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Ball-and-stick model of the lurasidone molecule
Clinical data
Trade names Latuda
AHFS/ Consumer Drug Information
MedlinePlus a611016
License data
  • AU: B1
  • US: B (No risk in non-human studies)
Routes of
By mouth
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability 9–19% (oral)[1]
Protein binding ~99%[2]
Metabolism Liver (CYP3A4-mediated)[1]
Biological half-life 18–40 hours[1][2]
Excretion Faecal (67–80%),
renal (9–19%)[1][2]
Synonyms SM-13,496
CAS Number
PubChem CID
ECHA InfoCard 100.225.187
Chemical and physical data
Formula C28H36N4O2S
Molar mass 492.68 g/mol
3D model (Jmol)
Specific rotation [α]20D −59°
Melting point 176 to 178 °C (349 to 352 °F)
Solubility in water 45 mg/mL (20 °C)

Lurasidone /lɜːr.ˈræ.sɪ.dn/ (trade name Latuda) is an atypical antipsychotic developed by Dainippon Sumitomo Pharma[3] and marketed by Sunovion in the USA. It has been approved for treatment of schizophrenia by the FDA since 2010. In the USA since 2013, it is also approved for the treatment of depressive episodes associated with bipolar I disorder as well as bipolar II disorder in adults when used alone or in combination with lithium, valproate, or lamotrigine.

Medical uses[edit]

Lurasidone is approved by the US Food and Drug Administration (FDA) for the treatment of schizophrenia since 2010[4] and depressive episodes associated with bipolar I disorder since 2013.[5] It received regulatory approval in the United Kingdom in September 2014. In October 2014, NHS Scotland advised use of lurasidone for schizophrenic adults who have not seen improvements with previous antipsychotics due to problems that arise from weight gain or changes in metabolic pathways when taking other medications.[6] It received approval by the European Medicines Agency on 24 January 2014. It was launched in Canada for the treatment of schizophrenia in September 2012, Health Canada giving their Summary Basis of Decision (SBD) as favourable on 15 October 2012.[7] European Commission has granted a marketing authorization for once-daily oral lurasidone for the treatment of schizophrenia in adults.[8] It is approved for use in the EU.[9]

In July 2013 lurasidone received approval for bipolar I depression.[5] Few available atypical antipsychotics are known to possess antidepressant efficacy in bipolar disorder (with the notable exceptions being quetiapine,[10][11][12][13] olanzapine[14][15][16] and possibly asenapine[17]) as a monotherapy, even though the majority of atypical antipsychotics are known to possess significant antimanic activity,[18] which is yet to be clearly demonstrated for lurasidone.

Lurasidone is not approved by the Food and Drug Administration (FDA) for the treatment of behavior disorders in older adults with dementia.[citation needed]


Lurasidone is contraindicated in individuals who are taking strong inhibitors of the liver enzyme CYP3A4 (ketoconazole, clarithromycin, ritonavir, levodropropizine, etc.) or inducers (carbamazepine, St. John's wort, phenytoin, rifampicin etc.).[19] The use of lurasidone in pregnant women has not been studied and is not recommended; in animal studies, no risks have been found.[20] Excretion in breast milk is also unknown; lurasidone is not recommended for breastfeeding women.[21] In the United States it is not indicated for use in children.[22]

Side effects[edit]

Side effects are generally similar to other antipsychotics. The drug has a relatively well-tolerated side effect profile, with low propensity for QTc interval changes, weight gain and lipid-related adverse effects.[23] In a recent meta-analysis of the efficacy and tolerability of 15 antipsychotic drugs it was found to produce the second least (after haloperidol) weight gain, the least QT interval prolongation, the fourth most extrapyramidal side effects (after haloperidol, zotepine and chlorpromazine) and the sixth least sedation (after paliperidone, sertindole, amisulpride, iloperidone and aripiprazole).[24]

As with other atypical neuroleptics, lurasidone should be used with caution in the elderly because it puts them at an increased risk for a stroke or transient ischemic attack;[25][26] however, these risks are not likely to be greater than those associated with antipsychotics of other classes.[27] Similarly, lurasidone should not be used to treat dementia-related psychosis, as evidence has shown increased mortality with antipsychotic use.[28]

Weight gain is reported in up to 15 and 16 percent of users.[29][30]


Blood plasma concentrations may be increased when combined with CYP3A4 inhibitors, possibly leading to more side effects. This has been clinically verified for ketoconazole, which increases lurasidone exposure by a factor of 9, and is also expected for other 3A4 inhibitors such as grapefruit juice. Co-administration of CYP3A4 inducers like rifampicin or St. John's wort can reduce plasma levels of lurasidone and its active metabolite, and consequently decrease the effects of the drug. For rifamipcin, the reduction was sixfold in a study.[2]


Mechanism of action[edit]

Lurasidone acts as an antagonist of the following sites[31][32] with the exception of 5-HT1A, where it acts as a partial agonist.[31] The α receptors are adrenergic receptors, D stands for dopamine receptors, and 5-HT for serotonin receptors. The higher the number in the second column, the lower the affinity.

Receptor Affinity (Ki (nM))
α1 receptor 48
α2A receptor 1.6
α2C receptor 10.8
D1 receptor 262
D2 receptor 0.9
D3 receptor 15.7
D4.4 receptor 30
5-HT1A receptor 6.8
5-HT2A receptor 2.0
5-HT2C receptor 415
5-HT3 receptor >1000
5-HT4 receptor >1000
5-HT7 receptor 0.5

Lurasidone has negligible actions at the histamine H1 and muscarinic acetylcholine receptors.[31][33]

No affinity for the H1 receptor[34] and low affinity for 5-HT2C explains the low weight gain.[32][34][35][verification needed]


ID-14283, the main active metabolite. The hydroxylation of the norbornane ring is highlighted.[36] The other active metabolite, ID-14326, has the OH group in endo position.[37]
The main inactivation step by oxidative N-dealkylation produces the metabolites ID-11614 and ID-20219.[37][38]

Lurasidone is taken by mouth and has an estimated absorption rate of 9 to 19%.[1] Studies have shown that when lurasidone is taken with food, absorption increases about twofold. Peak blood plasma concentrations are reached after one to three hours. About 99% of the circulating substance are bound to plasma proteins.[2]

Lurasidone is mainly metabolized in the liver via the enzyme CYP3A4, but has negligible affinity to other cytochrome P450 enzymes. It is transported by P-glycoprotein and ABCG2 and also inhibits these carrier proteins in vitro. It also inhibits the solute carrier protein SLC22A1, but no other relevant transporters.[2][25]

Main metabolism pathways are oxidative N-dealkylation between the piperazine and cycloheyane rings, hydroxylation of the norbornane ring, and S-oxidation.[2][38]:59 Other pathways are hydroxylation of the cyclohexane ring and reductive cleavage of the isothiazole ring followed by S-methylation.[37] The two relevant active metabolites are the norbornane hydroxylation products called ID-14283 and ID-14326, the former reaching pharmacologically relevant blood plasma concentrations. The two major inactive metabolites are the N-dealkylation products (the carboxylic acid ID-20219 and the piperazine ID-11614[37]), and a norbornane hydroxylated derivative of ID-20219 (ID-20220). Of lurasidone and its metabolites circulating in the blood, the native drug makes up 11%, the main active metabolite 4%, and the inactive carboxylic acids 24% and 11%, respectively.[1][2] Several dozen metabolites have been identified altogether.[38]:59–61

Biological half-life is given as 18 hours or 20 to 40 hours in different sources. 80% or 67% of a radiolabelled dose was recovered from the faeces, and 9% or 19% from the urine.[1][2]


The FDA approved the drug in 2010.[38]

Society and culture[edit]

Brand names[edit]

In India, this drug is available under the brand name of Lurafic.[citation needed]


Lurasidone may be useful for treating the cognitive and memory deficits seen in schizophrenia. In animal studies, it reversed dizocilpine-induced learning and memory impairment and was found to be superior in doing this to all of the other antipsychotics examined, including risperidone, olanzapine, quetiapine, clozapine, aripiprazole, and haloperidol.[31][39] Lurasidone has activity at several serotonin receptors that are involved in learning and memory, and unlike most other antipsychotics, lacks any anticholinergic effects (which are known to impair cognitive processes and memory).[31] These properties may underlie its improved effectiveness in treating these symptoms relative to older agents.[31]


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