Dexamfetamine 10mg tablets
Requires a prescription from a doctor or prescriber
Dextroamphetamine is the dextrorotatory enantiomer of amphetamine[A2505].
Strict controls: safe custody, register required
Legal requirements and restrictions
These are medicines with high potential for misuse but with accepted medical uses. Subject to the strictest controls.
Legal requirements
- Must be stored in a locked controlled drugs cabinet
- Pharmacy must keep a controlled drugs register
- Prescriptions valid for 28 days only
- Prescriptions must include specific details (dose, form, strength, total quantity)
- Cannot be emergency supplied by pharmacists
Other medicines in this category
Morphine, Oxycodone, Fentanyl, Methylphenidate (Ritalin), Amphetamines
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
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Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Dexamfetamine
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.
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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 Dexamfetamine
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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.
1 branded products available
MHRA licensed products
View all licensed products for Dexamfetamine on the MHRA register
Amfexa 10mg 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)
15 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 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(4)
Solriamfetol for treating excessive daytime sleepiness caused by narcolepsy (TA758)
Attention deficit hyperactivity disorder: diagnosis and management (NG87)
Narcolepsy with or without cataplexy in adults: pitolisant (ES8)
Attention deficit hyperactivity disorder (QS39)
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 & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
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. 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: 5 · Randomised trials: 2 · Trials: 10 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
Oliva HNP, Prudente TP, Mayerson TF, et al.
2025
- Central Nervous System Stimulants
- Attention Deficit Disorder with Hyperactivity
- Methylphenidate
ImportanceThe use of stimulant medications has expanded substantially beyond the traditional treatment of attention-deficit/hyperactivity disorder (ADHD) to encompass a variety of other clinical conditions. Understanding the safety of these medications is important as their use increases across diverse patient populations.ObjectiveTo assess the safety of stimulant medications as reported in randomized clinical trials (RCTs) investigating methylphenidate, lisdexamfetamine, and other amphetamines.Data sourcesA comprehensive literature search was conducted from July 1, 2024, through February 28, 2025, using CINAHL, Embase, PubMed or MEDLINE, ScienceDirect, and Web of Science for studies published since 2000. Keywords included safety, adverse event, side effect, amphetamine, dextroamphetamine, stimulant, lisdexamfetamine, and methylphenidate.Study selectionRCTs published between January 1, 2000, and December 13, 2024, were included. These trials investigated the safety of stimulants in various clinical conditions, including ADHD, depression, binge eating disorder, schizophrenia, Alzheimer disease, and stimulant use disorders as well as in healthy individuals. Trials not focused on safety or adverse events (AEs) of stimulants, nonoriginal research, nonhuman research, trials with concomitant prescriptions other than stimulants, and trials without a placebo group were excluded.Data extraction and synthesisData extraction followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guideline. Independent reviewers extracted study data, and a random-effects model was used to pool results. Heterogeneity was assessed using the I2 statistic.Main outcomes and measuresThe primary outcome was the risk ratio (RR) of developing any AE in participants taking stimulants vs placebo.ResultsA total of 93 RCTs were included after exclusions. The methodological quality assessment of the included trials showed overall low or unclear risk of bias. Trials with a duration of up to 52 weeks showed that stimulant medications were associated with an increased risk of overall AEs compared with placebo (RR, 1.34; 90% CI, 1.27-1.41), with high heterogeneity (I2 = 67%). Statistical significance of this finding was maintained when subgroups (ie, methylphenidate, lisdexamfetamine, and other amphetamines) were separately analyzed.Conclusions and relevanceThis meta-analysis found an increased risk of overall AEs associated with stimulants compared with placebo. Future research could provide more standardized and consistent assessments of this outcome and may improve understanding about misuse risk.
Abstract licence: CC BY
S. King, S. Griffin, Z. Hodges, et al.
Health technology assessment, 2006
M. Nuijten, P. Blanken, B. van de Wetering, et al.
Lancet, 2016
- Crack Cocaine
- Cocaine-Related Disorders
- Heroin Dependence
Barkla XM, McArdle PA, Newbury-Birch D
2015
- Substance-Related Disorders
- Dextroamphetamine
- Methylphenidate
BackgroundAmong young people up to 18 years of age, approximately 5% have attention deficit hyperactivity disorder (ADHD), many of whom have symptoms persisting into adulthood. ADHD is associated with increased risk of co-morbid psychiatric disorders, including substance misuse. Many will be prescribed medication, namely methylphenidate, atomoxetine, dexamphetamine and lisdexamfetamine. If so, it is important to know if interactions exist and if they are potentially toxic.MethodsThree databases (Medline, EMBASE and PsychINFO) from a 22 year period (1992 - June 2014) were searched systematically. Key search terms included alcohol, substance related disorders, methylphenidate, atomoxetine, dexamphetamine, lisdexamfetamine, and death, which identified 493 citations (344 after removal of duplicates). The eligibility of each study was assessed jointly by two investigators, leaving 20 relevant articles.ResultsWe identified only a minimal increase in side-effects when ADHD medication (therapeutic doses) was taken with alcohol. None of the reviewed studies showed severe sequelae among those who had overdosed on ADHD medication and other coingestants, including alcohol.ConclusionsThe numbers across all the papers studied remain too low to exclude uncommon effects. Also, studies of combined effects with novel psychoactive substances have not yet appeared in the literature. Nevertheless, no serious sequelae were identified from combining ADHD medication with alcohol/illicit substances from the pre-novel psychoactive substance era.
Abstract licence: CC BY
Natalie Gauci, Hazer Khalifa, Donald Lee, et al.
Sleep science, 2023
Daryl Efron, N. Coscini
Australian Prescriber, 2025
SUMMARY Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder characterised by developmentally inappropriate levels of hyperactivity, impulsivity and/or inattention, with substantial impact on functioning. Stimulants (methylphenidate, dexamfetamine, lisdexamfetamine) are the main pharmacological treatment for children and adolescents with ADHD and are highly effective at reducing core ADHD symptoms. Non-stimulants such as atomoxetine, clonidine and guanfacine can also be useful in some patients.
Abstract licence: CC BY-NC-ND
Shahnoor Adil
BJPsych Open, 2026
Aims: The prevalence of attention deficit/hyperactivity disorder (ADHD) diagnoses and stimulant prescribing among women of reproductive age has increased substantially over the past two decades. Dextro-/amphetamine formulations, particularly dexamphetamine, are now among the most commonly used ADHD medications during pregnancy. Clinical decision making is complicated by uncertainty regarding maternal, fetal and long term child outcomes, leading to high rates of medication discontinuation. This review aims to synthesise current evidence on maternal, neonatal, congenital and long term neurodevelopmental outcomes associated with dexamphetamine and related stimulant use during pregnancy. Methods: A narrative review of population based cohort studies, registry analyses and clinical guidelines examining perinatal stimulant exposure was conducted. Outcomes of interest included neonatal and obstetric outcomes, congenital malformations, maternal complications and long term neurodevelopmental outcomes, with careful consideration of confounding by maternal ADHD, behavioural and sociodemographic factors. Studies were selected based on their quality, relevance and inclusion of contemporary perinatal data. Results: Population level data demonstrate a marked rise in perinatal stimulant use, primarily driven by dexamphetamine, with an 11-fold increase observed in a British Columbia registry study (2000-2021). Retrospective cohort studies suggest that continuing dexamphetamine during pregnancy is generally not associated with adverse maternal or neonatal outcomes compared with cessation. Evidence for hypertensive disorders, however, remains inconclusive. International registry studies report no increased risk of major congenital malformations following amphetamine exposure, with a small signal observed for methylphenidate. Long term follow up studies, after adjusting for confounding by maternal ADHD, found no meaningful increase in neurodevelopmental disorders among children exposed in utero. Maternal ADHD and related behavioural or sociodemographic factors may act as confounders underlining the importance of accounting for these factors in research and clinical decision making. Conclusion: Current evidence suggests that dexamphetamine exposure during pregnancy is not associated with major increases in adverse maternal, neonatal, congenital or long term neurodevelopmental outcomes when confounding is appropriately addressed. Shared, individualised decision making remains essential. Given the limitations of observational study designs and residual confounding, future research should prioritise dexamphetamine-specific data and include qualitative measures of maternal functioning as well as long term childhood outcomes.
Abstract licence: CC BY 4.0
Stefan Spulber, Pascal Kilian, Wan Norhamidah Wan Ibrahim, et al.
PLoS ONE, 2014
- Zebrafish
- Akathisia, Drug-Induced
- Dextroamphetamine
Perfluorooctane sulfonate (PFOS) is a widely spread environmental contaminant. It accumulates in the brain and has potential neurotoxic effects. The exposure to PFOS has been associated with higher impulsivity and increased ADHD prevalence. We investigated the effects of developmental exposure to PFOS in zebrafish larvae, focusing on the modulation of activity by the dopaminergic system. We exposed zebrafish embryos to 0.1 or 1 mg/L PFOS (0.186 or 1.858 µM, respectively) and assessed swimming activity at 6 dpf. We analyzed the structure of spontaneous activity, the hyperactivity and the habituation during a brief dark period (visual motor response), and the vibrational startle response. The findings in zebrafish larvae were compared with historical data from 3 months old male mice exposed to 0.3 or 3 mg/kg/day PFOS throughout gestation. Finally, we investigated the effects of dexamfetamine on the alterations in spontaneous activity and startle response in zebrafish larvae. We found that zebrafish larvae exposed to 0.1 mg/L PFOS habituate faster than controls during a dark pulse, while the larvae exposed to 1 mg/L PFOS display a disorganized pattern of spontaneous activity and persistent hyperactivity. Similarly, mice exposed to 0.3 mg/kg/day PFOS habituated faster than controls to a new environment, while mice exposed to 3 mg/kg/day PFOS displayed more intense and disorganized spontaneous activity. Dexamfetamine partly corrected the hyperactive phenotype in zebrafish larvae. In conclusion, developmental exposure to PFOS in zebrafish induces spontaneous hyperactivity mediated by a dopaminergic deficit, which can be partially reversed by dexamfetamine in zebrafish larvae.
Abstract licence: CC BY 4.0
M. G. Madsen, Jin Liang Zhu, T. Munk-Olsen, et al.
Paediatric Drugs, 2025
- Pregnancy Complications
- Central Nervous System Stimulants
- Attention Deficit Disorder with Hyperactivity
Females of reproductive age are increasingly using attention deficit hyperactivity disorder (ADHD) medication, but its use during pregnancy and breastfeeding is largely unknown. The aim of this study is to examine the prevalence of ADHD medication fills during pregnancy and breastfeeding, including characteristics of these females and cohort differences over time. We conducted a descriptive study using Danish nationwide registers. Within cohorts of pregnant and breastfeeding females, we calculated the prevalence of ADHD medication (methylphenidate, amphetamine, dexamfetamine, lisdexamfetamine, modafinil, atomoxetine, clonidine and guanfacine) fills and described sociodemographic and clinical characteristics across groups with fills, no fills and previous fills. Cohort differences in ADHD medication fills during pregnancy for 2005–2010, 2011–2016 and 2017–2022 were examined. In this cohort of 1,077,279 pregnancies, ADHD medication fills increased from 0.08 to 7.71 per 1000 individuals between 2005 and 2022. Among 446,485 breastfeeding females, fills increased from 0.55 to 3.67 per 1000 individuals from 2012 to 2022. Compared with the group with no fills, females filling ADHD medication during pregnancy and breastfeeding were younger, had lower levels of education, were more often smoking during pregnancy, utilised more psychiatric healthcare and had concurrent fills of other psychotropic medication. Cohort differences over time revealed that females filling ADHD medication during pregnancy in 2017–2022 were older, had higher levels of education, smoked less during pregnancy, had fewer psychiatric contacts and were less likely to fill other psychotropic medications compared with females in the earlier cohorts. Results showed an increasing prevalence of ADHD medication fills during pregnancy and breastfeeding in Denmark over time, surpassing the increase observed generally in females of reproductive age filling ADHD medication. Results revealed a difference in characteristics of females filling ADHD medication during pregnancy over time, suggesting a shift in pregnancy treatment patterns.
Abstract licence: CC BY-NC
Shane Darke, Amy Peacock, Johan A Duflou, et al.
Medical Journal of Australia, 2025
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
91 found
Half-life
11.75 hours
Mechanism
The exact mechanism of amphetamines as a class is not known.
Food interactions
1 warning
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
[L52145]
…
Half-life
11.75 hours
[L52145]
In a study of post-stroke patients the half life was 16.0…
Volume of distribution
195L
[A177247]
Metabolism
[A174292]
…
Elimination
[A2505]
Clearance
17L/h
[A177247]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L52145]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1183 interactions
[L52145]
These effects were not seen in rat or rabbit studies, and the effects on human pregnancy have not been studied.
[L52145]
The risk and benefit of use during pregnancy should be weighed as bone deformities, tracheoesophageal fistula, anal atresia, low birthweight, and withdrawl have been reported in the children of mothers who were taking dextroamphetamine during pregnancy.
[L52145]
Mothers should not take amphetamines while nursing as the drug is excreted in breast milk.
[L52145]
Long term effects of dextroamphetamine have not bee determined in pediatric patients and dextroamphetamine should be avoided in children under 3 years.
[L52145]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L52145]
[L52145]
In a study of post-stroke patients the half life was 16.0 hours in females and 12.4 hours in males.
[A2505]
Studies in healthy populations show a half life of 7.9 hours.
[A177247]
[A177247]
[A174292]
[A2505]
[A177247]
Proteins and enzymes this drug interacts with in the body
PMID:23363473 PMID:37914936 PMID:38081299 PMID:38517752 PMID:8643547
Regulates the transvesicular monoaminergic gradient that determines the quantal size.
Mediates somatodendritic dopamine release in hippocampal neurons, likely as part of a regulated secretory pathway that integrates retrograde synaptic signals (By similarity). Acts as a primary transporter for striatal dopamine loading ensuring impulse-dependent release of dopamine at the synaptic cleft (By similarity). Responsible for histamine and serotonin storage and subsequent corelease from mast cell granules PMID:8860238
PMID:2008212 PMID:8125921 PMID:38750358
Is responsible for norepinephrine re-uptake and clearance from the synaptic cleft, thus playing a crucial role in norepinephrine inactivation and homeostasis (By similarity). Can also mediate sodium- and chloride-dependent transport of dopamine PMID:11093780 PMID:8125921 PMID:39395208 PMID:39048818
PMID:10375632 PMID:11093780 PMID:1406597 PMID:15505207 PMID:19478460 PMID:39112701 PMID:39112703 PMID:39112705 PMID:8302271
Also mediates sodium- and chloride-dependent transport of norepinephrine (also known as noradrenaline) (By similarity). Regulator of light-dependent retinal hyaloid vessel regression, downstream of OPN5 signaling (By similarity)
PMID:11459929 PMID:11723224 PMID:15718104 PMID:31399635 PMID:36100653 PMID:37935376 PMID:37935377 PMID:37963465 PMID:38168118
Also functions as a receptor for various drugs and psychoactive substances, such as amphetamine and methamphetamine .
PMID:31399635 PMID:37935376 PMID:37935377
Unresponsive to classical biogenic amines, such as epinephrine and histamine and only partially activated by dopamine and serotonin .
PMID:11459929 PMID:11723224
Expressed in both the central and peripheral nervous system: TAAR1 activation regulates the activity of several neurotransmitter signaling pathways by (1) decreasing the basal firing rates of the neurons involved and by (2) lowering the sensitivity of receptors to neurotransmitters .
PMID:37935376 PMID:37935377 PMID:37963465 PMID:38168118
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:31399635 PMID:37935376 PMID:37963465
TAAR1 is coupled with different G(i)/G(o)-, G(s)- or G(q)/G(11) classes of G alpha proteins depending on the ligand .
PMID:31399635 PMID:37935376 PMID:37963465
CAD-binding is coupled to G(i)/G(o) G alpha proteins and mediates inhibition of adenylate cyclase activity .
PMID:37935376 PMID:37963465
T1AM- or beta-PEA-binding is coupled to G(s) G alpha proteins and mediates activation of adenylate cyclase activity .
PMID:37935376 PMID:37963465
CHA- or IAA-binding 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 .
PMID:37935376 PMID:37963465
TMA-binding is coupled with all three G(i)/G(o)-, G(s)- or G(q)/G(11) G alpha protein subtypes .
PMID:37935376 PMID:37963465
Amphetamine-binding is coupled with G(s)- or G(12)/G(13) G alpha protein subtypes PMID:31399635
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:10375632 PMID:11093780 PMID:1406597 PMID:15505207 PMID:19478460 PMID:39112701 PMID:39112703 PMID:39112705 PMID:8302271
Also mediates sodium- and chloride-dependent transport of norepinephrine (also known as noradrenaline) (By similarity). Regulator of light-dependent retinal hyaloid vessel regression, downstream of OPN5 signaling (By similarity)
ATC N06BA02
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)
Dextroamphetamine
Matched from: Dexamfetamine
Additional database identifiers
Drugs Product Database (DPD)
8298
Drugs Product Database (DPD)
8295
ChemSpider
5621
BindingDB
50022723
PDB
1WE
Guide to Pharmacology
2147
ZINC
ZINC000006021033
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:11048
GenAtlas
SLC6A2
GeneCards
SLC6A2
GenBank Gene Database
M65105
GenBank Protein Database
189258
Guide to Pharmacology
926
UniProt Accession
SC6A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11049
GenAtlas
SLC6A3
GeneCards
SLC6A3
GenBank Gene Database
M96670
GenBank Protein Database
553260
Guide to Pharmacology
927
UniProt Accession
SC6A3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:17734
GenAtlas
TAAR1
GeneCards
TAAR1
GenBank Gene Database
AF380185
GenBank Protein Database
14600074
Guide to Pharmacology
364
UniProt Accession
TAAR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:278
GenAtlas
ADRA1B
GeneCards
ADRA1B
GenBank Gene Database
M99589
Guide to Pharmacology
23
UniProt Accession
ADA1B_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:278
GenAtlas
ADRA1B
GeneCards
ADRA1B
GenBank Gene Database
M99589
Guide to Pharmacology
23
UniProt Accession
ADA1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:280
GenAtlas
ADRA1D
GeneCards
ADRA1D
GenBank Gene Database
M76446
GenBank Protein Database
177807
Guide to Pharmacology
24
UniProt Accession
ADA1D_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:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
GenBank Gene Database
D23670
GenBank Protein Database
809499
UniProt Accession
AMO_ECOLI
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11049
GenAtlas
SLC6A3
GeneCards
SLC6A3
GenBank Gene Database
M96670
GenBank Protein Database
553260
Guide to Pharmacology
927
UniProt Accession
SC6A3_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72