Cariprazine 3mg capsules
Requires a prescription from a doctor or prescriber
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Suspected adverse reactions reported for Cariprazine
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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Suspected adverse reactions reported for Cariprazine
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1 branded products available
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Reagila 3mg capsules
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.
WHO defined daily dose (DDD)
3 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Codes for healthcare professionals and prescribing systems
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 code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 42 · Randomised trials: 8 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
M. Olivola, N. Bassetti, Serena Parente, et al.
Current Neuropharmacology, 2023
Cognitive deficits are associated with schizophrenia and show a progressive worsening, often being unresponsive to treatment. New antipsychotic molecules acting as antagonist at the serotoninergic 5-hydroxytryptamine receptor 7 (e.g. lurasidone) or partial agonists at dopamine D3 receptor (e.g. cariprazine) could have an impact on cognition in this patient group. The aim of the systematic review is to explore the efficacy of lurasidone and cariprazine in improving cognition in both animal models and human studies. The following terms: (lurasidone AND cognit*) OR (cariprazine AND cognit*) were searched in Web of Science from inception to December 2021. We included all studies that assessed changes in cognitive function after treatment with cariprazine or lurasidone. Of 201 selected articles, 36 were included. Twenty-four articles used animal models (rats, mice and marmosets), five evaluating the effects of cariprazine and 19 the effects of lurasidone. Twelve articles were clinical studies (cariprazine n = 2; lurasidone n = 10). In both animal and human studies lurasidone showed a greater efficacy on cognitive performance compared to placebo, quetiapine, ziprasidone or treatment-as-usual. Cariprazine was superior to other antipsychotics in improving cognitive functions in both animal and human studies. The cognitive effect of lurasidone could be explained by its potent antagonism at the 5-HT7 receptors combined with partial agonism at 5-HT1A receptors. The pro-cognitive effect of cariprazine is probably explained by its very high affinity for D3 receptors. Head-to-head studies comparing lurasidone and cariprazine are needed to establish the “first-choice” treatment for cognitive dysfunction associated with schizophrenia.
Abstract licence: CC BY
João Martins-Correia, L. A. Fernandes, R. Kenny, et al.
Journal of affective disorders, 2024
Á. Barabássy, R. Csehi, Z. Dombi, et al.
Pharmaceuticals, 2025
Eman Ali, Fakhar Latif, Yusra Mashkoor, et al.
Asian journal of psychiatry, 2024
H. Gill, D. Chen-Li, Sipan Haikazian, et al.
CNS Spectrums, 2024
Xiao N, Yin L, Lee S, et al.
2025
- Antipsychotic Agents
- Antidepressive Agents
- Bipolar Disorder
BackgroundThere is a need to provide up-to-date, clinically translatable data as it relates to the treatment of a major depressive episode (MDE) with mixed features.MethodsPubMed and OVID were searched from inception to July 22, 2024. Randomized controlled trials (RCTs) investigating the efficacy of pharmacological agents for adults with bipolar disorder (BD) or major depressive disorder (MDD) in an MDE with mixed features were included. Risk of bias was assessed using the Cochrane Risk of Bias Tool for Randomized Studies (RoB2).ResultsA total of seven studies were included in this systematic review. The studies identified were all short-term acute studies ranging from 6 to 8 weeks. Treatment with lurasidone, olanzapine, cariprazine, lumateperone, quetiapine, and ziprasidone was associated with statistically significant reduction of depressive symptoms in MDEs with mixed features. Only lumateperone is studied in both BD subtypes [bipolar I disorder (BD-I), bipolar II disorder (BD-II)] and MDD, wherein efficacy in mixed features was the prespecified primary outcome. Lurasidone has a single study in MDD, while ziprasidone has data in a mixed sample of BD-II and MDD. Data for the other agents in mixed features is post hoc. Co-occurring hypomanic symptoms generally improved, and there was no significant difference between the above treatments and placebo with respect to hypomanic symptom severity intensification or treatment-emergent affective switching.ConclusionSelect atypical antipsychotics are effective in alleviating depressive symptoms in persons with mixed features; albeit, much of the data is obtained from post hoc analysis. Minimal evidence exists for the efficacy of lithium or valproate in the treatment of depressive episodes with mixed features. Antidepressant monotherapy has not been adequately evaluated in depressive episodes with mixed features. In addition, there is a pressing need for a consistent definition of mixed presentations to guide future interventional studies.
Abstract licence: CC BY
L. García-Fernández, V. Romero-Ferreiro, Inmaculada Peñuelas-Calvo, et al.
Harvard Review of Psychiatry, 2024
Livio Tarchi, Susan Bugini, C. Dani, et al.
CNS Drugs, 2024
Pappa S, Csehi R, Caldwell-Dunn E, et al.
2025
- Piperazines
- Clozapine
- Antipsychotic Agents
Treatment-resistant schizophrenia affects over half of individuals with schizophrenia. Clozapine is the only approved treatment in the United States but often provides limited relief. Augmenting clozapine with cariprazine (CAR) (a D3-preferring dopamine D2-D3 partial agonist) may improve outcomes. This systematic review evaluated the efficacy and safety of this combination in patients with sub-optimal response. A search of PubMed, Embase, and Cochrane Library yielded 52 cases from 21 eligible studies to be included in the analysis. Patient and treatment characteristics and clinical outcomes were synthesized. Cariprazine replaced another antipsychotic or was added to clozapine monotherapy in 44.2% and 34.6% of cases, respectively. Before treatment, 90% of patients had positive and 81% had negative symptoms. Combination therapy improved these symptoms in 66% and 83% of cases, respectively. In 19 patients with Positive and Negative Symptom Scale scores available before and after treatment, total scores decreased by 43.4%, with positive and negative subscale reductions of 23.0% and 59.1%. The combination was generally well tolerated; some patients experienced weight loss and reduced clozapine-related side effects. New adverse events occurred in 19% (most commonly akathisia at 6%). Cariprazine was discontinued in 17% of cases due to side effects or lack of efficacy. Overall, the combination appears safe and promising, especially for persistent negative symptoms, likely due to complementary neuroreceptor effects. Larger controlled trials are needed to confirm these findings.
Abstract licence: CC BY
Koukopoulos A, Janiri D, Milintenda M, et al.
2025
Background/Objectives: Dopamine partial agonists are drugs initially developed to treat schizophrenia, seeking a double effect of increased dopaminergic transmission in the prefrontal cortex and decrease in the accumbens/striatum. Of these drugs, aripiprazole, brexpiprazole, and cariprazine are currently marketed and used in schizophrenia spectrum and mood disorders. It is debated whether patients with psychiatric disorders becoming pregnant should discontinue or continue their antipsychotic treatment despite some risks for the fetus, i.e., whether it is worse to have an untreated disorder or treating it with drugs. The safety of drugs for mother and baby extend from pregnancy to the postpartum, when breastfeeding assumes great importance. We set to investigate the use of dopamine partial agonists in pregnancy and lactation. Methods: On 23 June 2025, we used suitable strategies for identifying cases and studies of cariprazine, aripiprazole, brexpiprazole, dopamine partial agonists in pregnancy, perinatal period, and/or lactation on PubMed, CINAHL, PsycInfo/PsycArticles, Scopus, and ClinicalTrials.gov. We used the PRISMA Statement in developing our review. We included case reports and clinical studies. We excluded reports without pregnancy or focused on other drugs than the above. We reached consensus on eligibility with Delphi rounds among all authors. Results: Our searches produced 386 results on the above databases. We included 24 case reports/series and 15 studies. Most studies showed no negative pregnancy outcomes. There were serious concerns about the use of dopamine D2/D3 partial agonists during lactation. Conclusions: The use of dopamine partial agonists during pregnancy appears to be safe, but during breastfeeding they should be better avoided.
Abstract licence: CC BY
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study 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
19 found
Half-life
314 to 446 hours
Mechanism
While recent research points to the involvement of multiple neurotransmitters in…
Food interactions
4 warnings
Human targets
8 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
3.6 hours
Half-life
314 to 446 hours
[A247095]
Terminal half-lives of cariprazine, DCAR, and DDCAR ranged from 31.6…
Protein binding
91 to 97%
[L40198]
Metabolism
Elimination
12.5 mg/d
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L43307][L40198]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1238 interactions
The possibility of multiple drug involvement should also be considered.
[L40198]
The exact mechanism of action of cariprazine is not fully elucidated. Cariprazine potently binds to both of these receptors, more preferably to D3 receptors with higher affinity.[A3941] Preclinical studies suggest that D3 receptor blockade is associated with exerting pro-cognitive and antidepressant effects and attenuating negative symptoms in schizophrenia.[A247095] This unique mechanism of action differs from that of other antipsychotic agents that mostly target D2 and 5-HT2A receptors.[A247055] Cariprazine is also a partial agonist at 5-HT1A receptors, an antagonist at 5-HT2B and 5-HT2A receptors, an antagonist at histamine H1 receptors. It also binds to 5-HT2C, alpha (α)-1A adrenergic, and alpha (α)-1B adrenergic receptors with low affinity.[A3941][A247095]
As cariprazine is a partial agonist at dopamine D2 and D3 receptors, it produces an apparent lower blockade level than other antipsychotic agents that block dopamine receptors. This receptor binding profile is advantageous as dopamine receptor blockade is associated with extrapyramidal symptoms as side effects. Partial agonism would allow the dopamine receptor to be stimulated even at maximal receptor occupancy by the drug.[A247100] Antagonism at 5-HT1A [A247100] and 5-HT2A receptors by cariprazine can increase dopaminergic neurotransmission in the nigrostriatal pathway, thereby further reducing the risk of extrapyramidal symptoms.[A247055] However, cariprazine is still associated with a risk of akathisia, extrapyramidal disorder, restlessness, and tremor.[A3941][L40198]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A3941]
After single dose administration of cariprazine, the peak plasma cariprazine concentration occurred in approximately three to six hours.
[L40198]
In healthy volunteers, the Tmax following oral administration was 3.6 hours for cariprazine, 6.5 hours for DCAR, and 18.1 hours for DDCAR. The steady-state was reached dose-proportionally within three weeks for cariprazine, DCAR, and DDCAR in patients with schizophrenia.
[A3941]
Administration of a single dose of 1.5 mg cariprazine capsule with a high-fat meal did not significantly affect the Cmax and AUC of cariprazine or its metabolite, desmethyl cariprazine (DCAR).
[L40198]
[A247095]
Terminal half-lives of cariprazine, DCAR, and DDCAR ranged from 31.6 to 68.4, 29.7 to 37.5, and 314 to 446 hours, respectively. The effective half-life, calculated from time to steady state, or the functional half-life of total active moieties was approximately one week.
[A247060]
[L40198]
DDCAR can be metabolized by CYP3A4 to form a hydroxylated metabolite.
[A3940][A3941][L40198]
[L40198]
Proteins and enzymes this drug interacts with in the body
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity)
PMID:22957663 PMID:3138543 PMID:33762731 PMID:37935376 PMID:37935377 PMID:8138923 PMID:8393041
Also functions as a receptor for various drugs and psychoactive substances .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:38552625 PMID:8138923 PMID:8393041
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:8138923 PMID:8393041
HTR1A is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission: signaling inhibits adenylate cyclase activity and activates a phosphatidylinositol-calcium second messenger system that regulates the release of Ca(2+) ions from intracellular stores .
PMID:33762731 PMID:35610220
Beta-arrestin family members regulate signaling by mediating both receptor desensitization and resensitization processes .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of 5-hydroxytryptamine release and in the regulation of dopamine and 5-hydroxytryptamine metabolism .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of dopamine and 5-hydroxytryptamine levels in the brain, and thereby affects neural activity, mood and behavior .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the response to anxiogenic stimuli PMID:18476671 PMID:20363322 PMID:20945968
PMID:18703043 PMID:23519210 PMID:7926008 PMID:8078486 PMID:8143856 PMID:8882600
Also functions as a receptor for various ergot alkaloid derivatives and psychoactive substances .
PMID:12970106 PMID:18703043 PMID:23519210 PMID:23519215 PMID:24357322 PMID:28129538 PMID:30127358 PMID:36087581 PMID:7926008 PMID:8078486 PMID:8143856
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:23519215 PMID:28129538 PMID:8078486 PMID:8143856 PMID:8882600
HTR2B is coupled to G(q)/G(11) G alpha proteins and activates phospholipase C-beta, releasing diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3) second messengers that modulate the activity of phosphatidylinositol 3-kinase and promote the release of Ca(2+) ions from intracellular stores, respectively .
PMID:18703043 PMID:23519215 PMID:28129538 PMID:30127358 PMID:36087581 PMID:8078486 PMID:8143856 PMID:8882600
Beta-arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways .
PMID:23519215 PMID:28129538 PMID:30127358 PMID:36087581
Plays a role in the regulation of dopamine and 5-hydroxytryptamine release, 5-hydroxytryptamine uptake and in the regulation of extracellular dopamine and 5-hydroxytryptamine levels, and thereby affects neural activity. May play a role in the perception of pain (By similarity). Plays a role in the regulation of behavior, including impulsive behavior .
PMID:21179162
Required for normal proliferation of embryonic cardiac myocytes and normal heart development (By similarity).
Protects cardiomyocytes against apoptosis (By similarity). Plays a role in the adaptation of pulmonary arteries to chronic hypoxia (By similarity). Plays a role in vasoconstriction (By similarity).
Required for normal osteoblast function and proliferation, and for maintaining normal bone density (By similarity). Required for normal proliferation of the interstitial cells of Cajal in the intestine (By similarity)
PMID:1330647 PMID:18703043 PMID:19057895 PMID:21645528 PMID:22300836 PMID:35084960 PMID:38552625
Also functions as a receptor for various drugs and psychoactive substances, including mescaline, psilocybin, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and lysergic acid diethylamide (LSD) .
PMID:28129538 PMID:35084960
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:28129538 PMID:35084960
HTR2A is coupled to G(q)/G(11) G alpha proteins and activates phospholipase C-beta, releasing diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3) second messengers that modulate the activity of phosphatidylinositol 3-kinase and promote the release of Ca(2+) ions from intracellular stores, respectively .
PMID:18703043 PMID:28129538 PMID:35084960
Beta-arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways .
PMID:28129538 PMID:35084960
Affects neural activity, perception, cognition and mood .
PMID:18297054
Plays a role in the regulation of behavior, including responses to anxiogenic situations and psychoactive substances. Plays a role in intestinal smooth muscle contraction, and may play a role in arterial vasoconstriction (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
ATC N05AX15
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Cariprazine
Additional database identifiers
Drugs Product Database (DPD)
23719
ChemSpider
25999972
BindingDB
50382290
PDB
7RU
ZINC
ZINC000100907004
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3024
GenAtlas
DRD3
GeneCards
DRD3
GenBank Gene Database
U32499
GenBank Protein Database
927342
Guide to Pharmacology
216
UniProt Accession
DRD3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3023
GenAtlas
DRD2
GeneCards
DRD2
GenBank Gene Database
M30625
GenBank Protein Database
181432
Guide to Pharmacology
215
UniProt Accession
DRD2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5286
GenAtlas
HTR1A
GeneCards
HTR1A
GenBank Gene Database
M28269
GenBank Protein Database
189928
Guide to Pharmacology
1
UniProt Accession
5HT1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5294
GenAtlas
HTR2B
GeneCards
HTR2B
GenBank Gene Database
X77307
GenBank Protein Database
475198
Guide to Pharmacology
7
UniProt Accession
5HT2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5293
GenAtlas
HTR2A
GeneCards
HTR2A
GenBank Gene Database
S42168
GenBank Protein Database
36431
Guide to Pharmacology
6
UniProt Accession
5HT2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5182
GenAtlas
HRH1
GeneCards
HRH1
GenBank Gene Database
Z34897
GenBank Protein Database
510296
Guide to Pharmacology
262
UniProt Accession
HRH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5295
GenAtlas
HTR2C
GeneCards
HTR2C
GenBank Gene Database
M81778
GenBank Protein Database
338028
Guide to Pharmacology
8
UniProt Accession
5HT2C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:277
GenAtlas
ADRA1A
GeneCards
ADRA1A
GenBank Gene Database
D25235
GenBank Protein Database
433201
Guide to Pharmacology
22
UniProt Accession
ADA1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2631
GeneCards
CYP2E1
GenBank Gene Database
J02625
GenBank Protein Database
181360
Guide to Pharmacology
1330
UniProt Accession
CP2E1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q2938837), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.