Haloperidol 500microgram tablets
Requires a prescription from a doctor or prescriber
Drugs used in psychoses and related disorders
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Haloperidol
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
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.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Haloperidol
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
9 branded products available
Part of the Haldol brand family (generic: Haloperidol)
MHRA licensed products
View all licensed products for Haloperidol on the MHRA register
Haloperidol 500microgram tablets
Haloperidol 500microgram tablets
Haloperidol 500microgram tablets
Haloperidol 500microgram tablets
Haloperidol 500microgram tablets
Haloperidol 500microgram tablets
Haloperidol 500microgram tablets
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)
8 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 NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
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
Clinical guidelines and formulary information
British National Formulary
Haloperidol
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(7)
Delirium: prevention, diagnosis and management in hospital and long-term care (CG103)
Violence and aggression: short-term management in mental health, health and community settings (NG10)
Alcohol-use disorders: diagnosis and management of physical complications (CG100)
Bipolar disorder: assessment and management (CG185)
Dementia: assessment, management and support for people living with dementia and their carers (NG97)
End of life care for infants, children and young people with life-limiting conditions: planning and management (NG61)
Psychosis and schizophrenia in children and young people: recognition and management (CG155)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
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
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
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
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
1 found
Half-life
14.5-36.7 hours
Mechanism
While haloperidol has demonstrated pharmacologic activity at a number of recepto…
Food interactions
1 warning
Human targets
18 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.7-6.1 hours
[A32346]
Studies…
Half-life
14.5-36.7 hours
Protein binding
7.5-11.6%
Volume of distribution
9.5-21.7 L/kg
Metabolism
1%
[A32346]…
Elimination
30%
Clearance
0.39-0.708 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Use of the first-generation antipsychotics (including haloperidol) is considered highly effective for the management of the "positive" symptoms of schizophrenia including hallucinations, hearing voices, aggression/hostility, disorganized speech, and psychomotor agitation. However, this class of drugs is also limited by the development of movement disorders induced by dopamine-blockade such as drug-induced parkinsonism, akathisia, dystonia, tardive dyskinesia, as well as other side effects including sedation, weight gain, and prolactin changes. While there are limited high-quality studies comparing haloperidol to lower-potency first-generation antipsychotics such as DB00477, DB01624, DB00623, and DB01403, haloperidol typically demonstrates the least amount of side effects within this class, but demonstrates a stronger disposition for causing extrapyramidal symptoms (EPS).[A180613][A180616][A180625] These other low‐potency antipsychotics are limited by their lower affinity for dopamine receptors, which requires a higher dose to effectively treat symptoms of schizophrenia. In addition, they block many receptors other than the primary target (dopamine receptors), such as cholinergic or histaminergic receptors, resulting in a higher incidence of side effects such as sedation, weight gain, and hypotension.
Interestingly, in vivo pharmacogenetic studies have demonstrated that the metabolism of haloperidol may be modulated by genetically determined polymorphic CYP2D6 activity. However, these findings contradict the findings from studies in vitro with human liver microsomes and from drug interaction studies in vivo. Inter-ethnic and pharmacogenetic differences in haloperidol metabolism may possibly explain these observations.[A32346]
First-generation antipsychotic drugs have largely been replaced with second- and third-generation (atypical) antipsychotics such as DB00734, DB00334, DB00363, DB01224, DB01238, and DB00246. However, haloperidol use remains widespread and is considered the benchmark for comparison in trials of the newer generation antipsychotics.[A180625]
The efficacy of haloperidol was first established in controlled trials in the 1960s.[A180610]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 2324 interactions
While the exact mechanism is not entirely understood, haloperidol is known to inhibit the effects of dopamine and increase its turnover. Traditional antipsychotics, such as haloperidol, bind more tightly than dopamine itself to the dopamine D2 receptor, with dissociation constants that are lower than that for dopamine.[A4962] It is believed that haloperidol competitively blocks post-synaptic dopamine (D2) receptors in the brain, eliminating dopamine neurotransmission and leading to the relief of delusions and hallucinations that are commonly associated with psychosis. It acts primarily on the D2-receptors and has some effect on 5-HT2 and α1-receptors, with negligible effects on dopamine D1-receptors. The drug also exerts some blockade of α-adrenergic receptors of the autonomic system.[L2022]
Antagonistic activity regulated through dopamine D2 receptors in the chemoreceptive trigger zone (CTZ) of the brain renders its antiemetic activity. Of the three D2-like receptors, only the D2 receptor is blocked by antipsychotic drugs in direct relation to their clinical antipsychotic abilities.
Clinical brain-imaging findings show that haloperidol remains tightly bound to D2 dopamine receptors in humans undergoing 2 positron emission tomography (PET) scans with a 24h pause in between scans.[A4962] A common adverse effect of this drug is the development of extrapyramidal symptoms (EPS), due to this tight binding of haloperidol to the dopamine D2 receptor.
Due to the risk of unpleasant and sometimes lifelong extrapyramidal symptoms, newer antipsychotic medications than haloperidol have been discovered and formulated. Rapid dissociation of drugs from dopamine D2 receptors is a plausible explanation for the improved EPS profile of atypical antipsychotics such as DB00734. This is also consistent with the theory of a lower affinity for D2 receptors for these drugs. As mentioned above, haloperidol binds tightly to the dopamine receptor, potentiating the risk of extrapyramidal symptoms,[A4962] and therefore should only been used when necessary.
The balance between the wanted drug effects on psychotic symptoms and unwanted side effects are largely at play within dopaminergic brain pathways affected by haloperidol. Cortical dopamine-D2-pathways play an important role in regulating these effects and include the nigrostriatal pathway, which is responsible for causing extrapyramidal symptoms (EPS), the mesolimbic and mesocortical pathways, which are responsible for the improvement in positive schizophrenic symptoms, and the tuberoinfundibular dopamine pathway, which is responsible for hyperprolactinemia.
A syndrome consisting of potentially irreversible, involuntary, dyskinetic movements may develop in patients. Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome.F4645
Cases of sudden death, QT-prolongation, and Torsades de Pointes have been reported in patients receiving haloperidol. Higher than recommended doses of any formulation and intravenous administration of haloperidol appear to be associated with a higher risk of QT-prolongation and Torsades de Pointes. Although cases have been reported even in the absence of predisposing factors, particular caution is advised in treating patients with other QT-prolonging conditions (including electrolyte imbalance [particularly hypokalemia and hypomagnesemia], drugs known to prolong QT, underlying cardiac abnormalities, hypothyroidism, and familial long QT-syndrome).F4645
A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with antipsychotic drugs. Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status (including catatonic signs) and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmias). Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis) and acute renal failure.F4645
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A32346]
Studies have found a wide variance in pharmacokinetic values for orally administered haloperidol with 1.7-6.1 hours reported for time to peak plasma concentration (tmax), 14.5-36.7 hours reported for half-life (t1⁄2), and 43.73 μg/L•h [range 14.89-120.96 μg/L•h] reported for AUC.
[A32346]
Haloperidol is well-absorbed from the gastrointestinal tract when ingested orally, however, the first-pass hepatic metabolism decreases its oral bioavailability to 40 - 75%.
After intramuscular administration, the time to peak plasma concentration (tmax) is 20 minutes in healthy individuals or 33.8 minutes in patients with schizophrenia, with a mean half-life of 20.7 hours.
[A32346]
Bioavailability following intramuscular administration is higher than that for oral administration.
Administration of haloperidol decanoate (the depot form of haloperidol for long-term treatment) in sesame oil results in slow release of the drug for long-term effects. The plasma concentrations of haloperidol gradually rise, reaching its peak concentration at about 6 days after the injection, with an apparent half-life of about 21 days. Steady-state plasma concentrations are achieved after the third or fourth dose.F4645
[A32346]
[A32346]
[A32346]
This high volume of distribution is in accordance with its lipophilicity, which also suggests free movement through various tissues including the blood-brain barrier.
[A32346]
In humans, haloperidol is biotransformed to various metabolites, including p-fluorobenzoylpropionic acid, 4-(4-chlorophenyl)-4-hydroxypiperidine, reduced haloperidol, pyridinium metabolites, and haloperidol glucuronide. In psychiatric patients treated regularly with haloperidol, the concentration of haloperidol glucuronide in plasma is the highest among the metabolites, followed, in rank order, by unchanged haloperidol, reduced haloperidol and reduced haloperidol glucuronide.
The drug is thought to be metabolized primarily by oxidative N-dealkylation of the piperidine nitrogen to form fluorophenylcarbonic acids and piperidine metabolites (which appear to be inactive), and by reduction of the butyrophenone carbonyl to the carbinol, forming hydroxyhaloperidol.
The enzymes involved in the biotransformation of haloperidol include cytochrome P450 (CYP) including CYP3A4 and CYP2D6, carbonyl reductase and uridine di-phosphoglucose glucuronosyltransferase enzymes. The greatest proportion of the intrinsic hepatic clearance of haloperidol is performed by glucuronidation and followed by the reduction of haloperidol to reduced haloperidol and by CYP-mediated oxidation.
In studies of cytochrome-mediated disposition in vitro, CYP3A4 appears to be the major isoform of the enzyme responsible for the metabolism of haloperidol in humans.
The intrinsic clearance of the back-oxidation of reduced haloperidol to the parent compound, oxidative N-dealkylation and pyridinium formation are of the same order of magnitude. This suggests that the same enzyme system is responsible for the above three metabolic reactions.
In vivo human studies on haloperidol metabolism have shown that the glucuronidation of haloperidol accounts for 50 to 60% of haloperidol biotransformation and that approximately 23% of the biotransformation was accounted for by the reduction pathway. The remaining 20 to 30% ofthe biotransformation of haloperidol would be via N-dealkylation and pyridinium formation.
[A32346]
[A32346]
[A32346]
Haloperidol clearance after extravascular administration ranges from 0.9-1.5 l/h/kg, however this rate is reduced in poor metabolizers of C_YP2D6_ enzyme. Reduced CYP2D6 enzyme activity may result in increased concentrations of haloperidol.
The inter-subject variability (coefficient of variation, %) in haloperidol clearance was estimated to be 44% in a population pharmacokinetic analysis in patients with schizophrenia .
[L2028]
Genetic polymorphism of CYP2D6 has been demonstrated to be an important source of inter-patient variability in the pharmacokinetics of haloperidol and may affect therapeutic response and incidence of adverse effects.
[A32346]
Proteins and enzymes this drug interacts with in the body
PMID:12970106 PMID:18703043 PMID:19057895 PMID:29398112 PMID:7895773
Also functions as a receptor for various drugs and psychoactive substances, including ergot alkaloid derivatives, 1-2,5,-dimethoxy-4-iodophenyl-2-aminopropane (DOI) and lysergic acid diethylamide (LSD) .
PMID:19057895 PMID:29398112
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:18703043 PMID:29398112
HTR2C 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:29398112
Beta-arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways .
PMID:29398112
Regulates neuronal activity via the activation of short transient receptor potential calcium channels in the brain, and thereby modulates the activation of pro-opiomelanocortin neurons and the release of CRH that then regulates the release of corticosterone (By similarity). Plays a role in the regulation of appetite and eating behavior, responses to anxiogenic stimuli and stress (By similarity). Plays a role in insulin sensitivity and glucose homeostasis (By similarity)
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (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 N05AD01
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)
Haloperidol
Additional database identifiers
Drugs Product Database (DPD)
10146
Drugs Product Database (DPD)
1903
ChemSpider
3438
BindingDB
21398
PDB
GMJ
Guide to Pharmacology
86
ZINC
ZINC000000537822
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: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: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: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:4479
GenAtlas
MCHR1
GeneCards
MCHR1
GenBank Gene Database
U71092
Guide to Pharmacology
280
UniProt Accession
MCHR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10935
GenAtlas
SLC18A2
GeneCards
SLC18A2
GenBank Gene Database
L09118
GenBank Protein Database
292335
Guide to Pharmacology
1012
UniProt Accession
VMAT2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8157
GenAtlas
OPRS1
GeneCards
SIGMAR1
GenBank Gene Database
U75283
GenBank Protein Database
1783387
Guide to Pharmacology
2552
UniProt Accession
SGMR1_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:1952
GenAtlas
CHRM3
GeneCards
CHRM3
GenBank Gene Database
X15266
GenBank Protein Database
32324
Guide to Pharmacology
15
UniProt Accession
ACM3_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:281
GenAtlas
ADRA2A
GeneCards
ADRA2A
GenBank Gene Database
M23533
GenBank Protein Database
178196
Guide to Pharmacology
25
UniProt Accession
ADA2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:282
GenAtlas
ADRA2B
GeneCards
ADRA2B
GenBank Gene Database
M34041
GenBank Protein Database
178198
Guide to Pharmacology
26
UniProt Accession
ADA2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:283
GenAtlas
ADRA2C
GeneCards
ADRA2C
GenBank Gene Database
J03853
GenBank Protein Database
178194
Guide to Pharmacology
27
UniProt Accession
ADA2C_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:5301
GenAtlas
HTR6
GeneCards
HTR6
GenBank Gene Database
L41147
GenBank Protein Database
1162924
Guide to Pharmacology
11
UniProt Accession
5HT6R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5302
GenAtlas
HTR7
GeneCards
HTR7
GenBank Gene Database
U68487
GenBank Protein Database
1857143
Guide to Pharmacology
12
UniProt Accession
5HT7R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4586
GenAtlas
GRIN2B
GeneCards
GRIN2B
GenBank Gene Database
U90278
GenBank Protein Database
1899202
Guide to Pharmacology
457
UniProt Accession
NMDE2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3020
GenAtlas
DRD1
GeneCards
DRD1
GenBank Gene Database
X55760
GenBank Protein Database
30397
Guide to Pharmacology
214
UniProt Accession
DRD1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1548
GenAtlas
CBR1
GeneCards
CBR1
GenBank Gene Database
J04056
Guide to Pharmacology
1383
UniProt Accession
CBR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12541
GeneCards
UGT1A9
GenBank Gene Database
S55985
GenBank Protein Database
7690346
UniProt Accession
UD19_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:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2595
GeneCards
CYP1A1
GenBank Gene Database
K03191
GenBank Protein Database
181276
Guide to Pharmacology
1318
UniProt Accession
CP1A1_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: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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_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
International reference pricing
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: