NP THYROID 60 levothyroxine liothyronine 9 ug; 38 ug Tablet, 90-count
🆔 Identity & classification
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🏭 Manufacturer & labeler
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🩺 Clinical
Thyroid is used to treat the symptoms of hypothyroidism (a condition where the thyroid gland does not produce enough thyroid hormone). Symptoms of hypothyroidism include lack of energy, depression, constipation, weight gain, hair loss, dry skin, dry coarse hair, muscle cramps, decreased concentration, aches and pains, swelling of the legs, and increased sensitivity to cold. Thyroid is also used to treat goiter (enlarged thyroid gland). Thyroid is in a class of medications called thyroid agents. It works by supplying the thyroid hormone normally produced by the body.
Read the full MedlinePlus article ↗- Desiccated thyroid is made from dried pig (porcine) thyroid glands and naturally contains both T4 and T3 — the two main thyroid hormones your body makes. Synthetic options like lev...
- What exactly is desiccated thyroid, and is it the same as synthetic thyroid hormone?
- No — and this is really important. If your thyroid is working normally, taking thyroid hormone will not cause meaningful weight loss. Worse, taking it in higher doses to try to los...
- Can I use thyroid tablets to lose weight?
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🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
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UNII 776XM7047L
Calcium stearate is a white powder derived from stearic acid and calcium. It works as a lubricant and glidant to help the medicine flow smoothly during manufacturing and prevent ingredients from sticking to equipment.
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UNII LX22YL083G
A simple sugar derived from corn or other sources. It acts as a filler to give the medicine bulk and volume, and as a sweetener to improve taste in oral medications.
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UNII 7CVR7L4A2D
A starch-derived carbohydrate produced by breaking down corn, potato, or tapioca starch. It functions as a filler and binder to give the medicine bulk and texture, and sometimes as a mild sweetener or texture enhancer in powders and tablets.
3 inactive ingredients listed in the exact product block matched to this NDC.
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ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.Inactive ingredient FAQ
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💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per each | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | Not in the retail survey — common for institutional, discontinued, or low-volume packs. | |
| Medicaid paysCMS SDUD · 12 mo | No recent Medicaid claims on file for this NDC — rare and low-volume NDCs are suppressed in the public data. | |
| Medicare drug plans payPart D · quarterly | No Part D plan price is available for this NDC in our data. | |
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🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| NP Thyroid 60 38 ug/1; 9 ug 42192-0330-01 | Acella | 100 tablets | $0.665 | — | Availability likely | — |
| Thyroid 60 mg 62559-0742-01 | ANI | 100 tablets | $0.665 | — | Availability likely | — |
| Thyroid 60 mg 69680-0167-00 | Vitruvias | 100 tablets | $0.665 | — | Availability likely | — |
| EvexiTHROID 38 ug/1; 9 ug 73352-0696-10 | Trifluent | 100 tablets | $0.665 | — | Availability likely | — |
| Niva Thyroid 60 mg 75834-0312-01 | Nivagen | 100 tablets | $0.665 | — | Availability likely | — |
| Amerithroid 60 mg 82685-0343-01 | Oliva | 100 tablets | $0.665 | — | Availability likely | — |
| Armour Thyroid 60 mg 00456-0459-01 | Allergan, | 100 tablets | $1.127 | — | Availability likely | — |
| NP Thyroid 9 ug/1; 38 ug 17224-0503-28 | Calvin | 28 tablets | — | — | FDA listed | — |
| Armour Thyroid 60 mg 50090-0190-00 | A-S | 100 tablets | — | — | FDA listed | — |
| NP Thyroid 60 38 ug/1; 9 ug 50090-5216-00 | A-S | 90 tablets | — | — | FDA listed | — |
| NP Thyroid 60 38 ug/1; 9 ug 51655-0132-52 | Northwind | 30 tablets | — | — | FDA listed | — |
| RenThyroid 38 ug/1; 9 ug 64950-0172-01 | Genus | 100 tablets | — | — | FDA listed | — |
| NP Thyroid 60 38 ug/1; 9 ug 68071-3691-03 | NuCare | 30 tablets | — | — | FDA listed | — |
| NP Thyroid 60 38 ug/1; 9 ug 71335-0414-01 | Bryant | 60 tablets | — | — | FDA listed | — |
| Np Thyroid 60 9 ug/1; 38 ugthis 72189-0202-90 | DIRECT | 90 tablets | — | — | FDA listed | — |
| NP Thyroid 60 38 ug/1; 9 ug 76420-0568-01 | Asclemed | 100 tablets | — | — | FDA listed | — |
| Thyroid 60 mg 79739-7372-01 | LGM | 100 tablets | — | — | Discontinued | — |
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⏳ Availability & generic status
We did not find an FDA-approved generic match for this exact strength, form and route.
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📦 Packaging — all sizes for this product
| Package NDC | Description | Marketing start | Status |
|---|---|---|---|
| 72189-0202-90 You're viewing this | 90 TABLET in 1 BOTTLE (72189-202-90) | 2021-06-03 | Active |
🧭 About this NDC listing & data coverage
Listed without an FDA application
This product's marketing category indicates it is marketed without an approved FDA application (no NDA, ANDA, or BLA on file). Having an NDC does not by itself establish FDA approval — the NDC Directory is a listing system, not an approval decision. Approval-linked data such as Orange Book therapeutic-equivalence ratings therefore does not apply.
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| NDC identity (package / product / labeler codes) | ✓ Available |
| Labeler | ✓ Available |
| Product & package description | ✓ Available |
| Marketing category & status | ✓ Available |
| Active ingredient / dosage form / route | ✓ Available |
| FDA label (SPL via DailyMed) | ✓ Available |
| Package photos | ✓ Available |
| Inactive ingredients (structured) | ✓ Available |
| NADAC pharmacy acquisition price (CMS) | — Not published for this NDC CMS publishes NADAC only for NDCs reported in its retail-pharmacy survey. |
| Orange Book / therapeutic-equivalence data | — Not published for this NDC Applies only to products approved under an NDA/ANDA; many listings are out of scope. |
| HCPCS J-code billing crosswalk | — Not published for this NDC Most self-administered / retail products have no J-code — that is normal. |
| Medicaid utilization (CMS SDUD) | — Not published for this NDC CMS reports utilization only for NDCs with Medicaid claims above its privacy threshold. |
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📄 Full prescribing information FDA SPL
🎯 Indications and Usage ▾
INDICATIONS AND USAGE: NP Thyroid tablets (thyroid tablets, USP) are indicated: 1. As replacement or supplemental therapy in patients with hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. This category includes cretinism, myxedema, and ordinary hypothyroidism in patients of any age (children, adults, the elderly), or state (including pregnancy); primary hypothyroidism resulting from functional deficiency, primary atrophy, partial or total absence of thyroid gland, or the effects of surgery, radiation, or drugs, with or without the presence of goiter; and secondary (pituitary), or tertiary (hypothalamic) hypothyroidism (See WARNINGS).
2. As pituitary TSH suppressants, in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute or chronic Iymphocytic thyroiditis (Hashimoto’s), multinodular goiter, and in the management of thyroid cancer.
⏱️ Dosage and Administration ▾
DOSAGE AND ADMINISTRATION: The dosage of thyroid hormones is determined by the indication and must in every case be individualized according to patient response and laboratory findings. Thyroid hormones are given orally. In acute, emergency conditions, injectable levothyroxine sodium may be given intravenously when oral administration is not feasible or desirable, as in the treatment of myxedema coma, or during total parenteral nutrition.
Intramuscular administration is not advisable because of reported poor absorption. Hypothyroidism—Therapy is usually instituted using low doses, with increments which depend on the cardiovascular status of the patient. The usual starting dose is 30 mg NP Thyroid, with increments of 15 mg every 2 to 3 weeks.
A lower starting dosage, 15 mg/day, is recommended in patients with long standing myxedema, particularly if cardiovascular impairment is suspected, in which case extreme caution is recommended. The appearance of angina is an indication for a reduction in dosage. Most patients require 60 to 120 mg/day.
Failure to respond to doses of 180 mg suggests lack of compliance or malabsorption. Maintenance dosages 60 to 120 mg/day usually result in normal serum levothyroxine (T4) and triiodothyronine (T3) levels. Adequate therapy usually results in normal TSH and T4 levels after 2 to 3 weeks of therapy.
Readjustment of thyroid hormone dosage should be made within the first four weeks of therapy, after proper clinical and laboratory evaluations, including serum levels of T4, bound and free, and TSH. T3 may be used in preference to levothyroxine (T4) during radio-isotope scanning procedures, since induction of hypothyroidism in those cases is more abrupt and can be of shorter duration. It may also be preferred when impairment of peripheral conversion of T4 and T3 is suspected.
Myxedema Coma—Myxedema coma is usually precipitated in the hypothyroid patient of longstanding by intercurrent illness or drugs such as sedatives and anesthetics and should be considered a medical emergency. Therapy should be directed at the correction of electrolyte disturbances and possible infection besides the administration of thyroid hormones. Corticosteroids should be administered routinely.
T4 and T3 may be administered via a nasogastric tube but the preferred route of administration of both hormones is intravenous. Levothyroxine sodium (T4) is given at starting dose of 400 mcg (100 mcg/mL) given rapidly, and is usually well tolerated, even in the elderly. This initial dose is followed by daily supplements of 100 to 200 mcg given intravenously.
Normal T4 levels are achieved in 24 hours followed in 3 days by threefold elevation of T3. Oral therapy with thyroid hormone would be resumed as soon as the clinical situation has been stabilized and the patient is able to take oral medication. Thyroid Cancer—Exogenous thyroid hormone may produce regression of metastases from follicular and papillary carcinoma of the thyroid and is used as ancillary therapy of these conditions with radioactive iodine.
TSH should be suppressed to low or undetectable levels. Therefore, larger amounts of thyroid hormone than those used for replacement therapy are required. Medullary carcinoma of the thyroid is usually unresponsive to this therapy.
Thyroid Suppression Therapy—Administration of thyroid hormone in doses higher than those produced physiologically by the gland results in suppression of the production of endogenous hormone. This is the basis for the thyroid suppression test and is used as an aid in the diagnosis of patients with signs of mild hyperthyroidism in whom base line laboratory tests appear normal, or to demonstrate thyroid gland autonomy in patients with Grave’s ophthalmopathy. 131I uptake is determined before and after the administration of the exogenous hormone.
A 50 percent or greater suppression of uptake indicates a normal thyroid-pituitary axis and thus rules out thyroid gland autonomy. For adults, the usual suppressive dose…
⛔ Contraindications ▾
CONTRAINDICATIONS: Thyroid hormone preparations are generally contraindicated in patients with diagnosed but as yet uncorrected adrenal cortical insufficiency, untreated thyrotoxicosis, and apparent hypersensitivity to any of their active or extraneous constituents. There is no well-documented evidence from the literature, however, of true allergic or idiosyncratic reactions to thyroid hormone.
⚠️ Warnings ▾
WARNINGS Drugs with thyroid hormone activity, alone or together with other therapeutic agents, have been used for the treatment of obesity. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction. Larger doses may produce serious or even life-threatening manifestations of toxicity, particularly when given in association with sympathomimetic amines such as those used for their anorectic effects.
The use of thyroid hormones in the therapy of obesity, alone or combined with other drugs, is unjustified and has been shown to be ineffective. Neither is their use justified for the treatment of male or female infertility unless this condition is accompanied by hypothyroidism.
🤒 Adverse Reactions ▾
ADVERSE REACTIONS: Adverse reactions other than those indicative of hyperthyroidism because of therapeutic overdosage, either initially or during the maintenance period, are rare (See OVERDOSAGE).
🔄 Drug Interactions ▾
Drug Interactions—Oral Anticoagulants—Thyroid hormones appear to increase catabolism of vitamin K-dependent clotting factors. If oral anticoagulants are also being given, compensatory increases in clotting factor synthesis are impaired. Patients stabilized on oral anticoagulants who are found to require thyroid replacement therapy should be watched very closely when thyroid is started.
If a patient is truly hypothyroid, it is likely that a reduction in anticoagulant dosage will be required. No special precautions appear to be necessary when oral anticoagulant therapy is begun in a patient already stabilized on maintenance thyroid replacement therapy. Insulin or Oral Hypoglycemics—Initiating thyroid replacement therapy may cause increases in insulin or oral hypoglycemic requirements.
The effects seen are poorly understood and depend upon a variety of factors such as dose and type of thyroid preparations and endocrine status of the patient. Patients receiving insulin or oral hypoglycemics should be closely watched during initiation of thyroid replacement therapy. Cholestyramine - Cholestyramine binds both T4 and T3 in the intestine, thus impairing absorption of these thyroid hormones.
In vitro studies indicate that the binding is not easily removed. Therefore four to five hours should elapse between administration of cholestyramine and thyroid hormones. Estrogen, Oral Contraceptives—Estrogens tend to increase serum thyroxine-binding globulin (TBg).
In a patient with a nonfunctioning thyroid gland who is receiving thyroid replacement therapy, free levothyroxine may be decreased when estrogens are started thus increasing thyroid requirements. However, if the patient’s thyroid gland has sufficient function, the decreased free thyroxine will result in a compensatory increase in thyroxine output by the thyroid. Therefore, patients without a functioning thyroid gland who are on thyroid replacement therapy may need to increase their thyroid dose if estrogens or estrogen-containing oral contraceptives are given.
🔄 Drug / Laboratory Test Interactions ▾
Drug/Laboratory Test Interactions—The following drugs or moieties are known to interfere with laboratory tests performed in patients on thyroid hormone therapy: androgens, corticosteroids, estrogens, oral contraceptives containing estrogens, iodine-containing preparations, and the numerous preparations containing salicylates. 1. Changes in TBg concentration should be taken into consideration in the interpretation of T4 and T3 values.
In such cases, the unbound (free) hormone should be measured. Pregnancy, estrogens, and estrogencontaining oral contraceptives increase TBg concentrations. TBg may also be increased during infectious hepatitis.
Decreases in TBg concentrations are observed in nephrosis, acromegaly, and after androgen or corticosteroid therapy. Familial hyper- or hypothyroxine-binding-globulinemias have been described. The incidence of TBg deficiency approximates 1 in 9,000.
The binding of levothyroxine by TBPA is inhibited by salicylates. 2. Medicinal or dietary iodine interferes with all in vivo tests of radio-iodine uptake, producing low uptakes which may not be relative of a true decrease in hormone synthesis.
3. The persistence of clinical and laboratory evidence of hypothyroidism in spite of adequate dosage replacement indicates either poor patient compliance, poor absorption, excessive fecal loss, or inactivity of the preparation. Intracellular resistance to thyroid hormone is quite rare.
🤰 Pregnancy ▾
Pregnancy-Category A—Thyroid hormones do not readily cross the placental barrier. The clinical experience to date does not indicate any adverse effect on fetuses when thyroid hormones are administered to pregnant women. On the basis of current knowledge, thyroid replacement therapy to hypothyroid women should not be discontinued during pregnancy.
🧒 Pediatric Use ▾
Pediatric Use—Pregnant mothers provide little or no thyroid hormone to the fetus. The incidence of congenital hypothyroidism is relatively high (1:4,000) and the hypothyroid fetus would not derive any benefit from the small amounts of hormone crossing the placental barrier. Routine determinations of serum T4 and/or TSH is strongly advised in neonates in view of the deleterious effects of thyroid deficiency on growth and development.
Treatment should be initiated immediately upon diagnosis, and maintained for life, unless transient hypothyroidism is suspected; in which case, therapy may be interrupted for 2 to 8 weeks after the age of 3 years to reassess the condition. Cessation of therapy is justified in patients who have maintained a normal TSH during those 2 to 8 weeks.
🆘 Overdosage ▾
OVERDOSAGE: Signs and Symptoms—Excessive doses of thyroid result in a hypermetabolic state resembling in every respect the condition of endogenous origin. The condition may be selfinduced. Treatment of Overdosage—Dosage should be reduced or therapy temporarily discontinued if signs and symptoms of overdosage appear.
Treatment may be reinstituted at a lower dosage. In normal individuals, normal hypothalamic-pituitary-thyroid axis function is restored in 6 to 8 weeks after thyroid suppression. Treatment of acute massive thyroid hormone overdosage is aimed at reducing gastrointestinal absorption of the drugs and counteracting central and peripheral effects, mainly those of increased sympathetic activity.
Vomiting may be induced initially if further gastrointestinal absorption can reasonably be prevented and barring contraindications such as coma, convulsions, or loss of the gagging reflex. Treatment is symptomatic and supportive. Oxygen may be administered and ventilation maintained.
Cardiac glycosides may be indicated if congestive heart failure develops. Measures to control fever, hypoglycemia, or fluid loss should be instituted if needed. Antiadrenergic agents, particularly propranolol, have been used advantageously in the treatment of increased sympathetic activity.
Propranolol may be administered intravenously at a dosage of 1 to 3 mg, over a 10-minute period or orally, 80 to 160 mg/day, initially, especially when no contraindications exist for its use.
🧬 Clinical Pharmacology ▾
CLINICAL PHARMACOLOGY: The steps in the synthesis of the thyroid hormones are controlled by thyrotropin (Thyroid Stimulating Hormone, TSH) secreted by the anterior pituitary. This hormone’s secretion is in turn controlled by a feedback mechanism effected by the thyroid hormones themselves and by thyrotropin releasing hormone (TRH), a tripeptide of hypothalamic origin. Endogenous thyroid hormone secretion is suppressed when exogenous thyroid hormones are administered to euthyroid individuals in excess of the normal gland’s secretion.
The mechanisms by which thyroid hormones exert their physiologic action are not well understood. These hormones enhance oxygen consumption by most tissues of the body, increase the basal metabolic rate, and the metabolism of carbohydrates, lipids, and proteins. Thus, they exert a profound influence on every organ system in the body and are of particular importance in the development of the central nervous system.
The normal thyroid gland contains approximately 200 mcg of levothyroxine (T4) per gram of gland, and 15 mcg of liodothyronine (T3) per gram. The ratio of these two hormones in the circulation does not represent the ratio in the thyroid gland, since about 80 percent of peripheral triiodothyronine comes from monodeiodination of levothyroxine. Peripheral monodeiodination of levothyroxine at the 5 position (inner ring) also results in the formation of reverse triiodothyronine (T3), which is calorigenically inactive.
Triiodothyronine (T3) levels are low in the fetus and newborn, in old age, in chronic caloric deprivation, hepatic cirrhosis, renal failure, surgical stress, and chronic illnesses representing what has been called the “T3 thyronine syndrome.”
📦 How Supplied / Storage and Handling ▾
HOW SUPPLIED: NP Thyroid tablets (thyroid tablets, USP) are supplied as follows: 30 mg (1/2 gr)), 60 mg (1 gr) , and 90 mg (1 1/2 gr) . NP Thyroid tablets are light tan, round tablets, debossed on one side with “AP” and a 3-digit code on the other side as follows: 30 mg (1/2 grain) - “329” 60 mg (1 grain) - “330” 90 mg (1 1/2 grain) - “331” MANUFACTURED FOR: Acella Pharmaceuticals, LLC 9005 Westside Parkway Alpharetta, GA 30009 1-800-541-4802 Rev 0818-01
📦 Storage and Handling ▾
Store in a tight container protected from light and moisture. Store between 15° - 30°C (59° - 86°F).
📋 Description ▾
NP Thyroid (thyroid tablets, USP) for oral use is a natural preparation derived from porcine thyroid glands. They contain both tetraiodothyronine sodium (T4 levothyroxine) and triiodothyronine sodium (T3 liothyronine) providing 38 mcg levothyroxine (T4) and 9 mcg liothyronine (T3) per grain of thyroid. The inactive ingredients are calcium stearate, dextrose monohydrate, maltodextrin and mineral oil.
💬 Information for Patients ▾
Information for the Patient—Patients on thyroid hormone preparations and parents of children on thyroid therapy should be informed that: 1. Replacement therapy is to be taken essentially for life, with the exception of cases of transient hypothyroidism, usually associated with thyroiditis, and in those patients receiving a therapeutic trial of the drug. 2.
They should immediately report during the course of therapy any signs or symptoms of thyroid hormone toxicity, e.g., chest pain, increased pulse rate, palpitations, excessive sweating, heat intolerance, nervousness, or any other unusual event. 3. In case of concomitant diabetes mellitus, the daily dosage of antidiabetic medication may need readjustment as thyroid hormone replacement is achieved.
If thyroid medication is stopped, a downward readjustment of the dosage of insulin or oral hypoglycemic agent may be necessary to avoid hypoglycemia. At all times, close monitoring of urinary glucose levels is mandatory in such patients. 4.
In case of concomitant oral anticoagulant therapy, the prothrombin time should be measured frequently to determine if the dosage of oral anticoagulants is to be readjusted. 5. Partial loss of hair may be experienced by children in the first few months of thyroid therapy, but this is usually a transient phenomenon and later recovery is usually the rule.