Thyroid by LGM PHARMA SOLUTIONS, LLC Thyroid Tablets, USP
Thyroid by
Drug Labeling and Warnings
Thyroid by is a Prescription medication manufactured, distributed, or labeled by LGM PHARMA SOLUTIONS, LLC. Drug facts, warnings, and ingredients follow.
Drug Details [pdf]
THYROID- thyroid, unspecified tablet
LGM PHARMA SOLUTIONS, LLC
Disclaimer: This drug has not been found by FDA to be safe and effective, and this labeling has not been approved by FDA. For further information about unapproved drugs, click here.
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Thyroid Tablets, USP
DESCRIPTION
Thyroid Tablets, USP* for oral use is a natural preparation derived from porcine thyroid glands and
may have a strong, characteristic odor. (T3 liothyronine is approximately four times as potent as T4
levothyroxine on a microgram for microgram basis.) They provide 38 mcg levothyroxine (T4) and 9
mcg liothyronine (T3) per grain of thyroid. The inactive ingredients are microcrystalline cellulose,
lactose, silicon dioxide, and magnesium stearate.
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 liothyronine (T3) per gram. The ratio of these two hormones in the circulation does not
represent the ratio in the thyroid gland, since about 80% of peripheral liothyronine (T3) comes from
monodeiodination of levothyroxine (T4). Peripheral monodeiodination of levothyroxine (T4) at the 5
position (inner ring) also results in the formation of reverse liothyronine (T3), which is calorigenically
inactive.
Liothyronine (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.”
Pharmacokinetics
Animal studies have shown that levothyroxine (T4) is only partially absorbed from the gastrointestinal
tract. The degree of absorption is dependent on the vehicle used for its administration and by the
character of the intestinal contents, the intestinal flora, including plasma protein, and soluble dietary
factors, all of which bind thyroid and thereby make it unavailable for diffusion. Only 41% is absorbed
when given in a gelatin capsule as opposed to a 74% absorption when given with an albumin carrier.
Depending on other factors, absorption has varied from 48 to 79% of the administered dose. Fasting
increases absorption. Malabsorption syndromes, as well as dietary factors, (children’s soybean
formula, concomitant use of anionic exchange resins such as cholestyramine) cause excessive fecal
loss. Liothyronine (T3) is almost totally absorbed, 95 % in 4 hours. The hormones contained in the
natural preparations are absorbed in a manner similar to the synthetic hormones.
More than 99% of circulating hormones are bound to serum proteins, including thyroid-binding
globulin (TBg), thyroid-binding prealbumin (TBPA), and albumin (TBa), whose capacities and affinities
vary for the hormones. The higher affinity of levothyroxine (T4) for both TBg and TBPA as compared to
liothyronine (T3) partially explains the higher serum levels and longer half-life of the former hormone.
Both protein-bound hormones exist in reverse equilibrium with minute amounts of free hormone, the
latter accounting for the metabolic activity.
Deiodination of levothyroxine (T4) occurs at a number of sites, including liver, kidney, and other
tissues. The conjugated hormone, in the form of glucuronide or sulfate, is found in the bile and gut
where it may complete an enterohepatic circulation. 85% of levothyroxine (T4) metabolized daily is
deiodinated.
INDICATIONS AND USAGE
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 lymphocytic thyroiditis (Hashimoto’s), multinodular
goiter, and in the management of thyroid cancer.
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
| 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.
The active ingredient (desiccated natural thyroid) in Thyroid Tablets, USP is derived from porcine (pig)
thyroid glands of pigs processed for human food consumption. Vitruvias is not aware of any cases of
disease transmission associated with the use of Thyroid Tablets, USP.
PRECAUTIONS
General
Thyroid hormones should be used with great caution in a number of circumstances where the
integrity of the cardiovascular system, particularly the coronary arteries, is suspected. These include
patients with angina pectoris or the elderly, in whom there is a greater likelihood of occult cardiac
disease. In these patients therapy should be initiated with low doses, i.e., 15-30 mg Thyroid Tablets,
USP. When, in such patients, a euthyroid state can only be reached at the expense of an aggravation
of the cardiovascular disease, thyroid hormone dosage should be reduced.
Thyroid hormone therapy in patients with concomitant diabetes mellitus or diabetes insipidus or
adrenal cortical insufficiency aggravates the intensity of their symptoms. Appropriate adjustments of
the various therapeutic measures directed at these concomitant endocrine diseases are required. The
therapy of myxedema coma requires simultaneous administration of glucocorticoids (See DOSAGE
AND ADMINISTRATION).
Hypothyroidism decreases and hyperthyroidism increases the sensitivity to oral anticoagulants.
Prothrombin time should be closely monitored in thyroid-treated patients on oral anticoagulants and
dosage of the latter agents adjusted on the basis of frequent prothrombin time determinations. In
infants, excessive doses of thyroid hormone preparations may produce craniosynostosis.
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.
Laboratory Tests
Treatment of patients with thyroid hormones requires the periodic assessment of thyroid status by
means of appropriate laboratory tests besides the full clinical evaluation. The TSH suppression test
can be used to test the effectiveness of any thyroid preparation bearing in mind the relative
insensitivity of the infant pituitary to the negative feedback effect of thyroid hormones. Serum T4
levels can be used to test the effectiveness of all thyroid medications except T3. When the total serum
T4 is low but TSH is normal, a test specific to assess unbound (free) T4 levels is warranted. Specific
measurements of T4 and T3 by competitive protein binding or radioimmunoassay are not influenced
by blood levels of organic or inorganic iodine.
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 or Colestipol—Cholestyramine or colestipol binds both levothyroxine (T4) and
liothyronine (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 or colestipol 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 (T4) may be decreased when estrogens are started thus increasing thyroid
requirements. However, if the patient’s thyroid gland has sufficient function, the decreased free
levothyroxine (T4) will result in a compensatory increase in levothyroxine (T4) 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
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
levothyroxine (T4) and liothyronine (T3) values. In such cases, the unbound (free) hormone should be
measured. Pregnancy, estrogens, and estrogen-containing 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 9000. 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.
Carcinogenesis, Mutagenesis, and Impairment of Fertility
A reportedly apparent association between prolonged thyroid therapy and breast cancer has not been
confirmed and patients on thyroid for established indications should not discontinue therapy. No
confirmatory long-term studies in animals have been performed to evaluate carcinogenic potential,
mutagenicity, or impairment of fertility in either males or females.
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.
Nursing Mothers
Minimal amounts of thyroid hormones are excreted in human milk. Thyroid is not associated with
serious adverse reactions and does not have a known tumorigenic potential. However, caution should
be exercised when thyroid is administered to a nursing woman.
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.
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).
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 self-induced.
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.
Other adjunctive measures may include administration of cholestyramine to interfere with thyroxine
absorption, and glucocorticoids to inhibit conversion of T4 to T3.
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
(T4) 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 Thyroid Tablets, USP, 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 T4 and 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.
Liothyronine (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 levothyroxine (T4) and
liothyronine (T3) is suspected.
Myxedema Coma
Myxedema coma is usually precipitated in the hypothyroid patient of long-standing 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.
Levothyroxine (T4) and liothyronine (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 a
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 IV. 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% or greater suppression of uptake indicates a normal
thyroid-pituitary axis and thus rules out thyroid gland autonomy.
For adults, the usual suppressive dose of levothyroxine (T4) is 1.56 mcg/kg of body weight per day
given for 7 to 10 days. These doses usually yield normal serum T4 and T3 levels and lack of response
to TSH.
Thyroid hormones should be administered cautiously to patients in whom there is strong suspicion of
thyroid gland autonomy, in view of the fact that the exogenous hormone effects will be additive to the
endogenous source.
Pediatric Dosage
Pediatric dosage should follow the recommendations summarized in Table 1. In infants with
congenital hypothyroidism, therapy with full doses should be instituted as soon as the diagnosis has
been made.
| Age | Thyroid Tablets, USP | |
| Dose per day | Daily dose per kg of body weight | |
| 0- 6 months | 15-30 mg | 4.8-6 mg |
| 6- 12 months | 30-45 mg | 3.6-4.8 mg |
| 1 – 5 years | 45-60 mg | 3-3.6 mg |
| 6- 12 years | 60-90 mg | 2.4-3 mg |
| Over 12 years | Over 90 mg | 1.2-1.8 mg |
HOW SUPPLIED
Thyroid Tablets, USP are supplied as follows: 15 mg (1/4 grain) are available in bottles of 100
(NDC: 79739-7370-1). 30 mg (1/2 grain) are available in bottles of 100 (NDC: 79739-7371-1).
60 mg (1 grain) are available in bottles of 100 (NDC: 79739-7372-1). 90 mg (1 & 1/2 grain) are
available in bottles of 100 (NDC: 79739-7373-1). 120 mg (2 grain) are available in bottles of 100
(NDC: 79739-7374-1). The bottles of 100 have child-resistant closures.
Thyroid Tablets, USP is an off-white to pale brown, round tablet, which may display flecks. The 15 mg
and 30 mg tablets are flat-faced with a bevel edge, and the 60 mg, 90 mg, and 120 mg tablets have
concave faces. One side is debossed with the letters "THY" and the other side with the strength code
numbers as defined below.
| Strength | Code |
| ¼ grain | 025 |
| ½ grain | 050 |
| 1 grain | 100 |
| 1 ½ grain | 150 |
| 2 grain | 200 |
Note: (T3 liothyronine is approximately four times as potent as T4 levothyroxine on a microgram for
microgram basis.)
Store in a tight container protected from light and moisture. Store between 15°C and 30°C (59°F and
86°F).
*Thyroid Tablets, USP has not been approved by FDA as a new drug.
All prescription substitutions and/or recommendations using this product shall be made subject to
state and federal statutes as applicable. Please note: this is not an Orange Book product and has
not been subjected to FDA therapeutic equivalency or other equivalency testing. No
representation is made as to generic status or bioequivalency. Each person recommending a
prescription substitution using this product shall make such recommendations based on each such
person’s professional opinion and knowledge, upon evaluating the active ingredients, excipients,
inactive ingredients and chemical information provided herein.
Manufactured by:
LGM Pharma Solutions, LLC
Irvine, CA 92614
Product of USA
7370-0000-99-OS-PD
Rev 01/2024
PRINCIPAL DISPLAY PANEL
LGM Pharma Solutions, LLC
NDC 79739-7370-1
Thyroid Tablets, USP
1/4 GRAIN (15 mg)
Each tablet contains:
levothyroxine (T4)
9.5 mcg
liothyronine (T3)
2.25 mcg
100 TABLETS Rx only
Directions for use: See insert.
Usual dose: 15 mg – 180 mg once a day. Thyroid Tablets, USP is a natural product with a strong, characteristic odor.
Storage: Store in a tight container protected from light and moisture. Store between 15°C-30°C (59°F-86°F)
Manufactured by:
LGM Pharma Solutions, LLC
Irvine, CA 92614
Product of USA
7370-PD Rev 01/2024
PRINCIPAL DISPLAY PANEL
LGM Pharma Solutions, LLC
NDC 79739-7371-1
Thyroid Tablets, USP
1/2 GRAIN (30 mg)
Each tablet contains:
levothyroxine (T4)
19 mcg
liothyronine (T3)
4.5 mcg
100 TABLETS Rx only
Directions for use: See insert.
Usual dose: 15 mg – 180 mg once a day. Thyroid Tablets, USP is a natural product with a strong, characteristic odor.
Storage: Store in a tight container protected from light and moisture. Store between 15°C-30°C (59°F-86°F)
Manufactured by:
LGM Pharma Solutions, LLC
Irvine, CA 92614
Product of USA
7371-PD Rev 01/2024
PRINCIPAL DISPLAY PANEL
LGM Pharma Solutions, LLC
NDC 79739-7372-1
Thyroid Tablets, USP
1 GRAIN (60 mg)
Each tablet contains:
levothyroxine (T4)
38 mcg
liothyronine (T3)
9 mcg
100 TABLETS Rx only
Directions for use: See insert.
Usual dose: 15 mg – 180 mg once a day. Thyroid Tablets, USP is a natural product with a strong, characteristic odor.
Storage: Store in a tight container protected from light and moisture. Store between 15°C-30°C (59°F-86°F)
Manufactured by:
LGM Pharma Solutions, LLC
Irvine, CA 92614
Product of USA
7372-PD Rev 01/2024
PRINCIPAL DISPLAY PANEL
LGM Pharma Solutions, LLC
NDC 79739-7373-1
Thyroid Tablets, USP
1 & 1/2 GRAIN (90 mg)
Each tablet contains:
levothyroxine (T4)
57 mcg
liothyronine (T3)
13.5 mcg
100 TABLETS Rx only
Directions for use: See insert.
Usual dose: 15 mg – 180 mg once a day. Thyroid Tablets, USP is a natural product with a strong, characteristic odor.
Storage: Store in a tight container protected from light and moisture. Store between 15°C-30°C (59°F-86°F)
Manufactured by:
LGM Pharma Solutions, LLC
Irvine, CA 92614
Product of USA
7373-PD Rev 01/2024
PRINCIPAL DISPLAY PANEL
LGM Pharma Solutions, LLC
NDC 79739-7374-1
Thyroid Tablets, USP
2 GRAIN (120 mg)
Each tablet contains:
levothyroxine (T4)
76 mcg
liothyronine (T3)
18 mcg
100 TABLETS Rx only
Directions for use: See insert.
Usual dose: 15 mg – 180 mg once a day. Thyroid Tablets, USP is a natural product with a strong, characteristic odor.
Storage: Store in a tight container protected from light and moisture. Store between 15°C-30°C (59°F-86°F)
Manufactured by:
LGM Pharma Solutions, LLC
Irvine, CA 92614
Product of USA
7374-PD Rev 01/2024
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| Labeler - LGM PHARMA SOLUTIONS, LLC (117549198) |
Trademark Results [Thyroid]
Mark Image Registration | Serial | Company Trademark Application Date |
|---|---|
 THYROID 86947461 5253778 Live/Registered |
American Thyroid Association, Inc. 2016-03-21 |
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