U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS


Stereochemistry ACHIRAL
Molecular Formula C4H5O4.Li
Molecular Weight 124.021
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0







Molecular Formula C4H5O4
Molecular Weight 117.0801
Charge -1
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Molecular Formula Li
Molecular Weight 6.941
Charge 1
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Curator's Comment: Description was created based on several sources, including https://www.ncbi.nlm.nih.gov/pubmed/19538681 | https://www.ncbi.nlm.nih.gov/pubmed/23371914 | http://www.rsc.org/periodic-table/element/3/lithium

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and John Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.


Curator's Comment: The first lithium mineral petalite, LiAlSi4O10, was discovered on the Swedish island of Utö by the Brazilian, Jozé Bonifácio de Andralda e Silva in the 1790s. It was observed to give an intense crimson flame when thrown onto a fire. In 1817, Johan August Arfvedson of Stockholm analysed it and deduced it contained a previously unknown metal, which he called lithium. He realised this was a new alkali metal and a lighter version of sodium. However, unlike sodium he was not able to separate it by electrolysis. In 1821 William Brande obtained a tiny amount this way but not enough on which to make measurements. It was not until 1855 that the German chemist Robert Bunsen and the British chemist Augustus Matthiessen obtained it in bulk by the electrolysis of molten lithium chloride.

Approval Year



Primary TargetPharmacologyConditionPotency
6.53 µM [IC50]
2.0 mM [Ki]
Target ID: O95861
Gene ID: 10380.0
Gene Symbol: BPNT1
Target Organism: Homo sapiens (Human)
0.3 mM [IC50]


ConditionModalityTargetsHighest PhaseProduct

Approved Use

Lithium is indicated in the treatment of manic episodes of Bipolar Disorder.

Launch Date



Sodium bicarbonate and systemic hemodynamics in volunteers anesthetized with halothane.
1975 May
Obsolete but dangerous antacid preparations.
1978 Jan
Organophosphate poisoning: modifications in acid base equilibrium and use of sodium bicarbonate as an aid in the treatment of toxicity in dogs.
1983 Feb
Calcification of superficial scalp veins secondary to intravenous infusion of sodium bicarbonate and calcium chloride.
1983 Jul
Bupivacaine cardiotoxicity in a pregnant patient with mitral valve prolapse.
1983 Jun
[Effect of antacids on mineral metabolism].
1983 Mar
Experimental amitriptyline intoxication: electrophysiologic manifestations and management.
1984 Jan-Feb
Treatment of ventricular tachyarrhythmias resulting from amitriptyline toxicity in dogs.
1984 Nov
Urothelial injury to the rabbit bladder from various alkaline and acidic solutions used to dissolve kidney stones.
1986 Jul
Experimental amitriptyline intoxication: treatment of cardiac toxicity with sodium bicarbonate.
1986 Sep
Incidence of hypotension associated with epidural anesthesia using alkalinized and nonalkalinized lidocaine for cesarean section.
1987 Nov
The effect of pH buffering on reducing the pain associated with subcutaneous infiltration of bupivicaine.
1991 Mar
Summation effects of uracil and other promoters on epithelial lesion development in the F344 rat urinary bladder initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine.
1991 Nov
Reversal of desipramine toxicity in rats using drug-specific antibody Fab' fragment: effects on hypotension and interaction with sodium bicarbonate.
1992 Mar
Sodium bicarbonate alleviates penile pain induced by intracavernous injections for erectile dysfunction.
1993 May
Alkalinization of local anesthesia with sodium bicarbonate--preferred method of local anesthesia.
1994 Jan
Effects of magnesium sulfate and lidocaine in the treatment of ventricular arrhythmias in experimental amitriptyline poisoning in the rat.
1994 Mar
Reversal of flecainide-induced ventricular arrhythmia by hypertonic sodium bicarbonate in dogs.
1995 May
Neutralizing pH of lidocaine reduces pain during Norplant system insertion procedure.
1995 May
Reduction of desipramine cardiotoxicity and prolongation of survival in rats with the use of polyclonal drug-specific antibody Fab fragments.
1995 Sep
Effect of calcium chloride and 4-aminopyridine therapy on desipramine toxicity in rats.
Pathophysiology and treatment of cocaine toxicity: implications for the heart and cardiovascular system.
1996 Dec
Metabolic alkalosis and myoclonus from antacid ingestion.
1996 Jun
Therapy of Sjögren's syndrome. New aspects and future directions.
1998 Feb
Oral sodium bicarbonate reduces proximal renal tubular peptide catabolism, ammoniogenesis, and tubular damage in renal patients.
1998 Mar
The effects of sodium bicarbonate on thioridazine-induced cardiac dysfunction in the isolated perfused rat heart.
2001 Apr
Renal tubular peptide catabolism in chronic vascular rejection.
2001 May-Jul
The prevention of pain from injection of rocuronium by magnesium sulphate, lignocaine, sodium bicarbonate and alfentanil.
2003 Jun
Fanconi syndrome caused by antiepileptic therapy with valproic Acid.
2004 Jul
Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial.
2004 May 19
Alkaline induces metallothionein gene expression and potentiates cell proliferation in Chinese hamster ovary cells.
2005 Dec
Reversal of citalopram-induced junctional bradycardia with intravenous sodium bicarbonate.
2005 Jan
Quinidine cardiotoxicity.
2005 May
Early bicarbonate loading and dantroline for ziprasidone/haloperidol-induced neuroleptic malignant syndrome.
2006 Apr
Nalidixic acid overdose and metabolic acidosis.
2006 Mar
Acute renal failure due to phenazopyridine (Pyridium) overdose: case report and review of the literature.
2006 Nov
Deregulation of the p16-cyclin D1/cyclin-dependent kinase 4-retinoblastoma pathway involved in the rat bladder carcinogenesis induced by terephthalic acid-calculi.
2006 Oct
Comparison of usefulness of sodium bicarbonate versus sodium chloride to prevent contrast-induced nephropathy in patients undergoing an emergent coronary procedure.
2007 Sep 1
Contrast medium-induced nephropathy: strategies for prevention.
2008 Sep
G418-mediated ribosomal read-through of a nonsense mutation causing autosomal recessive proximal renal tubular acidosis.
2008 Sep
Sodium bicarbonate versus normal saline for protection against contrast nephropathy.
Mass casualties from acute inhalation of chlorine gas.
2009 Dec
Iatrogenic Flecainide toxicity.
2010 Dec
Randomized controlled trial: lisinopril reduces proteinuria, ammonia, and renal polypeptide tubular catabolism in patients with chronic allograft nephropathy.
2010 Jan 15
Acute propafenone toxicity after two exposures at standard dosing.
2010 Jun-Jul
Hyper-alkalinization without hyper-hydration for the prevention of high-dose methotrexate acute nephrotoxicity in patients with osteosarcoma.
2010 Nov
High sensitivity of RBL-2H3 cells to cadmium and manganese: an implication of the role of ZIP8.
2011 Jul
Chemicals inducing acute irritant contact dermatitis mobilize intracellular calcium in human keratinocytes.
2013 Feb
Evaluation of aggregating brain cell cultures for the detection of acute organ-specific toxicity.
2013 Jun
Hexavalent chromium affects sperm motility by influencing protein tyrosine phosphorylation in the midpiece of boar spermatozoa.
2016 Jan

Sample Use Guides

Optimal patient response to Lithium Carbonate usually can be established and maintained with 600 mg t.i.d. Optimal patient response to Lithium Oral Solution usually can be established and maintained with 10 mL (2 full teaspoons) (16 mEq of lithium) t.i.d. Such doses will normally produce an effective serum lithium level ranging between 1.0 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 of 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.
Route of Administration: Oral
Although lithium at a high concentration (10 mM) activated β-catenin in different types of neurons, β-catenin shifted to the nucleus at a therapeutically relevant concentration (1 mM) only in thalamic neurons, both in vivo and in vitro.
Substance Class Chemical
by admin
on Thu Jul 06 01:01:33 UTC 2023
by admin
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