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| Product NDC Code | 63323-895 | ||||
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| Drug Name | Levothyroxine sodium |
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| Type | Generic | ||||
| Pharm Class | Thyroxine [CS], l-Thyroxine [EPC] |
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| Route | INTRAVENOUS | ||||
| Dosage Form | INJECTION, SOLUTION | ||||
| RxCUI drug identifier | 2166148, 2166193, 2166196 |
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| Application Number | NDA210632 | ||||
| Labeler Name | Fresenius Kabi USA, LLC | ||||
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Overdosage of Levothyroxine Sodium
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 ) and Adverse Reactions ( 6 )]. In addition, confusion and disorientation may occur. Cerebral embolism, shock, coma, and death have been reported. Reduce the Levothyroxine Sodium Injection dose or temporarily discontinue if signs or symptoms of overdosage occur. Initiate appropriate supportive treatment as dictated by the patient's medical status.
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 Adverse reactions associated with levothyroxine are primarily those of hyperthyroidism due to therapeutic overdosage [see Warnings and Precautions ( 5 ) , 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, muscle spasm 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: flushing, rash Seizures have been reported rarely with the institution of levothyroxine therapy. Adverse reactions associated with Levothyroxine Sodium Injection are primarily those of hyperthyroidism due to therapeutic overdosage: fatigue, increased appetite, weight loss, heat intolerance, fever, excessive sweating, headache, hyperactivity, nervousness, anxiety, irritability, emotional lability, insomnia, tremors, muscle weakness, muscle spasm, palpitations, tachycardia, arrhythmias, increased pulse and blood pressure, heart failure, angina, myocardial infarction, cardiac arrest, dyspnea, diarrhea, vomiting, abdominal cramps, elevations in liver function tests, flushing, and rash. ( 6 ) To report SUSPECTED ADVERSE REACTIONS, contact Fresenius Kabi USA, LLC at 1-800-551-7176 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch. 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.
Drug and or laboratory test interactions
Information about any known interference by the drug with laboratory tests.7.8 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 9,000.
Levothyroxine Sodium 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., synthesis, secretion, catabolism, protein binding, and target tissue response) that may alter the therapeutic response to Levothyroxine Sodium Injection. ( 7 ) 7.1 Drugs Known to Affect Thyroid Hormone Pharmacokinetics Many drugs affect thyroid hormone pharmacokinetics and metabolism (e.g., synthesis, secretion, catabolism, protein binding, and target tissue response) and may alter the therapeutic response to Levothyroxine Sodium Injection (see Tables 1 - 3 ). Table 1: Drugs That May Alter T 4 and Triiodothyronine (T 3 ) Serum Transport Without Effecting Free Thyroxine (FT 4 ) 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 levothyroxine results in an initial transient increase in FT 4 . Continued administration results in a decrease in serum T 4 and normal FT 4 and TSH concentrations. Salicylates (> 2 g/day) Salicylates inhibit binding of T 4 and T 3 to TBG and transthyretin. An initial increase in serum FT 4 is followed by return of FT 4 to normal levels with sustained therapeutic serum salicylate concentrations, although total T 4 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 increase 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 free T4 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 2: Drugs That May Alter Hepatic Metabolism of T 4 (Hypothyroidism) Potential impact: Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of levothyroxine, resulting in increased levothyroxine 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 3: Drugs That May Decrease Conversion of T 4 to T 3 Potential impact: Administration of these enzyme inhibitors decreases the peripheral conversion of T 4 to T 3 , leading to decreased T 3 levels. However, serum T 4 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), T 3 and T 4 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 T 3 concentrations by 30% with minimal change in serum T 4 levels. However, long-term glucocorticoid therapy may result in slightly decreased T 3 and T 4 levels due to decreased TBG production (See above). Other drugs: 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 levothyroxine to antidiabetic or insulin therapy may result in increased antidiabetic agent or insulin requirements. Careful monitoring of glycemic control is recommended. 7.3 Oral Anticoagulants Levothyroxine increases the response to oral anticoagulant therapy. Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state. Closely monitor coagulation tests to permit appropriate and timely dosage adjustments. 7.4 Digitalis Glycosides Levothyroxine 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 levothyroxine 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. Levothyroxine may accelerate the onset of action of tricyclics. Administration of sertraline in patients stabilized on levothyroxine may result in increased levothyroxine requirements. 7.6 Ketamine Concurrent use of ketamine and levothyroxine may produce marked hypertension and tachycardia. Closely monitor blood pressure and heart rate in these patients. 7.7 Sympathomimetics Concurrent use may of sympathomimetics and levothyroxine 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 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 9,000.
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| 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 levothyroxine 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 increase 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 free T4 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 levothyroxine requirements. | |
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| 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. | |
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| 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 drugs: 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 levothyroxine (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 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 Distribution Circulating thyroid hormones are greater than 99% bound to plasma proteins, including thyroxine binding globulin (TBG), thyroxine binding prealbumin (TBPA), and 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 )]. Metabolism T4 is slowly eliminated. The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately eighty percent 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 amounts of T3 and reverse T3 (rT3). 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, where it is hydrolyzed and eliminated in feces as the free hormones. Urinary excretion of T4 decreases with age. Table 1: Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients T 4 : Levothyroxine T 3 : Liothyronine 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 Half-Life (Days) Protein Binding (%) 2 T 4 10 to 20 1 6 to 8 1 99.96 T 3 1 4 ≤ 2 99.5
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| T4 | 10 to 20 | 1 | 6 to 81 | 99.96 |
| 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 levothyroxine (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 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 Distribution Circulating thyroid hormones are greater than 99% bound to plasma proteins, including thyroxine binding globulin (TBG), thyroxine binding prealbumin (TBPA), and 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 )]. Metabolism T4 is slowly eliminated. The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately eighty percent 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 amounts of T3 and reverse T3 (rT3). 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, where it is hydrolyzed and eliminated in feces as the free hormones. Urinary excretion of T4 decreases with age. Table 1: Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients T 4 : Levothyroxine T 3 : Liothyronine 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 Half-Life (Days) Protein Binding (%) 2 T 4 10 to 20 1 6 to 8 1 99.96 T 3 1 4 ≤ 2 99.5
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| T4 | 10 to 20 | 1 | 6 to 81 | 99.96 |
| 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 Uncorrected adrenal insufficiency [see Warnings and Precautions ( 5.2 )] 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 Levothyroxine Sodium Injection contains synthetic crystalline levothyroxine (T4) in sodium salt form. Levothyroxine sodium has an empirical formula of C 15 H 10 I 4 NNaO 4 , a molecular weight of 798.85 g/mol (anhydrous), and the following structural formula: Levothyroxine Sodium Injection is a sterile, preservative free, clear, colorless, sterile solution for intravenous administration available as: 100 mcg per 5 mL (20 mcg per mL), 200 mcg per 5 mL (40 mcg per mL), and 500 mcg per 5 mL (100 mcg per mL). Each mL of Levothyroxine Sodium Injection also contains 10 mg Tromethamine, USP; 0.14 mg Sodium Iodide, USP; 6.48 mg Sodium Chloride, USP; and Water for Injection, USP Sodium hydroxide, NF and/or Hydrochloric acid, USP may have been added for pH adjustment (9.5 – 10.8). Levothyroxine Sodium Injection is in single dose clear glass vials. Structural Formula
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 Consider the age, general physical condition, cardiac risk factors, and clinical severity of myxedema and duration of myxedema symptoms when determining dosages of Levothyroxine Sodium Injection. ( 2.1 ) Start with lower doses in elderly patients and in patients with underlying cardiovascular disease. ( 2.1 ) The recommended loading dose is 300 mcg to 500 mcg administered intravenously. ( 2.1 ) The recommended maintenance dose is 50 mcg to 100 mcg administered intravenously daily until the patient can tolerate oral therapy. ( 2.1 ) Administer Levothyroxine Sodium Injection intravenously at a rate not to exceed 100 mcg per minute. ( 2.2 ) Do not add Levothyroxine Sodium Injection to intravenous fluids. ( 2.2 ) 2.1 Dosage Consider the age, general physical condition, cardiac risk factors, and clinical severity of myxedema and duration of myxedema symptoms when determining the starting and maintenance dosages of Levothyroxine Sodium Injection. Start with lower doses in elderly patients and in patients with underlying cardiovascular disease [see Warnings and Precautions ( 5.1 ) and Use in Specific Populations ( 8.5 )]. The recommended loading dose of Levothyroxine Sodium Injection is 300 mcg to 500 mcg administered intravenously. The recommended maintenance dose of Levothyroxine Sodium Injection is 50 mcg to 100 mcg administered intravenously daily until the patient can tolerate oral therapy. 2.2 Administration Instructions Administer Levothyroxine Sodium Injection as an intravenous injection at a rate not to exceed 100 mcg per minute. Do not add Levothyroxine Sodium Injection to intravenous fluids. Inspect Levothyroxine Sodium Injection visually prior to injection. It should appear clear and colorless, solution free of visible particulates. Do not use if particulate matter or coloration is seen. Discard any unused portion.
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 Levothyroxine Sodium Injection is clear, colorless solution supplied as: 100 mcg per 5 mL (20 mcg per mL) single-dose vial 200 mcg per 5 mL (40 mcg per mL) single-dose vial 500 mcg per 5 mL (100 mcg per mL) single-dose vial Injection: 100 mcg per 5 mL (20 mcg per mL) single-dose vial 200 mcg per 5 mL (40 mcg per mL) single-dose vial 500 mcg per 5 mL (100 mcg per mL) single-dose vial ( 3 )
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 Levothyroxine Sodium Injection is indicated for the treatment of myxedema coma. Levothyroxine Sodium Injection is L-thyroxine (T4) indicated in adult patients for the treatment of myxedema coma. ( 1 ) Limitations of Use: Not recommended as a substitute for oral levothyroxine sodium because the relative bioavailability of Levothyroxine Sodium Injection to oral levothyroxine sodium has not been established and there is a risk of inaccurate dose conversion. ( 1 ) Limitations of Use: Not recommended as a substitute for oral levothyroxine sodium because the relative bioavailability of Levothyroxine Sodium Injection to oral levothyroxine sodium has not been established and there is a risk of inaccurate dose conversion.
Spl product data elements
Usually a list of ingredients in a drug product.Levothyroxine Sodium Levothyroxine Sodium Levothyroxine sodium Levothyroxine Levothyroxine Sodium Anhydrous Tromethamine Sodium Iodide Sodium Chloride Sodium Hydroxide Hydrochloric Acid Levothyroxine Sodium Levothyroxine Sodium Levothyroxine sodium Levothyroxine Levothyroxine Sodium Anhydrous Tromethamine Sodium Iodide Sodium Chloride Sodium Hydroxide Hydrochloric Acid Levothyroxine Sodium Levothyroxine Sodium Levothyroxine sodium Levothyroxine Levothyroxine Sodium Anhydrous Tromethamine Sodium Iodide Sodium Chloride Sodium Hydroxide Hydrochloric Acid
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 Injection.
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 Injection.
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.PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Vial Label NDC 63323-885-10 Levothyroxine Sodium Injection 100 mcg per 5 mL (20 mcg per mL) For intravenous use. Preservative free. 5 mL Single-Dose Vial- Discard Unused Portion PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Vial Label
PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Carton Panel NDC 63323-885-10 Levothyroxine Sodium Injection 100 mcg per 5 mL (20 mcg per mL) For intravenous use. Preservative free. 5 mL Single-Dose Vial- Discard Unused Portion Rx only PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Carton Panel
PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Vial Label NDC 63323-895-10 Levothyroxine Sodium Injection 500 mcg per 5 mL (100 mcg per mL) For intravenous use. Preservative free. 5 mL Single-Dose Vial- Discard Unused Portion PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Vial Label
PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Carton Panel NDC 63323-895-10 Levothyroxine Sodium Injection 500 mcg per 5 mL (100 mcg per mL) For intravenous use. Preservative free. 5 mL Single-Dose Vial- Discard Unused Portion Rx only PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Carton Panel
PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Vial Label NDC 63323-890-10 Levothyroxine Sodium Injection 200 mcg per 5 mL (40 mcg per mL) For intravenous use. Preservative free. 5 mL Single-Dose Vial- Discard Unused Portion PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Vial Label
PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Carton Panel NDC 63323-890-10 Levothyroxine Sodium Injection 200 mcg per 5 mL (40 mcg per mL) For intravenous use. Preservative free. 5 mL Single-Dose Vial- Discard Unused Portion Rx only PACKAGE LABEL - PRINCIPAL DISPLAY – Levothyroxine Sodium Injection 5 mL Carton Panel
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 Levothyroxine Sodium Injection with lower doses in elderly patients and in patients with underlying cardiovascular disease and closely monitor for cardiac adverse reactions. Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with levothyroxine overtreatment in the elderly [see Dosage and Administration ( 2.1 ) and Warnings and Precautions ( 5.1 )].
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 safety and efficacy of Levothyroxine Sodium Injection have not been established in pediatric patients.
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 There is no available data with use of Levothyroxine Sodium Injection in pregnant women. The clinical data in pregnant women treated with oral levothyroxine to maintain a euthyroid state have not reported increased rates of major birth defects, miscarriages, or adverse maternal or fetal outcomes (see Data ). There are risks to the mother and fetus associated with myxedema coma in pregnancy (see Clinical Considerations ) . Animal reproduction studies have not been conducted with levothyroxine sodium. 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 Myxedema coma is a medical emergency which can be fatal, if left untreated. Delaying treatment in pregnant women with myxedema coma increases the risk of maternal and fetal morbidity and mortality. Life-sustaining therapy for the pregnant woman should not be withheld due to potential concerns regarding the effects of Levothyroxine Sodium Injection on the fetus. Data Human Data There is no available data with use of Levothyroxine Sodium Injection in pregnant women. Oral levothyroxine is approved for use as a replacement therapy in hypothyroidism. There is a long experience of oral levothyroxine use in pregnant women that has 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 8.1 Pregnancy Risk Summary There is no available data with use of Levothyroxine Sodium Injection in pregnant women. The clinical data in pregnant women treated with oral levothyroxine to maintain a euthyroid state have not reported increased rates of major birth defects, miscarriages, or adverse maternal or fetal outcomes (see Data ). There are risks to the mother and fetus associated with myxedema coma in pregnancy (see Clinical Considerations ) . Animal reproduction studies have not been conducted with levothyroxine sodium. 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 Myxedema coma is a medical emergency which can be fatal, if left untreated. Delaying treatment in pregnant women with myxedema coma increases the risk of maternal and fetal morbidity and mortality. Life-sustaining therapy for the pregnant woman should not be withheld due to potential concerns regarding the effects of Levothyroxine Sodium Injection on the fetus. Data Human Data There is no available data with use of Levothyroxine Sodium Injection in pregnant women. Oral levothyroxine is approved for use as a replacement therapy in hypothyroidism. There is a long experience of oral levothyroxine use in pregnant women that has 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 Published studies report that levothyroxine is present in human milk following the administration of oral levothyroxine. 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. There is no available data with use of Levothyroxine Sodium Injection in lactating women. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for levothyroxine and any potential adverse effects on the breastfed infant from levothyroxine or from the underlying maternal condition. 8.4 Pediatric Use The safety and efficacy of Levothyroxine Sodium Injection have not been established in pediatric patients. 8.5 Geriatric Use Because of the increased prevalence of cardiovascular disease among the elderly, initiate Levothyroxine Sodium Injection with lower doses in elderly patients and in patients with underlying cardiovascular disease and closely monitor for cardiac adverse reactions. Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with levothyroxine overtreatment in the elderly [see Dosage and Administration ( 2.1 ) and Warnings and Precautions ( 5.1 )].
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 Levothyroxine Sodium Injection is a clear, colorless solution available as follows: NDC Total Strength per Total Volume Concentration 63323-885-10 100 mcg per 5 mL 20 mcg per mL 63323-890-10 200 mcg per 5 mL 40 mcg per mL 63323-895-10 500 mcg per 5 mL 100 mcg per mL Protect from light in the original vial in a carton and store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature]. The unopened vial may be stored for up to 24 hours exposed to indoor lighting outside of the carton. The drug product is preservative free. Discard any unused portion. Lake Zurich, IL 60047 www.fresenius-kabi.com/us 451617 Issued: April 2019 Fresenius Logo
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| 63323-885-10 | 100 mcg per 5 mL | 20 mcg per mL |
| 63323-890-10 | 200 mcg per 5 mL | 40 mcg per mL |
| 63323-895-10 | 500 mcg per 5 mL | 100 mcg per mL |
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 Levothyroxine Sodium Injection, should not be used for the treatment of obesity or for weight loss. Larger doses may produce serious or even life threatening manifestations of toxicity. ( 6 , 10 ) WARNING: NOT FOR TREATMENT OF OBESITY OR FOR WEIGHT LOSS Thyroid hormones, including Levothyroxine Sodium Injection, should not be used for the treatment of obesity or for weight loss. Larger doses 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