Label: LITHIUM CARBONATE tablet, extended release
- NDC Code(s): 0054-0020-25
- Packager: Hikma Pharmaceuticals USA Inc.
- Category: HUMAN PRESCRIPTION DRUG LABEL
- DEA Schedule: None
- Marketing Status: Abbreviated New Drug Application
Updated October 12, 2022
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Lithium toxicity is closely related to serum lithium levels, and can occur at doses close to therapeutic levels. Facilities for prompt and accurate serum lithium determinations should be available before initiating therapy [see DOSAGE AND ADMINISTRATION].
- Rx Only
Lithium Carbonate Extended-Release Tablets, USP contain lithium carbonate, USP a white, light alkaline powder with molecular formula Li2CO3 and molecular weight 73.89. Lithium is an element of the alkali-metal group with atomic number 3, atomic weight 6.94 and an emission line at 671 nm on the flame photometer. The tablets meet the requirements of USP Dissolution Test 2 in the USP monograph for Lithium Carbonate Extended-release Tablets, USP.
Lithium Carbonate Extended-Release Tablets: Each speckled, off-white to yellow, round biconvex tablet, debossed with “54 346” on one side and scored on the other side, contains lithium carbonate, 450 mg. Inactive ingredients consist of iron oxide (yellow), magnesium stearate, povidone, sodium alginate and sodium starch glycolate.
Lithium Carbonate Extended-Release Tablets USP, 450 mg are designed to release a portion of the dose initially and the remainder gradually; the release pattern of the controlled release tablets reduces the variability in lithium blood levels seen with the immediate release dosage forms.
- CLINICAL PHARMACOLOGY
INDICATIONS AND USAGE
Lithium Carbonate Extended-Release Tablets are indicated in the treatment of manic episodes of manic-depressive illness. Maintenance therapy prevents or diminishes the intensity of subsequent episodes in those manic-depressive patients with a history of mania.
Typical symptoms of mania include pressure of speech, motor hyperactivity, reduced need for sleep, flight of ideas, grandiosity, elation, poor judgment, aggressiveness and possibly hostility. When given to a patient experiencing a manic episode, Lithium Carbonate Extended-Release Tablets may produce a normalization of symptomatology within 1 to 3 weeks.
The toxic concentrations for lithium (≥1.5 mEq/L) are close to the therapeutic range (0.8 to 1.2mEq/L). Some patients abnormally sensitive to lithium may exhibit toxic signs at serum concentrations that are considered within the therapeutic range [see Boxed Warning, DOSAGE AND ADMINISTRATION]. Lithium may take up to 24 hours to distribute into brain tissue, so occurrence of acute toxicity symptoms may be delayed.
Neurological signs of lithium toxicity range from mild neurological adverse reactions such as fine tremor, lightheadedness, lack of coordination, and weakness; to moderate manifestations like giddiness, apathy, drowsiness, hyperreflexia, muscle twitching, ataxia, blurred vision, tinnitus, and slurred speech; and severe manifestations such as clonus, confusion, seizure, coma, and death. In rare cases, neurological sequelae may persist despite discontinuing lithium treatment and may be associated with cerebellar atrophy. Cardiac manifestations involve electrocardiographic changes, such as prolonged QT interval, ST and T-wave changes and myocarditis. Renal manifestations include urine concentrating defect, nephrogenic diabetes insipidus, and renal failure. Respiratory manifestations include dyspnea, aspiration pneumonia, and respiratory failure. Gastrointestinal manifestations include nausea, vomiting, diarrhea, and bloating. No specific antidote for lithium poisoning is known [see OVERDOSAGE].
The risk of lithium toxicity is increased by:
- Recent onset of concurrent febrile illness
- Concomitant administration of drugs which increase lithium serum concentrations by pharmacokinetic interactions or drugs affecting kidney function [see PRECAUTIONS: Drug Interactions]
- Acute ingestion
- Impaired renal function
- Volume depletion or dehydration
- Significant cardiovascular disease
- Changes in electrolyte concentrations (especially sodium and potassium)
Monitor for signs and symptoms of lithium toxicity. If symptoms occur, decrease dosage or discontinue lithium treatment.
Unmasking of Brugada Syndrome
There have been postmarketing reports of a possible association between treatment with lithium and the unmasking of Brugada Syndrome. Brugada Syndrome is a disorder characterized by abnormal electrocardiographic (ECG) findings and a risk of sudden death. Lithium should generally be avoided in patients with Brugada Syndrome or those suspected of having Brugada Syndrome. Consultation with a cardiologist is recommended if: (1) treatment with lithium is under consideration for patients suspected of having Brugada Syndrome or patients who have risk factors for Brugada Syndrome, e.g., unexplained syncope, a family history of Brugada Syndrome, or a family history of sudden unexplained death before the age of 45 years, (2) patients who develop unexplained syncope or palpitations after starting lithium therapy.
Cases of pseudotumor cerebri (increased intracranial pressure and papilledema) have been reported with lithium use. If undetected, this condition may result in enlargement of the blind spot, constriction of visual fields, and eventual blindness due to optic atrophy. Lithium should be discontinued, if clinically possible, if this syndrome occurs.
Chronic lithium therapy may be associated with diminution of renal concentrating ability, occasionally presenting as nephrogenic diabetes insipidus, with polyuria and polydipsia. Such patients should be carefully managed to avoid dehydration with resulting lithium retention and toxicity. This condition is usually reversible when lithium is discontinued.
Post marketing cases consistent with nephrotic syndrome have been reported with the use of lithium. Biopsy findings in patients with nephrotic syndrome include minimal change disease and focal segmental glomerulosclerosis. Discontinuation of lithium in patients with nephrotic syndrome has resulted in remission of nephrotic syndrome.
Morphologic changes with glomerular and interstitial fibrosis and nephron atrophy have been reported in patients on chronic lithium therapy. Morphologic changes have also been seen in manic-depressive patients never exposed to lithium. The relationship between renal functional and morphologic changes and their association with lithium therapy have not been established.
Kidney function should be assessed prior to and during lithium therapy. Routine urinalysis and other tests may be used to evaluate tubular function (e.g., urine specific gravity or osmolality following a period of water deprivation, or 24-hour urine volume) and glomerular function (e.g., serum creatinine, creatinine clearance or proteinuria). During lithium therapy, progressive or sudden changes in renal function, even within the normal range, indicate the need for reevaluation of treatment.
An encephalopathic syndrome (characterized by weakness, lethargy, fever, tremulousness and confusion, extrapyramidal symptoms, leukocytosis, elevated serum enzymes, BUN and FBS) has occurred in a few patients treated with lithium plus a neuroleptic. In some instances, the syndrome was followed by irreversible brain damage. Because of a possible causal relationship between these events and the concomitant administration of lithium and neuroleptics, patients receiving such combined therapy should be monitored closely for early evidence of neurologic toxicity and treatment discontinued promptly if such signs appear. This encephalopathic syndrome may be similar to or the same as neuroleptic malignant syndrome (NMS).
Lithium can precipitate serotonin syndrome, a potentially life-threatening condition. The risk is increased with concomitant use of other serotonergic drugs (including selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, triptans, tricyclic antidepressants, fentanyl, tramadol, tryptophan, buspirone, and St. John’s Wort) and with drugs that impair metabolism of serotonin, i.e., MAOIs [see PRECAUTIONS].
Serotonin syndrome signs and symptoms may include mental status changes (e.g., agitation, hallucinations, delirium, and coma), autonomic instability (e.g., tachycardia, labile blood pressure, dizziness, diaphoresis, flushing, hyperthermia), neuromuscular symptoms (e.g., tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, and gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea).
Monitor all patients taking lithium for the emergence of serotonin syndrome. Discontinue treatment with lithium and any concomitant serotonergic agents immediately if the above symptoms occur, and initiate supportive symptomatic treatment. If concomitant use of lithium with other serotonergic drugs is clinically warranted, inform patients of the increased risk for serotonin syndrome and monitor for symptoms.
Concomitant Use with Neuromuscular Blocking Agents
Lithium may prolong the effects of neuromuscular blocking agents. Therefore, neuromuscular blocking agents should be given with caution to patients receiving lithium.
Usage in Pregnancy
Adverse effects on implantation in rats, embryo viability in mice and metabolism in vitro of rat testes and human spermatozoa have been attributed to lithium, as have teratogenicity in submammalian species and cleft palates in mice.
In humans, lithium carbonate may cause fetal harm when administered to a pregnant woman. Data from lithium birth registries suggest an increase in cardiac and other anomalies, especially Ebstein’s anomaly. If this drug is used in women of childbearing potential, or during pregnancy, or if a patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.
Usage in Nursing Mothers
Lithium is excreted in human milk. Nursing should not be undertaken during lithium therapy except in rare and unusual circumstances where, in the view of the physician, the potential benefits to the mother outweigh possible hazards to the infant or neonate. Signs and symptoms of lithium toxicity such as hypertonia, hypothermia, cyanosis, and ECG changes have been reported in some infants and neonates.
Usage in Pediatric Patients
Safety and effectiveness in pediatric patients under 12 years of age have not been determined; its use in these patients is not recommended.
There has been a report of a transient syndrome of acute dystonia and hyperreflexia occurring in a 15 kg child who ingested 300 mg of lithium carbonate.
The ability to tolerate lithium is greater during the acute manic phase and decreases when manic symptoms subside [see DOSAGE AND ADMINISTRATION].
The distribution space of lithium approximates that of total body water. Lithium is primarily excreted in urine with insignificant excretion in feces. Renal excretion of lithium is proportional to its plasma concentration. The half-life of elimination of lithium is approximately 24 hours. Lithium decreases sodium reabsorption by the renal tubules which could lead to sodium depletion. Therefore, it is essential for the patient to maintain a normal diet, including salt, and an adequate fluid intake (2500 to 3000 mL) at least during the initial stabilization period. Decreased tolerance to lithium has been reported to ensue from protracted sweating or diarrhea and, if such occur, supplemental fluid and salt should be administered under careful medical supervision and lithium intake reduced or suspended until the condition is resolved.
In addition to sweating and diarrhea, concomitant infection with elevated temperatures may also necessitate a temporary reduction or cessation of medication.
Previously existing underlying thyroid disorders do not necessarily constitute a contraindication to lithium treatment; where hypothyroidism pre-exists, careful monitoring of thyroid function during lithium stabilization and maintenance allows for correction of changing thyroid parameters, if any; where hypothyroidism occurs during lithium stabilization and maintenance, supplemental thyroid treatment may be used.
Information for Patients
Lithium carbonate may impair mental and/or physical abilities. Caution patients about activities requiring alertness (e.g. operating vehicles or machinery).
A condition known as Brugada Syndrome may pre-exist and be unmasked by lithium therapy. Brugada Syndrome is a heart disorder characterized by abnormal electrocardiographic (ECG) findings and risk of sudden death. Patients should be advised to seek immediate emergency assistance if they experience fainting, lightheadedness, abnormal heart beats, or shortness of breath because they may have a potentially life-threatening heart disorder known as Brugada Syndrome.
Caution should be used when lithium and diuretics are used concomitantly because diuretic-induced sodium loss may reduce the renal clearance of lithium and increase serum lithium levels with risk of lithium toxicity. Patients receiving such combined therapy should have serum lithium levels monitored closely and the lithium dosage adjusted if necessary.
Lithium levels should be closely monitored when patients initiate or discontinue NSAID use. In some cases, lithium toxicity has resulted from interactions between an NSAID and lithium. Indomethacin and piroxicam have been reported to increase significantly steady-state plasma lithium concentrations. There is also evidence that other nonsteroidal anti-inflammatory agents, including the selective cyclooxygenase-2 (COX-2) inhibitors, have the same effect. In a study conducted in healthy subjects, mean steady-state lithium plasma levels increased approximately 17% in subjects receiving lithium 450 mg b.i.d. with celecoxib 200 mg b.i.d. as compared to subjects receiving lithium alone.
Concomitant use of lithium with a Sodium-Glucose Cotransporter 2 (SGLT2) inhibitor may decrease serum lithium concentrations. Monitor serum lithium concentration more frequently during SGLT2 inhibitor initiation and dosage changes.
Concurrent use of metronidazole with lithium may provoke lithium toxicity due to reduced renal clearance. Patients receiving such combined therapy should be monitored closely.
There is evidence that angiotensin-converting enzyme inhibitors, such as enalapril and captopril, and angiotensin II receptor antagonists, such as losartan, may substantially increase steady-state plasma lithium levels, sometimes resulting in lithium toxicity. When such combinations are used, lithium dosage may need to be decreased, and plasma lithium levels should be measured more often.
Concurrent use of calcium channel blocking agents with lithium may increase the risk of neurotoxicity in the form of ataxia, tremors, nausea, vomiting, diarrhea and/or tinnitus. Caution is recommended. Concomitant administration of lithium with serotonergic drugs can precipitate serotonin syndrome. Monitor patients for signs and symptoms of serotonin syndrome, particularly during lithium initiation. If serotonin syndrome occurs, consider discontinuation of lithium and/or concomitant serotonergic drugs. Examples of serotonergic drugs include selective serotonin reuptake inhibitors (SSRI), serotonin and norepinephrine reuptake inhibitors (SNRI), and monoamine oxidase inhibitors (MAOI).
The following drugs can lower serum lithium concentrations by increasing urinary lithium excretion: acetazolamide, urea, xanthine preparations, and alkalinizing agents such as sodium bicarbonate.
Concomitant administration of methyldopa, phenytoin, or carbamazepine with lithium may increase the risk of toxic effects of these drugs.
Concomitant extended use of iodide preparations, especially potassium iodide, with lithium may produce hypothyroidism.
Usage in Pregnancy
Teratogenic Effects: [see WARNINGS].
Usage in Nursing Mothers
Because of the potential for serious adverse reactions in nursing infants and neonates from lithium, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother [see WARNINGS].
Safety and effectiveness in pediatric patients below the age of 12 have not been established [see WARNINGS].
Clinical studies of Lithium Carbonate Extended-Release Tablets did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other therapy.
This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function.
The occurrence and severity of adverse reactions are generally directly related to serum lithium concentrations as well as to individual patient sensitivity to lithium, and generally occur more frequently and with greater severity at higher concentrations.
Adverse reactions may be encountered at serum lithium levels below 1.5 mEq/L. Mild to moderate adverse reactions may occur at levels from 1.5 to 2.5 mEq/L, and moderate to severe reactions may be seen at levels of 2 mEq/L and above.
Fine hand tremor, polyuria and mild thirst may occur during initial therapy for the acute manic phase, and may persist throughout treatment. Transient and mild nausea and general discomfort may also appear during the first few days of lithium administration.
These side effects usually subside with continued treatment or a temporary reduction or cessation of dosage. If persistent, cessation of lithium therapy may be required.
Diarrhea, vomiting, drowsiness, muscular weakness and lack of coordination may be early signs of lithium intoxication, and can occur at lithium levels below 2 mEq/L. At higher levels, ataxia, giddiness, tinnitus, blurred vision and a large output of dilute urine may be seen. Serum lithium levels above 3 mEq/L may produce a complex clinical picture, involving multiple organs and organ systems. Serum lithium levels should not be permitted to exceed 2 mEq/L during the acute treatment phase.
The following reactions have been reported and appear to be related to serum lithium levels, including levels within the therapeutic range:
Neuromuscular/Central Nervous System: Tremor, muscle hyperirritability (fasciculations, twitching, clonic movements of whole limbs), hypertonicity, ataxia, choreo-athetotic movements, hyperactive deep tendon reflex, extrapyramidal symptoms including acute dystonia, cogwheel rigidity, blackout spells, epileptiform seizures, slurred speech, dizziness, vertigo, downbeat nystagmus, incontinence of urine or feces, somnolence, psychomotor retardation, restlessness, confusion, stupor, coma, tongue movements, tics, tinnitus, hallucinations, poor memory, slowed intellectual functioning, startled response, worsening of organic brain syndromes, myasthenia gravis (rarely).
Cardiovascular: Cardiac arrhythmia, hypotension, peripheral circulatory collapse, bradycardia, sinus node dysfunction with severe bradycardia (which may result in syncope), Unmasking of Brugada Syndrome [see WARNINGS and PRECAUTIONS: Information for Patients].
Gastrointestinal: Anorexia, nausea, vomiting, diarrhea, gastritis, salivary gland swelling, abdominal pain, excessive salivation, flatulence, indigestion.
Genitourinary: Glycosuria, decreased creatinine clearance, albuminuria, oliguria, and symptoms of nephrogenic diabetes insipidus including polyuria, thirst and polydipsia.
Dermatologic: Drying and thinning of hair, alopecia, anesthesia of skin, chronic folliculitis, xerosis cutis, psoriasis onset or exacerbation, generalized pruritus with or without rash, cutaneous ulcers, angioedema, drug reaction with eosinophilia and systemic symptoms (DRESS).
Autonomic Nervous System: Blurred vision, dry mouth, impotence/sexual dysfunction.
Thyroid Abnormalities: Euthyroid goiter and/or hypothyroidism (including myxedema) accompanied by lower T3 and T4. I131 uptake may be elevated [see PRECAUTIONS]. Paradoxically, rare cases of hyperthyroidism have been reported.
EEG Changes: Diffuse slowing, widening of the frequency spectrum, potentiation and disorganization of background rhythm.
EKG Changes: Reversible flattening, isoelectricity or inversion of T-waves.
Miscellaneous: Fatigue, lethargy, transient scotomata, exophthalmos, dehydration, weight loss, leukocytosis, headache, transient hyperglycemia, hypercalcemia, hyperparathyroidism, excessive weight gain, edematous swelling of ankles or wrists, metallic taste, dysgeusia/taste distortion, salty taste, thirst, swollen lips, tightness in chest, swollen and/or painful joints, fever, polyarthralgia, dental caries.
Some reports of nephrogenic diabetes insipidus, hyperparathyroidism, and hypothyroidism which persist after lithium discontinuation have been received.
A few reports have been received of the development of painful discoloration of fingers and toes and coldness of the extremities within one day of the starting of treatment with lithium. The mechanism through which these symptoms (resembling Raynaud’s syndrome) developed is not known. Recovery followed discontinuance.
The toxic levels for lithium (≥ 1.5 mEq/L) are close to the therapeutic levels (0.6 to 1.2 mEq/L). It is therefore important that patients and their families be cautioned to watch for early toxic symptoms and to discontinue the drug and inform the physician should they occur. Toxic symptoms are listed in detail under ADVERSE REACTIONS.
No specific antidote for lithium poisoning is known. Early symptoms of lithium toxicity can usually be treated by reduction or cessation of dosage of the drug and resumption of the treatment at a lower dose after 24 to 48 hours. In severe cases of lithium poisoning, the first and foremost goal of treatment consists of elimination of this ion from the patient. Treatment is essentially the same as that used in barbiturate poisoning: 1) gastric lavage, 2) correction of fluid and electrolyte imbalance, and 3) regulation of kidney function. Urea, mannitol and aminophylline all produce significant increases in lithium excretion. Hemodialysis is an effective and rapid means of removing the ion from the severely toxic patient.
Infection prophylaxis, regular chest X-rays and preservation of adequate respiration are essential.
DOSAGE AND ADMINISTRATION
Doses of controlled-release tablets are usually given b.i.d. (approximately 12-hour intervals). When initiating therapy with controlled-release lithium, dosage must be individualized according to serum levels and clinical response.
When switching a patient from immediate-release capsules to Lithium Carbonate Extended-Release Tablets, give the same total daily dose when possible. Most patients on maintenance therapy are stabilized on 900 mg daily, e.g., Lithium Carbonate Extended-Release Tablets, 450 mg b.i.d. When the previous dosage of immediate-release lithium is not a multiple of 450 mg, e.g., 1,500 mg, initiate Lithium Carbonate Extended-Release Tablets at the multiple of 450 mg nearest to, but below, the original daily dose, i.e., 1,350 mg. When the 2 doses are unequal, give the larger dose in the evening. In the above example, with a total daily dose of 1,350 mg, generally 450 mg of Lithium Carbonate Extended-Release Tablets should be given in the morning and 900 mg of Lithium Carbonate Extended-Release Tablets in the evening. If desired, the total daily dose of 1,350 mg can be given in three equal 450 mg doses of Lithium Carbonate Extended-Release Tablets. These patients should be monitored at 1- to 2-week intervals, and dosage adjusted if necessary, until stable and satisfactory serum levels and clinical state are achieved.
When patients require closer titration than that available with doses of Lithium Carbonate Extended-Release Tablets in increments of 450 mg, immediate-release capsules should be used.
Optimal patient response to Lithium Carbonate Extended-Release Tablets can usually be established and maintained with 1800 mg per day in divided doses. Such doses will normally produce the desired serum lithium level ranging between 1 and 1.5 mEq/L.
Dosage must be individualized according to serum levels and clinical response. Regular monitoring of the patient’s clinical state and serum lithium levels is necessary. Serum levels should be determined twice per week during the acute phase, and until the serum level and clinical condition of the patient have been stabilized.
The desirable serum lithium levels are 0.6 to 1.2 mEq/L. Dosage will vary from one individual to another, but usually 900 mg to 1200 mg per day in divided doses will maintain this level. Serum lithium levels in uncomplicated cases receiving maintenance therapy during remission should be monitored at least every two months.
Patients unusually sensitive to lithium may exhibit toxic signs at serum levels below 1 mEq/L.
- Blood samples for serum lithium determinations should be drawn immediately prior to the next dose when lithium concentrations are relatively stable (i.e., 8 to 12 hours after the previous dose). Total reliance must not be placed on serum levels alone. Accurate patient evaluation requires both clinical and laboratory analysis.
- Elderly patients often respond to reduced dosage, and may exhibit signs of toxicity at serum levels ordinarily tolerated by younger patients.
- Lithium Carbonate Extended-Release Tablets must be swallowed whole and never chewed or crushed.
Lithium Carbonate Extended-Release Tablets, USP
450 mg tablets are speckled, off-white to yellow, round biconvex tablets with “54 346” debossed on one side and scored on the other side.
(NDC 0054-0020-25) Bottle of 100 Tablets
Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature.]
Hikma Pharmaceuticals USA Inc.
Berkeley Heights, NJ 07922
Revised October 2022
- PACKAGE/LABEL PRINCIPAL DISPLAY PANEL
INGREDIENTS AND APPEARANCE
lithium carbonate tablet, extended release
Product Information Product Type HUMAN PRESCRIPTION DRUG Item Code (Source) NDC:0054-0020 Route of Administration ORAL Active Ingredient/Active Moiety Ingredient Name Basis of Strength Strength LITHIUM CARBONATE (UNII: 2BMD2GNA4V) (LITHIUM CATION - UNII:8H8Z5UER66) LITHIUM CARBONATE 450 mg Inactive Ingredients Ingredient Name Strength FERRIC OXIDE YELLOW (UNII: EX438O2MRT) MAGNESIUM STEARATE (UNII: 70097M6I30) POVIDONE, UNSPECIFIED (UNII: FZ989GH94E) SODIUM ALGINATE (UNII: C269C4G2ZQ) SODIUM STARCH GLYCOLATE TYPE A POTATO (UNII: 5856J3G2A2) Product Characteristics Color WHITE (speckled, off-white to yellow) Score 2 pieces Shape ROUND (biconvex) Size 11mm Flavor Imprint Code 54;346 Contains Packaging # Item Code Package Description Marketing Start Date Marketing End Date 1 NDC:0054-0020-25 100 in 1 BOTTLE, PLASTIC; Type 0: Not a Combination Product 01/13/2004 Marketing Information Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date ANDA ANDA076691 01/13/2004 Labeler - Hikma Pharmaceuticals USA Inc. (080189610) Establishment Name Address ID/FEI Business Operations West-Ward Columbus Inc. 058839929 MANUFACTURE(0054-0020) Establishment Name Address ID/FEI Business Operations Livent 126144408 API MANUFACTURE(0054-0020)