Purple JSP / 515 NDC 60846-803-01 88 Olive JSP / 561 NDC 60846-804-01 100 Yellow JSP / 516 NDC 60846-805-01 112 Rose JSP / 562 NDC 60846-806-01 125 Tan JSP / 519 NDC 60846-807-01 137 Blue JSP / 564 NDC 60846-808-01 150 Light Blue JSP / 520 NDC 60846-809-01 175 Lilac JSP / 563 NDC 60846-810-01 200 Pink JSP / 522 NDC 60846-811-01 300 Green JSP / 523 NDC 60846-812-01 STORAGE CONDITIONS Store between 20°C-25°C (68°F-77°F) with excursions permitted between 15°C-30°C (59°F-86°F).
| Strength (mcg) | Color | Tablet Markings | NDC - bottles of 100 |
|---|---|---|---|
| 25 | Peach | JSP / 513 | NDC 60846-801-01 |
| 50 | White | JSP / 514 | NDC 60846-802-01 |
| 75 | Purple | JSP / 515 | NDC 60846-803-01 |
| 88 | Olive | JSP / 561 | NDC 60846-804-01 |
| 100 | Yellow | JSP / 516 | NDC 60846-805-01 |
| 112 | Rose | JSP / 562 | NDC 60846-806-01 |
| 125 | Tan | JSP / 519 | NDC 60846-807-01 |
| 137 | Blue | JSP / 564 | NDC 60846-808-01 |
| 150 | Light Blue | JSP / 520 | NDC 60846-809-01 |
| 175 | Lilac | JSP / 563 | NDC 60846-810-01 |
| 200 | Pink | JSP / 522 | NDC 60846-811-01 |
| 300 | Green | JSP / 523 | NDC 60846-812-01 |
Boxed warning
Information about contraindications or serious warnings, particularly those that may lead to death or serious injury.WARNING: NOT FOR TREATMENT OF OBESITY OR FOR WEIGHT LOSS Thyroid hormones, including UNITHROID, either alone or with other therapeutic agents, should not be used for the treatment of obesity or for weight loss. 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 [see Adverse Reactions ( 6 ), Drug Interactions ( 7.7 ), and Overdosage ( 10 )] . WARNING: NOT FOR TREATMENT OF OBESITY OR FOR WEIGHT LOSS See full prescribing information for complete boxed warning. Thyroid hormones, including UNITHROID, should not be used for the treatment of obesity or for weight loss. Doses beyond the range of daily hormonal requirements may produce serious or even life threatening manifestations of toxicity ( 6 , 10 ).
Disclaimer: Do not rely on openFDA or Phanrmacy Near Me to make decisions regarding medical care. While we make every effort to ensure that data is accurate, you should assume all results are unvalidated. Source: OpenFDA, Healthporta Drugs API