Lithium carbonate 400mg modified-release tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
400mg
Oral
Lithium has been used to treat manic episodes since the 19th century[A176642].
Active ingredients:
Lithium carbonate
1 safety notice
Safety information for pregnancy and breastfeeding
Pregnancy
There is conflicting evidence regarding the incidence of cardiovascular abnormalities in first trimester administration of lithium[FDA Label].
Animal studies have shown adverse effects on the fetus and fertility overall[FDA Label].
The risk and benefit of lithium use in pregnancy must be weighed and should lithium treatment continue in pregnancy, serum lithium concentrations should be regularly monitored, dosages should be adjusted, and lithium should be decreased or stopped 2 or 3 days before delivery to avoid maternal and/or neonatal toxicity[FDA Label].
Breastfeeding is not recommended with maternal lithium use but if it is continued, the infant should be monitored for thyroid function and symptoms of lithium toxicity such as hypertonia, hypothermia, cyanosis, and ECG changes[FDA Label].
Breastfeeding
Breastfeeding is not recommended with maternal lithium use but if it is continued, the infant should be monitored for thyroid function and symptoms of lithium toxicity such as hypertonia, hypothermia, cyanosis, and ECG changes[FDA Label].
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
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EudraVigilance
EMA
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
21 branded products available
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Part of the Priadel brand family (generic: Lithium carbonate)
21 products
MHRA licensed products
View all licensed products for Lithium carbonate on the MHRA register
Camcolit 400 modified-release tablets
Camcolit 400 modified-release tablets
Priadel 400mg modified-release tablets
Priadel 400mg modified-release tablets
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£18.60indicative price
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
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Lithium citrate 509mg/5ml oral solution
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Lithium carbonate 200mg/5ml oral suspension
Oral suspension
200mg/5ml
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Lithium citrate 564mg modified-release tablets
Tablet
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Lithium citrate 520mg/5ml oral solution sugar free
Oral solution
520mg/5ml
Same therapeutic group
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Lithium carbonate
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(2)
Chronic kidney disease: assessment and management (NG203)
NG203
NICE guideline
Updated Nov 2021Bipolar disorder: assessment and management (CG185)
CG185
Clinical guideline
Updated Sept 2025Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
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These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
56 found
Half-life
18 to 36 hours
Mechanism
Lithium's mechanism of action is still unknown[FDA Label].
Food interactions
4 warnings
Human targets
5 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
100%
Lithium absorption is rapid and oral bioavailability is close to 100%.
[A176639]
[A176639]
Half-life
18 to 36 hours
The half life of lithium carbonate is 18 to 36 hours[FDA Label]. Other sources say it may be 7 to 20 hours.
[L5858]
[L5858]
Protein binding
Lithium carbonate is not significantly protein bound[FDA Label].
[A176639]
[A176639]
Volume of distribution
0.7 to 1.0L/kg
Apparent volume of distribution is 0.7 to 1.0L/kg[FDA Label].
[L5858]
[L5858]
Metabolism
Lithium carbonate is not metabolized before excretion[FDA Label].
Elimination
Lithium is primarily eliminated through the kidneys and elimination in the feces is insignificant[FDA Label].
Clearance
40mL/min
Clearance is generally between 10 and 40mL/min but may be as low as 15mL/min in elderly patients and those with renal impairment.
[A176639]
[A176639]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Lithium has been used to treat manic episodes since the 19th century[A176642]. Though it is widely used, its mechanism of action is still unknown[FDA Label][A14585][A176642][A176651][L5843]. Lithium carbonate has a narrow therapeutic range and so careful monitoring is required to avoid adverse effects[FDA Label].
Properties:
View FDA drug labelAvg. mass: 73.89 Da
DrugBank indication
Lithium carbonate is indicated as a monotherapy for the treatment of acute manic and mixed episodes associated with bipolar 1 disorder in patients ≥7 years of age.
[L1275]
It is also indicated as a maintenance treatment for bipolar 1 disorder in patients ≥7 years of age.
[L1275]
[L1275]
It is also indicated as a maintenance treatment for bipolar 1 disorder in patients ≥7 years of age.
[L1275]
Also known as(60)
Carbonic acid, dilithium salt
Dilithium carbonate
Lithii carbonas
Lithium carbonate
Lithiumcarbonate
Lithonate
3.1.3.25
IMP 2
Dosage forms(29)
Capsule, liquid filled (Oral) — 300 mg
Tablet, film coated (Oral)
Tablet, film coated (Oral) — 400 mg
Capsule (Oral) — 600 mg
Capsule (Oral) — 150 MG
Capsule (Oral) — 300 MG
Capsule, gelatin coated (Oral) — 300 mg/1
Tablet, extended release (Oral) — 450 mg/1
Molecular properties(18)
Drug interactions(1547)
Known interactions with other medications. Always consult a healthcare professional.
Desmopressin
Moderate
The therapeutic efficacy of Desmopressin can be decreased when used in combination with Lithium carbonate.
The serum concentration of Lithium carbonate can be increased when it is combined with Valsartan.
Olmesartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Olmesartan.
The serum concentration of Lithium carbonate can be increased when it is combined with Losartan.
Candesartan cilexetil
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Candesartan cilexetil.
Eprosartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Eprosartan.
Telmisartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Telmisartan.
Irbesartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Irbesartan.
Forasartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Forasartan.
Saprisartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Saprisartan.
Tasosartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Tasosartan.
The serum concentration of Lithium carbonate can be increased when it is combined with Saralasin.
Azilsartan medoxomil
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Azilsartan medoxomil.
Fimasartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Fimasartan.
Candesartan
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Candesartan.
The serum concentration of Lithium carbonate can be increased when it is combined with Ramipril.
Fosinopril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Fosinopril.
Trandolapril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Trandolapril.
Benazepril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Benazepril.
The serum concentration of Lithium carbonate can be increased when it is combined with Enalapril.
The serum concentration of Lithium carbonate can be increased when it is combined with Moexipril.
Lisinopril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Lisinopril.
Perindopril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Perindopril.
The serum concentration of Lithium carbonate can be increased when it is combined with Quinapril.
Omapatrilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Omapatrilat.
Rescinnamine
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Rescinnamine.
The serum concentration of Lithium carbonate can be increased when it is combined with Captopril.
Cilazapril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Cilazapril.
The serum concentration of Lithium carbonate can be increased when it is combined with Spirapril.
Temocapril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Temocapril.
The serum concentration of Lithium carbonate can be increased when it is combined with Imidapril.
Zofenopril
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Zofenopril.
The serum concentration of Lithium carbonate can be increased when it is combined with Delapril.
Benazeprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Benazeprilat.
Fosinoprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Fosinoprilat.
Ramiprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Ramiprilat.
Trandolaprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Trandolaprilat.
Moexiprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Moexiprilat.
Perindoprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Perindoprilat.
Quinaprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Quinaprilat.
Cilazaprilat
Unknown severity
The serum concentration of Lithium carbonate can be increased when it is combined with Cilazaprilat.
Buprenorphine
Moderate
Lithium carbonate may increase the central nervous system depressant (CNS depressant) activities of Buprenorphine.
Doxylamine
Moderate
Doxylamine may increase the central nervous system depressant (CNS depressant) activities of Lithium carbonate.
Dronabinol
Moderate
Dronabinol may increase the central nervous system depressant (CNS depressant) activities of Lithium carbonate.
Droperidol
Moderate
Droperidol may increase the central nervous system depressant (CNS depressant) activities of Lithium carbonate.
Hydrocodone
Moderate
Lithium carbonate may increase the central nervous system depressant (CNS depressant) activities of Hydrocodone.
Hydroxyzine
Moderate
Hydroxyzine may increase the central nervous system depressant (CNS depressant) activities of Lithium carbonate.
Magnesium sulfate
Moderate
The therapeutic efficacy of Lithium carbonate can be increased when used in combination with Magnesium sulfate.
Methotrimeprazine
Moderate
Lithium carbonate may increase the central nervous system depressant (CNS depressant) activities of Methotrimeprazine.
Metyrosine
Moderate
Lithium carbonate may increase the sedative activities of Metyrosine.
Showing 50 of 1547 interactions
Food & lifestyle interactions
Avoid Alcohol
Avoid alcohol. Alcohol increased peak serum concentrations of lithium.
Advice
Avoid iodine-containing foods and supplements. Iodine and lithium may synergistically produce hypothyroidism.
Caffeine Notice
Limit caffeine intake. Caffeine may decrease lithium concentrations.
Take With Food
Take with food. Food reduces gastrointestinal upset.
Toxicity & overdose
In rats, the oral LD50 is 525mg/kg and the inhalation LC50 is >2.17mg/L over 4 hoursMSDS.
There is insufficient data regarding the carcinogenicity, mutagenicity, or fertility impairment of lithium carbonate[FDA Label]. However, studies in rats and mice have shown repeated daily dosing of lithium carbonate result in adverse effects on male reproductive organs, spermatogenesis, and testosterone levels[FDA Label].
There is conflicting evidence regarding the incidence of cardiovascular abnormalities in first trimester administration of lithium[FDA Label]. Animal studies have shown adverse effects on the fetus and fertility overall[FDA Label].
The risk and benefit of lithium use in pregnancy must be weighed and should lithium treatment continue in pregnancy, serum lithium concentrations should be regularly monitored, dosages should be adjusted, and lithium should be decreased or stopped 2 or 3 days before delivery to avoid maternal and/or neonatal toxicity[FDA Label].
Breastfeeding is not recommended with maternal lithium use but if it is continued, the infant should be monitored for thyroid function and symptoms of lithium toxicity such as hypertonia, hypothermia, cyanosis, and ECG changes[FDA Label].
Safety in effectiveness in patients under 12 years has not been established, however dosing for patients 12 years and older is similar to that of adult patients[FDA Label].
Safety in geriatric patients has not been established, however caution is advised when using lithium as this population is more likely to have impaired renal function[FDA Label].
Patients with creatinine clearance between 30mL/min and 89mL/min should be started at a lower dose and slowly titrated to the correct dose while monitoring serum lithium levels[FDA Label]. Patients with a creatinine clearance less than 30mL/min should not take lithium, especially in the case of a low sodium diet[FDA Label].
There is insufficient data regarding the carcinogenicity, mutagenicity, or fertility impairment of lithium carbonate[FDA Label]. However, studies in rats and mice have shown repeated daily dosing of lithium carbonate result in adverse effects on male reproductive organs, spermatogenesis, and testosterone levels[FDA Label].
There is conflicting evidence regarding the incidence of cardiovascular abnormalities in first trimester administration of lithium[FDA Label]. Animal studies have shown adverse effects on the fetus and fertility overall[FDA Label].
The risk and benefit of lithium use in pregnancy must be weighed and should lithium treatment continue in pregnancy, serum lithium concentrations should be regularly monitored, dosages should be adjusted, and lithium should be decreased or stopped 2 or 3 days before delivery to avoid maternal and/or neonatal toxicity[FDA Label].
Breastfeeding is not recommended with maternal lithium use but if it is continued, the infant should be monitored for thyroid function and symptoms of lithium toxicity such as hypertonia, hypothermia, cyanosis, and ECG changes[FDA Label].
Safety in effectiveness in patients under 12 years has not been established, however dosing for patients 12 years and older is similar to that of adult patients[FDA Label].
Safety in geriatric patients has not been established, however caution is advised when using lithium as this population is more likely to have impaired renal function[FDA Label].
Patients with creatinine clearance between 30mL/min and 89mL/min should be started at a lower dose and slowly titrated to the correct dose while monitoring serum lithium levels[FDA Label]. Patients with a creatinine clearance less than 30mL/min should not take lithium, especially in the case of a low sodium diet[FDA Label].
How it works
Mechanism of action
Lithium's mechanism of action is still unknown[FDA Label]. However, the “inositol depletion theory” suggests 3 main potential targets[A176642]. These targets are inositol monophosphatase, inositol polyphosphatase, and glycogen synthase kinase 3(GSK-3)[A176642][L5843].
The “Inositol depletion theory” suggests lithium behaves as an uncompetitive inhibitor of inositol monophosphatase in a manner inversely proportional to the degree of stimulus[A176642]. This inhibition lowers levels of inositol triphosphate[L5843]. However, stronger inhibitors of inositol monophosphatase are not as clinically effective and low levels of inositol triphosphate are associated with memory impairment[A176642][L5843].
Lithium acts on inositol polyphosphatase as an uncompetitive inhibitor[A176642]. This inhibition is thought to have multiple downstream effects that have yet to be clarified[A176642].
Lithium regulates phosphorylation of GSK-3 which regulates other enzymes through phosphorylation[A176642]. Lithium can also inhibit GSK-3 through interfering with the magnesium ion in the active site[A176642].
The “Inositol depletion theory” suggests lithium behaves as an uncompetitive inhibitor of inositol monophosphatase in a manner inversely proportional to the degree of stimulus[A176642]. This inhibition lowers levels of inositol triphosphate[L5843]. However, stronger inhibitors of inositol monophosphatase are not as clinically effective and low levels of inositol triphosphate are associated with memory impairment[A176642][L5843].
Lithium acts on inositol polyphosphatase as an uncompetitive inhibitor[A176642]. This inhibition is thought to have multiple downstream effects that have yet to be clarified[A176642].
Lithium regulates phosphorylation of GSK-3 which regulates other enzymes through phosphorylation[A176642]. Lithium can also inhibit GSK-3 through interfering with the magnesium ion in the active site[A176642].
Pharmacodynamics
Lithium's mechanism of action is still unknown[FDA Label]. Lithium's therapeutic action may be due to a number of effects, ranging from inhibition of enzymes such as glycogen synthase kinase 3, inositol phosphatases, or modulation of glutamate receptors[A176642][A176651].
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Lithium absorption is rapid and oral bioavailability is close to 100%.
[A176639]
[A176639]
Half-life
The half life of lithium carbonate is 18 to 36 hours[FDA Label]. Other sources say it may be 7 to 20 hours.
[L5858]
[L5858]
Protein binding
Lithium carbonate is not significantly protein bound[FDA Label].
[A176639]
[A176639]
Volume of distribution
Apparent volume of distribution is 0.7 to 1.0L/kg[FDA Label].
[L5858]
[L5858]
Metabolism
Lithium carbonate is not metabolized before excretion[FDA Label].
Route of elimination
Lithium is primarily eliminated through the kidneys and elimination in the feces is insignificant[FDA Label].
Clearance
Clearance is generally between 10 and 40mL/min but may be as low as 15mL/min in elderly patients and those with renal impairment.
[A176639]
[A176639]
Drug targets(5)
Proteins and enzymes this drug interacts with in the body
Inositol monophosphatase 2
IMPA2
Specific functionglucose-1-phosphatase activity
Cellular location
Cytoplasm
General function & pharmacology
Phosphatase that can use myo-inositol monophosphates, myo-inositol 1,4-diphosphate, scyllo-inositol-1,4-diphosphate, glucose-1-phosphate, beta-glycerophosphate and 2'-AMP as substrates in vitro .
PMID:17068342
It is likely that IMPA2 has an as yet unidentified in vivo substrate(s) .
PMID:17068342
Has been implicated as the pharmacological target for lithium (Li(+)) action in brain PMID:17068342
PMID:17068342
It is likely that IMPA2 has an as yet unidentified in vivo substrate(s) .
PMID:17068342
Has been implicated as the pharmacological target for lithium (Li(+)) action in brain PMID:17068342
Glycogen synthase kinase-3 alpha
GSK3A
inhibitor
Specific functionATP binding
General function & pharmacology
Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), CTNNB1/beta-catenin, APC and AXIN1 .
PMID:11749387 PMID:17478001 PMID:19366350
Requires primed phosphorylation of the majority of its substrates .
PMID:11749387 PMID:17478001 PMID:19366350
Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis .
PMID:11749387 PMID:17478001 PMID:19366350
Regulates glycogen metabolism in liver, but not in muscle (By similarity). May also mediate the development of insulin resistance by regulating activation of transcription factors .
PMID:10868943 PMID:17478001
In Wnt signaling, regulates the level and transcriptional activity of nuclear CTNNB1/beta-catenin .
PMID:17229088
Facilitates amyloid precursor protein (APP) processing and the generation of APP-derived amyloid plaques found in Alzheimer disease .
PMID:12761548
May be involved in the regulation of replication in pancreatic beta-cells (By similarity). Is necessary for the establishment of neuronal polarity and axon outgrowth (By similarity).
Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation (By similarity). Acts as a regulator of autophagy by mediating phosphorylation of KAT5/TIP60 under starvation conditions which activates KAT5/TIP60 acetyltransferase activity and promotes acetylation of key autophagy regulators, such as ULK1 and RUBCNL/Pacer .
PMID:30704899
Negatively regulates extrinsic apoptotic signaling pathway via death domain receptors. Promotes the formation of an anti-apoptotic complex, made of DDX3X, BRIC2 and GSK3B, at death receptors, including TNFRSF10B.
The anti-apoptotic function is most effective with weak apoptotic signals and can be overcome by stronger stimulation (By similarity). Phosphorylates mTORC2 complex component RICTOR at 'Thr-1695' which facilitates FBXW7-mediated ubiquitination and subsequent degradation of RICTOR PMID:25897075
PMID:11749387 PMID:17478001 PMID:19366350
Requires primed phosphorylation of the majority of its substrates .
PMID:11749387 PMID:17478001 PMID:19366350
Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis .
PMID:11749387 PMID:17478001 PMID:19366350
Regulates glycogen metabolism in liver, but not in muscle (By similarity). May also mediate the development of insulin resistance by regulating activation of transcription factors .
PMID:10868943 PMID:17478001
In Wnt signaling, regulates the level and transcriptional activity of nuclear CTNNB1/beta-catenin .
PMID:17229088
Facilitates amyloid precursor protein (APP) processing and the generation of APP-derived amyloid plaques found in Alzheimer disease .
PMID:12761548
May be involved in the regulation of replication in pancreatic beta-cells (By similarity). Is necessary for the establishment of neuronal polarity and axon outgrowth (By similarity).
Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation (By similarity). Acts as a regulator of autophagy by mediating phosphorylation of KAT5/TIP60 under starvation conditions which activates KAT5/TIP60 acetyltransferase activity and promotes acetylation of key autophagy regulators, such as ULK1 and RUBCNL/Pacer .
PMID:30704899
Negatively regulates extrinsic apoptotic signaling pathway via death domain receptors. Promotes the formation of an anti-apoptotic complex, made of DDX3X, BRIC2 and GSK3B, at death receptors, including TNFRSF10B.
The anti-apoptotic function is most effective with weak apoptotic signals and can be overcome by stronger stimulation (By similarity). Phosphorylates mTORC2 complex component RICTOR at 'Thr-1695' which facilitates FBXW7-mediated ubiquitination and subsequent degradation of RICTOR PMID:25897075
Inositol monophosphatase 1
IMPA1
Specific functionfructose-1-phosphatase activity
Cellular location
Cytoplasm
General function & pharmacology
Phosphatase involved in the dephosphorylation of myo-inositol monophosphates to generate myo-inositol .
PMID:17068342 PMID:8718889 PMID:9462881
Is also able to dephosphorylate scyllo-inositol-phosphate, myo-inositol 1,4-diphosphate, scyllo-inositol-1,3-diphosphate and scyllo-inositol-1,4-diphosphate .
PMID:17068342
Also dephosphorylates in vitro other sugar-phosphates including D-galactose-1-phosphate, glucose-1-phosphate, glucose-6-phosphate, fructose-1-phosphate, beta-glycerophosphate and 2'-AMP .
PMID:17068342 PMID:8718889 PMID:9462881
Responsible for the provision of inositol required for synthesis of phosphatidylinositols and polyphosphoinositides, and involved in maintaining normal brain function .
PMID:26416544 PMID:8718889
Has been implicated as the pharmacological target for lithium (Li(+)) action in brain, which is used to treat bipolar affective disorder .
PMID:17068342
Is equally active with 1D-myo-inositol 1-phosphate, 1D-myo-inositol 3-phosphate and D-galactose 1-phosphate PMID:9462881
PMID:17068342 PMID:8718889 PMID:9462881
Is also able to dephosphorylate scyllo-inositol-phosphate, myo-inositol 1,4-diphosphate, scyllo-inositol-1,3-diphosphate and scyllo-inositol-1,4-diphosphate .
PMID:17068342
Also dephosphorylates in vitro other sugar-phosphates including D-galactose-1-phosphate, glucose-1-phosphate, glucose-6-phosphate, fructose-1-phosphate, beta-glycerophosphate and 2'-AMP .
PMID:17068342 PMID:8718889 PMID:9462881
Responsible for the provision of inositol required for synthesis of phosphatidylinositols and polyphosphoinositides, and involved in maintaining normal brain function .
PMID:26416544 PMID:8718889
Has been implicated as the pharmacological target for lithium (Li(+)) action in brain, which is used to treat bipolar affective disorder .
PMID:17068342
Is equally active with 1D-myo-inositol 1-phosphate, 1D-myo-inositol 3-phosphate and D-galactose 1-phosphate PMID:9462881
Glycogen synthase kinase-3 beta
GSK3B
Specific functionATP binding
Cellular location
Cytoplasm
General function & pharmacology
Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), EIF2B, CTNNB1/beta-catenin, APC, AXIN1, DPYSL2/CRMP2, JUN, NFATC1/NFATC, MAPT/TAU and MACF1 .
PMID:11430833 PMID:12554650 PMID:14690523 PMID:16484495 PMID:1846781 PMID:20937854 PMID:9072970
Requires primed phosphorylation of the majority of its substrates .
PMID:11430833 PMID:16484495
In skeletal muscle, contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis .
PMID:8397507
May also mediate the development of insulin resistance by regulating activation of transcription factors .
PMID:8397507
Regulates protein synthesis by controlling the activity of initiation factor 2B (EIF2BE/EIF2B5) in the same manner as glycogen synthase .
PMID:8397507
In Wnt signaling, GSK3B forms a multimeric complex with APC, AXIN1 and CTNNB1/beta-catenin and phosphorylates the N-terminus of CTNNB1 leading to its degradation mediated by ubiquitin/proteasomes .
PMID:12554650
Phosphorylates JUN at sites proximal to its DNA-binding domain, thereby reducing its affinity for DNA .
PMID:1846781
Phosphorylates NFATC1/NFATC on conserved serine residues promoting NFATC1/NFATC nuclear export, shutting off NFATC1/NFATC gene regulation, and thereby opposing the action of calcineurin .
PMID:9072970
Phosphorylates MAPT/TAU on 'Thr-548', decreasing significantly MAPT/TAU ability to bind and stabilize microtubules .
PMID:14690523
MAPT/TAU is the principal component of neurofibrillary tangles in Alzheimer disease .
PMID:14690523
Plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex .
PMID:20937854
Phosphorylates MACF1, inhibiting its binding to microtubules which is critical for its role in bulge stem cell migration and skin wound repair (By similarity). Probably regulates NF-kappa-B (NFKB1) at the transcriptional level and is required for the NF-kappa-B-mediated anti-apoptotic response to TNF-alpha (TNF/TNFA) (By similarity). Negatively regulates replication in pancreatic beta-cells, resulting in apoptosis, loss of beta-cells and diabetes (By similarity).
Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation (By similarity). Phosphorylates MUC1 in breast cancer cells, decreasing the interaction of MUC1 with CTNNB1/beta-catenin .
PMID:9819408
Is necessary for the establishment of neuronal polarity and axon outgrowth .
PMID:20067585
Phosphorylates MARK2, leading to inhibition of its activity (By similarity). Phosphorylates SIK1 at 'Thr-182', leading to sustainment of its activity .
PMID:18348280
Phosphorylates ZC3HAV1 which enhances its antiviral activity .
PMID:22514281
Phosphorylates SNAI1, leading to its ubiquitination and proteasomal degradation .
PMID:15448698 PMID:15647282 PMID:25827072 PMID:29059170
Phosphorylates SFPQ at 'Thr-687' upon T-cell activation .
PMID:20932480
Phosphorylates NR1D1 st 'Ser-55' and 'Ser-59' and stabilizes it by protecting it from proteasomal degradation.
Regulates the circadian clock via phosphorylation of the major clock components including BMAL1, CLOCK and PER2 .
PMID:19946213 PMID:28903391
Phosphorylates FBXL2 at 'Thr-404' and primes it for ubiquitination by the SCF(FBXO3) complex and proteasomal degradation (By similarity). Phosphorylates CLOCK AT 'Ser-427' and targets it for proteasomal degradation .
PMID:19946213
Phosphorylates BMAL1 at 'Ser-17' and 'Ser-21' and primes it for ubiquitination and proteasomal degradation .
PMID:28903391
Phosphorylates OGT at 'Ser-3' or 'Ser-4' which positively regulates its activity. Phosphorylates MYCN in neuroblastoma cells which may promote its degradation .
PMID:24391509
Regulates the circadian rhythmicity of hippocampal long-term potentiation and BMAL1 and PER2 expression (By similarity).
Acts as a regulator of autophagy by mediating phosphorylation of KAT5/TIP60 under starvation conditions, activating KAT5/TIP60 acetyltransferase activity and promoting acetylation of key autophagy regulators, such as ULK1 and RUBCNL/Pacer .
PMID:30704899
Negatively regulates extrinsic apoptotic signaling pathway via death domain receptors. Promotes the formation of an anti-apoptotic complex, made of DDX3X, BRIC2 and GSK3B, at death receptors, including TNFRSF10B. The anti-apoptotic function is most effective with weak apoptotic signals and can be overcome by stronger stimulation .
PMID:18846110
Phosphorylates E2F1, promoting the interaction between E2F1 and USP11, stabilizing E2F1 and promoting its activity .
PMID:17050006 PMID:28992046
Phosphorylates mTORC2 complex component RICTOR at 'Ser-1235' in response to endoplasmic stress, inhibiting mTORC2 .
PMID:21343617
Phosphorylates mTORC2 complex component RICTOR at 'Thr-1695' which facilitates FBXW7-mediated ubiquitination and subsequent degradation of RICTOR .
PMID:25897075
Phosphorylates FXR1, promoting FXR1 ubiquitination by the SCF(FBXO4) complex and FXR1 degradation by the proteasome (By similarity).
Phosphorylates interleukin-22 receptor subunit IL22RA1, preventing its proteasomal degradation (By similarity)
PMID:11430833 PMID:12554650 PMID:14690523 PMID:16484495 PMID:1846781 PMID:20937854 PMID:9072970
Requires primed phosphorylation of the majority of its substrates .
PMID:11430833 PMID:16484495
In skeletal muscle, contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis .
PMID:8397507
May also mediate the development of insulin resistance by regulating activation of transcription factors .
PMID:8397507
Regulates protein synthesis by controlling the activity of initiation factor 2B (EIF2BE/EIF2B5) in the same manner as glycogen synthase .
PMID:8397507
In Wnt signaling, GSK3B forms a multimeric complex with APC, AXIN1 and CTNNB1/beta-catenin and phosphorylates the N-terminus of CTNNB1 leading to its degradation mediated by ubiquitin/proteasomes .
PMID:12554650
Phosphorylates JUN at sites proximal to its DNA-binding domain, thereby reducing its affinity for DNA .
PMID:1846781
Phosphorylates NFATC1/NFATC on conserved serine residues promoting NFATC1/NFATC nuclear export, shutting off NFATC1/NFATC gene regulation, and thereby opposing the action of calcineurin .
PMID:9072970
Phosphorylates MAPT/TAU on 'Thr-548', decreasing significantly MAPT/TAU ability to bind and stabilize microtubules .
PMID:14690523
MAPT/TAU is the principal component of neurofibrillary tangles in Alzheimer disease .
PMID:14690523
Plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex .
PMID:20937854
Phosphorylates MACF1, inhibiting its binding to microtubules which is critical for its role in bulge stem cell migration and skin wound repair (By similarity). Probably regulates NF-kappa-B (NFKB1) at the transcriptional level and is required for the NF-kappa-B-mediated anti-apoptotic response to TNF-alpha (TNF/TNFA) (By similarity). Negatively regulates replication in pancreatic beta-cells, resulting in apoptosis, loss of beta-cells and diabetes (By similarity).
Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation (By similarity). Phosphorylates MUC1 in breast cancer cells, decreasing the interaction of MUC1 with CTNNB1/beta-catenin .
PMID:9819408
Is necessary for the establishment of neuronal polarity and axon outgrowth .
PMID:20067585
Phosphorylates MARK2, leading to inhibition of its activity (By similarity). Phosphorylates SIK1 at 'Thr-182', leading to sustainment of its activity .
PMID:18348280
Phosphorylates ZC3HAV1 which enhances its antiviral activity .
PMID:22514281
Phosphorylates SNAI1, leading to its ubiquitination and proteasomal degradation .
PMID:15448698 PMID:15647282 PMID:25827072 PMID:29059170
Phosphorylates SFPQ at 'Thr-687' upon T-cell activation .
PMID:20932480
Phosphorylates NR1D1 st 'Ser-55' and 'Ser-59' and stabilizes it by protecting it from proteasomal degradation.
Regulates the circadian clock via phosphorylation of the major clock components including BMAL1, CLOCK and PER2 .
PMID:19946213 PMID:28903391
Phosphorylates FBXL2 at 'Thr-404' and primes it for ubiquitination by the SCF(FBXO3) complex and proteasomal degradation (By similarity). Phosphorylates CLOCK AT 'Ser-427' and targets it for proteasomal degradation .
PMID:19946213
Phosphorylates BMAL1 at 'Ser-17' and 'Ser-21' and primes it for ubiquitination and proteasomal degradation .
PMID:28903391
Phosphorylates OGT at 'Ser-3' or 'Ser-4' which positively regulates its activity. Phosphorylates MYCN in neuroblastoma cells which may promote its degradation .
PMID:24391509
Regulates the circadian rhythmicity of hippocampal long-term potentiation and BMAL1 and PER2 expression (By similarity).
Acts as a regulator of autophagy by mediating phosphorylation of KAT5/TIP60 under starvation conditions, activating KAT5/TIP60 acetyltransferase activity and promoting acetylation of key autophagy regulators, such as ULK1 and RUBCNL/Pacer .
PMID:30704899
Negatively regulates extrinsic apoptotic signaling pathway via death domain receptors. Promotes the formation of an anti-apoptotic complex, made of DDX3X, BRIC2 and GSK3B, at death receptors, including TNFRSF10B. The anti-apoptotic function is most effective with weak apoptotic signals and can be overcome by stronger stimulation .
PMID:18846110
Phosphorylates E2F1, promoting the interaction between E2F1 and USP11, stabilizing E2F1 and promoting its activity .
PMID:17050006 PMID:28992046
Phosphorylates mTORC2 complex component RICTOR at 'Ser-1235' in response to endoplasmic stress, inhibiting mTORC2 .
PMID:21343617
Phosphorylates mTORC2 complex component RICTOR at 'Thr-1695' which facilitates FBXW7-mediated ubiquitination and subsequent degradation of RICTOR .
PMID:25897075
Phosphorylates FXR1, promoting FXR1 ubiquitination by the SCF(FBXO4) complex and FXR1 degradation by the proteasome (By similarity).
Phosphorylates interleukin-22 receptor subunit IL22RA1, preventing its proteasomal degradation (By similarity)
Glutamate receptor 3
GRIA3
Specific functionAMPA glutamate receptor activity
Cellular location
Cell membrane
General function & pharmacology
Ionotropic glutamate receptor that functions as a ligand-gated cation channel, gated by L-glutamate and glutamatergic agonists such as alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), quisqualic acid, and kainic acid (By similarity). L-glutamate acts as an excitatory neurotransmitter at many synapses in the central nervous system and plays an important role in fast excitatory synaptic transmission by inducing long-term potentiation (By similarity). Binding of the excitatory neurotransmitter L-glutamate induces a conformation change, leading to the opening of the cation channel, and thereby converts the chemical signal to an electrical impulse upon entry of calcium .
PMID:17989220
The receptor then desensitizes rapidly and enters a transient inactive state, characterized by the presence of bound agonist .
PMID:17989220
In the presence of CACNG8, shows resensitization which is characterized by a delayed accumulation of current flux upon continued application of glutamate PMID:21172611
PMID:17989220
The receptor then desensitizes rapidly and enters a transient inactive state, characterized by the presence of bound agonist .
PMID:17989220
In the presence of CACNG8, shows resensitization which is characterized by a delayed accumulation of current flux upon continued application of glutamate PMID:21172611
Transporters(3)
Proteins that transport this drug across cell membranes
Epithelial sodium channel subunit alpha
SCNN1A
Specific functionligand-gated sodium channel activity
Cellular location
Apical cell membrane
General function & pharmacology
This is one of the three pore-forming subunits of the heterotrimeric epithelial sodium channel (ENaC), a critical regulator of sodium balance and fluid homeostasis .
PMID:30251954 PMID:32729833 PMID:8023962 PMID:8278374 PMID:9792722
ENaC operates in epithelial tissues, where it mediates the electrodiffusion of sodium ions from extracellular fluid through the apical membrane of cells, with water following osmotically .
PMID:24124190 PMID:28710092 PMID:8278374
It plays a key role in maintaining sodium homeostasis through electrogenic sodium reabsorption in the kidneys .
PMID:12107247
Additionally, ENaC is essential for airway surface liquid homeostasis, which is crucial for proper mucus clearance PMID:24124190 PMID:28710092
PMID:30251954 PMID:32729833 PMID:8023962 PMID:8278374 PMID:9792722
ENaC operates in epithelial tissues, where it mediates the electrodiffusion of sodium ions from extracellular fluid through the apical membrane of cells, with water following osmotically .
PMID:24124190 PMID:28710092 PMID:8278374
It plays a key role in maintaining sodium homeostasis through electrogenic sodium reabsorption in the kidneys .
PMID:12107247
Additionally, ENaC is essential for airway surface liquid homeostasis, which is crucial for proper mucus clearance PMID:24124190 PMID:28710092
Epithelial sodium channel subunit beta
SCNN1B
Specific functionligand-gated sodium channel activity
Cellular location
Apical cell membrane
General function & pharmacology
This is one of the three pore-forming subunits of the heterotrimeric epithelial sodium channel (ENaC), a critical regulator of sodium balance and fluid homeostasis .
PMID:30251954 PMID:32729833 PMID:7762608 PMID:9792722
ENaC operates in epithelial tissues, where it mediates the electrodiffusion of sodium ions from extracellular fluid through the apical membrane of cells, with water following osmotically .
PMID:24124190
It plays a key role in maintaining sodium homeostasis through electrogenic sodium reabsorption in the kidneys .
PMID:12107247
Additionally, ENaC is essential for airway surface liquid homeostasis, which is crucial for proper mucus clearance PMID:24124190
PMID:30251954 PMID:32729833 PMID:7762608 PMID:9792722
ENaC operates in epithelial tissues, where it mediates the electrodiffusion of sodium ions from extracellular fluid through the apical membrane of cells, with water following osmotically .
PMID:24124190
It plays a key role in maintaining sodium homeostasis through electrogenic sodium reabsorption in the kidneys .
PMID:12107247
Additionally, ENaC is essential for airway surface liquid homeostasis, which is crucial for proper mucus clearance PMID:24124190
Epithelial sodium channel subunit gamma
SCNN1G
Specific functionligand-gated sodium channel activity
Cellular location
Apical cell membrane
General function & pharmacology
This is one of the three pore-forming subunits of the heterotrimeric epithelial sodium channel (ENaC), a critical regulator of sodium balance and fluid homeostasis .
PMID:30251954 PMID:32729833 PMID:7550319 PMID:7762608 PMID:9792722
ENaC operates in epithelial tissues, where it mediates the electrodiffusion of sodium ions from extracellular fluid through the apical membrane of cells, with water following osmotically .
PMID:24124190
It plays a key role in maintaining sodium homeostasis through electrogenic sodium reabsorption in the kidneys .
PMID:12107247 PMID:7550319 PMID:8640238
Additionally, ENaC is essential for airway surface liquid homeostasis, which is crucial for proper mucus clearance PMID:18507830 PMID:19017867 PMID:24124190
PMID:30251954 PMID:32729833 PMID:7550319 PMID:7762608 PMID:9792722
ENaC operates in epithelial tissues, where it mediates the electrodiffusion of sodium ions from extracellular fluid through the apical membrane of cells, with water following osmotically .
PMID:24124190
It plays a key role in maintaining sodium homeostasis through electrogenic sodium reabsorption in the kidneys .
PMID:12107247 PMID:7550319 PMID:8640238
Additionally, ENaC is essential for airway surface liquid homeostasis, which is crucial for proper mucus clearance PMID:18507830 PMID:19017867 PMID:24124190
Scientific references(4)
Quiroz J.A., Machado-Vieira R., Zarate CA Jr, Manji H.K.
Novel insights into lithium's mechanism of action: neurotrophic and neuroprotective effects.
Neuropsychobiology
201062(1):50-60. doi: 10.1159/000314310. Epub 2010 May 7
Hedya S.A., Swoboda H.D.
Hedya nubiferana (bud moth). CABI Compendium. 2021. doi: 10.
1079/cabicompendium
6905
Serretti A., Drago A., De Ronchi D.
Lithium Pharmacodynamics and Pharmacogenetics: Focus on Inositol Mono Phosphatase (IMPase), Inositol Poliphosphatase (IPPase) and Glycogen Sinthase Kinase 3 Beta (GSK-3 Beta).
Current Medicinal Chemistry
200916(15):1917-1948. doi: 10.2174/092986709788186101
Chalecka-Franaszek E., Chuang D.M.
Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons.
Proceedings of the National Academy of Sciences
199996(15):8745-8750. doi: 10.1073/pnas.96.15.8745
Affected organisms(1)
Humans and other mammals
International brands(1)
Experimental properties(3)
Commercial products(206)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Lithium carbonate
Additional database identifiers
Drugs Product Database (DPD)
10227
ChemSpider
10654
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6051
GenAtlas
IMPA2
GeneCards
IMPA2
GenBank Gene Database
AF014398
GenBank Protein Database
2406666
UniProt Accession
IMPA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4616
GeneCards
GSK3A
Guide to Pharmacology
2029
UniProt Accession
GSK3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6050
GenAtlas
IMPA1
GeneCards
IMPA1
GenBank Gene Database
X66922
GenBank Protein Database
395340
Guide to Pharmacology
1463
UniProt Accession
IMPA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4617
GenAtlas
GSK3B
GeneCards
GSK3B
GenBank Gene Database
L33801
GenBank Protein Database
529237
Guide to Pharmacology
2030
UniProt Accession
GSK3B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4573
GenAtlas
GRIA3
GeneCards
GRIA3
GenBank Gene Database
U10302
GenBank Protein Database
507829
Guide to Pharmacology
446
UniProt Accession
GRIA3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10599
GenAtlas
SCNN1A
GeneCards
SCNN1A
GenBank Gene Database
X76180
GenBank Protein Database
452650
Guide to Pharmacology
738
UniProt Accession
SCNNA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10600
GenAtlas
SCNN1B
GeneCards
SCNN1B
GenBank Gene Database
X87159
GenBank Protein Database
1004271
Guide to Pharmacology
739
UniProt Accession
SCNNB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10602
GenAtlas
SCNN1G
GeneCards
SCNN1G
GenBank Gene Database
X87160
GenBank Protein Database
1004273
Guide to Pharmacology
741
UniProt Accession
SCNNG_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)