Caffeine citrate 200mg/5ml oral solution
Requires a prescription from a doctor or prescriber
Caffeine is a drug of the methylxanthine class used for a variety of purposes, including certain respiratory conditions of the premature newborn, pain relief, and to combat drowsiness.
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Suspected adverse reactions reported for Caffeine citrate
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Suspected adverse reactions reported for Caffeine citrate
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1 branded products available
WHO defined daily dose (DDD)
400 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
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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: 17 · Randomised trials: 19 · 1977–2026
Showing the 50 most relevant studies, sorted by most relevant.
E. Oliphant, Sara M Hanning, Christopher J. D. McKinlay, et al.
Journal of Perinatology, 2024
P. Steer, V Flenady, A Shearman, et al.
Archives of Disease in Childhood Fetal & Neonatal, 2004
- Caffeine
- Citrates
- Doxapram
Jing Chen, Lu Jin, Xiao Chen
BioMed Research International, 2018
- Apnea
- Caffeine
- Citrates
BACKGROUND: Caffeine is widely used for the treatment of neonatal apnea, but there is no agreement on the optimum maintenance dose for preterm infants. OBJECTIVE: The aims of this meta-analysis were to compare the efficacy and safety of high versus low maintenance doses of caffeine citrate for the treatment of apnea in premature infants. METHODS: Literature searches were conducted using PubMed, Cochrane Library, OVID, Embase, Web of Science, Chinese Biomedical Literature, Weipu Journal, Wanfang, and CNKI databases up to September 2018. Only randomized controlled trials (RCTs) of caffeine citrate for apnea treatment in premature infants were included. Trials were divided into those testing high maintenance doses (10-20 mg/kg daily) and low maintenance doses (5-10 mg/kg daily) for comparison. Data collection and extraction, quality assessment, and data analyses were performed according to the Cochrane standards. RESULTS: Among the 345 studies initially identified, thirteen RCTs involving 1515 patients were included. Compared to the low-dose group, the high-dose group exhibited greater effective treatment rate (RR: 1.37, 95%CI: 1.18 to 1.60, P0.05). CONCLUSIONS: Higher maintenance doses of caffeine citrate appear more effective and safer than low maintenance doses for treatment of premature apnea, despite a higher incidence of tachycardia.
Abstract licence: CC BY 4.0
Amponsah SK, Nartey CM, Ofori EK
2025
Background and aimsCaffeine citrate is an example of a methylxanthine approved for managing apnea of prematurity (AOP). However, there is limited evidence of its use in low- and middle-income countries (LMICs). This rapid systematic review aims to appraise the literature on using caffeine citrate in managing neonatal apnea in LMICs.MethodsA comprehensive search was conducted on literature reporting the treatment of AOP in LMICs. The search was based on a population, intervention, comparison, and outcome format using medical subject heading terms. The PRISMA and PRISMA extension for scoping reviews guidelines were meticulously followed. PubMed, Science Direct, and Scopus were among the bibliographic databases searched. Initially, 2638 articles were identified based on the keywords used. However, after eliminating duplicates and implementing advanced options (only full-text, language, and year), the articles were further screened by abstract and title, ensuring a rigorous selection process.ResultsThe evaluation of 10 studies involving 1010 preterm infants provided compelling evidence. Our findings demonstrated that caffeine citrate, compared to aminophylline, had fewer adverse effects. The adverse effects, including feeding intolerance, tachycardia, central nervous system derailment, and hyperglycemia, were significantly reduced with caffeine citrate. Furthermore, data from the included studies revealed that caffeine citrate had a lower risk of recurrent apnea and was less likely to fall out of the recommended therapeutic range than aminophylline. These results unequivocally establish caffeine citrate's safety, efficacy, and cost-effectiveness in treating prematurity apnea in LMICs, providing a reliable and beneficial intervention for neonatal care in these regions.ConclusionCaffeine may be a preferred option in managing AOP in LMICs. However, high drug prices and lack of availability of caffeine may be factors limiting its use in these settings.
Abstract licence: CC BY-NC 4.0
Neamțu AV, Zlatian OM, Manda CV, et al.
2025
Background: Apnea of prematurity affects at least 85% of infants born before 34 weeks' gestation and represents a significant clinical challenge in neonatal intensive care. Methylxanthines, including caffeine, theophylline, and aminophylline, have emerged as the primary pharmacological intervention for this condition. Objective: To conduct a comprehensive systematic review of the use of methylxanthine in the treatment and prevention of apnea episodes in preterm infants, evaluating efficacy, safety, and long-term outcomes. Methods: We searched multiple databases including PubMed, Embase, Web of Science for randomized controlled trials, retrospective studies, or case-control studies of methylxanthine effects in preterm apnea. Risk of bias was assessed using the Cochrane Risk of Bias tool. Results were summarized narratively and grouped by methylxanthine type, study design, and primary outcomes (reduction in frequency and severity of apnea episodes, success of extubation, risk of bronchopulmonary dysplasia). Results: Twenty-five studies (n = 4599 preterm infants) were included. The landmark Caffeine for Apnea of Prematurity (CAP) trial (n = 2006) demonstrated that caffeine therapy significantly reduced bronchopulmonary dysplasia (36.3% vs. 46.9%, adjusted OR 0.63) and facilitated the earlier discontinuation of positive airway pressure (median 1 week earlier). Studies with a smaller number of cases have consistently demonstrated the efficacy of methylxanthines in reducing the incidence of bronchopulmonary dysplasia and apneic episodes and in supporting successful extubation. Long-term follow-up at 11 years showed improved pulmonary function (FEV1 z-score -1.00 vs. -1.53). Discussion: Limitations of this review include heterogeneity in outcome definitions, small sample sizes in early studies, and the dominance of evidence from the CAP trial. Methylxanthines, particularly caffeine, are an evidence-based intervention used for apnea of prematurity, with demonstrated benefits that extend beyond reducing the frequency and severity of apnea episodes, including decreasing the risk of bronchopulmonary dysplasia as well as reducing the need for mechanical ventilation. No external funding was received for this review. No registration record exists for this systematic review.
Abstract licence: CC BY
Renata Cristina da Silva Ferreira, Ana Carolina Felderheimer da Silva, Michel Carlos Mocellin, et al.
Complementary Therapies in Medicine, 2023
Yu M, Sharifi H, Quon S, et al.
2026
BackgroundCaffeine citrate is recommended to treat apnea of prematurity in premature neonates based on high-quality evidence demonstrating improved outcomes. In contrast, the prescription of caffeine for mature neonates and infants hospitalized with apnea is based on a paucity of evidence. We present here our protocol for a systematic review to synthesize existing data on the safety and effectiveness of caffeine treatment for apnea in hospitalized pediatric patients, with findings expected to focus on mature neonates and infants.MethodsWe developed this systematic review protocol in accordance with the PRISMA guidelines and PRISMA-P checklist. The search strategy was developed with the assistance of an information specialist. Information sources will include MEDLINE, Embase, CINAHL, and CENTRAL databases, as well as unpublished literature sources. Eligible studies will include randomized controlled trials, non-randomized trials, and observational studies investigating caffeine (of any formulation, administered by any route, of any duration) versus placebo, usual care, or non-methylxanthine comparator. The population of interest is children aged 0-17 years with apnea presenting to emergency, critical care, or in-patient settings; studies of premature babies receiving treatment for apnea of prematurity will be excluded. Critical outcomes include total duration of respiratory support, ventilator-free days, duration of invasive mechanical ventilation, duration of non-invasive respiratory support, time to apnea cessation, and serious adverse events. Two authors will independently screen identified studies against prespecified eligibility criteria. Data from included studies will be abstracted in duplicate and entered into our data abstraction form. Risk of bias for each included study will be independently assessed by two reviewers using the appropriate risk of bias tool. If appropriate, we will perform a meta-analysis. The quality of evidence will be assessed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology, with results presented in a summary of findings table.DiscussionWe will undertake the first rigorous evidence synthesis examining the safety and efficacy of caffeine treatment for apnea in hospitalized pediatric patients, where studies of premature babies with apnea of prematurity will be specifically excluded. We aim to fill the identified knowledge gap with this systematic review.Systematic review registrationPROSPERO CRD420251146484.
Abstract licence: CC BY
Coutiño Díaz M, Prieto Martínez A, Zare R, et al.
2025
- Wrestling
- Dietary Supplements
- Body Composition
BackgroundWrestling is a popular combat sport that requires muscular strength, power, agility, and endurance. Weight classes have motivated wrestlers to compete at a lower weight to optimise power-to-weight ratio and performance. To achieve these characteristics, athletes may use dietary supplements, however, their efficacy in wrestlers has not been systematically evaluated.ObjectiveThe purpose was to systematically review the literature to determine the efficacy of dietary supplements to improve body composition, physiological status, and performance in wrestlers.MethodsA systematic search was conducted in PubMed, ProQuest Medline, Web of Science, Cochrane Library, and Scopus on the 21st of January 2024 and updated on the 6th of January 2025. Studies were included if the participants were healthy wrestlers ingesting any type of dietary supplement in comparison to a control. Data associated with intervention type and characteristics, target populations, outcomes, and analysis methods were extracted.ResultsA total of 24 eligible original articles were included that assessed various supplementation strategies on body composition, exercise performance, and metabolic markers in wrestlers. Individual studies revealed significant effects of sodium citrate, creatine monohydrate, spirulina, green tea and oolong tea extracts, and branched-chain amino acids on body mass or composition. β-Hydroxy-β-methylbutyrate (HMB-FA), creatine monohydrate, and iron supplementation improved recovery and may improve exercise performance. Beet-root juice supplementation enhanced muscular strength and balance. BCAA supplementation produced mixed results on muscle damage biomarkers and performance, while sodium citrate, creatine, and spirulina can act as buffering agents. Thyme tea appears to improve antioxidant capacity.ConclusionsOverall, individual studies show some promise for several dietary supplements to alter body mass and body composition, improve exercise recovery and performance, delay fatigue, and modify serum biomarkers; nevertheless, effect sizes were often small, and results were often mixed.
Abstract licence: CC BY
Yiqun Miao, Yun Zhou, Shuliang Zhao, et al.
PLoS ONE, 2022
- Infant, Newborn, Diseases
- Infant, Premature, Diseases
- Aminophylline
BACKGROUND: Methylxanthine, including caffeine citrate and aminophylline, is the most common pharmacologic treatment for apnea of prematurity. However, due to the lack of high-quality evidence, there are no clear recommendations or guidelines on how to choose between caffeine and aminophylline. OBJECTIVE: This meta-analysis aimed to assess the comparative efficacy and safety of caffeine and aminophylline for apnea of prematurity, and provide reliable evidence for clinical medication in the treatment for apnea of prematurity. METHODS: PubMed, Scopus, Embase, EBSCO, Web of Science, and Cochrane databases were systematically searched from May 1975 to June 2022. RESULTS: Ten studies including a total of 923 preterm infants were evaluated. Our results showed that there was no significant difference in the effective rate of 1-3days between caffeine and aminophylline (OR 1.05, 95%CI: 0.40-2.74, P = 0.914). However, for side effects such as tachycardia (OR 0.22, 95%CI: 0.13-0.37, P<0.001) and feeding intolerance (OR 0.40, 95%CI: 0.23-0.70, P = 0.001), the incidence rate was lower in the caffeine group compared with the aminophylline group. No significant difference was found in hyperglycemia (OR 0.45, 95%CI: 0.19-1.05, P = 0.064). CONCLUSION: This meta-analysis reveals that caffeine citrate and aminophylline have similar therapeutic effectiveness on respiratory function, but caffeine has fewer side effects and should be considered first for treatment.
Abstract licence: CC BY 4.0
Hye Won Park, Gina Lim, Sung-Hoon Chung, et al.
Journal of Korean Medical Science, 2015
- Apnea
- Bronchopulmonary Dysplasia
- Caffeine
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
None known
Half-life
5 hours
Mechanism
The mechanism of action of caffeine is complex, as it impacts several body systems, which are listed below.
Food interactions
None known
Human targets
15 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
30 minutes
[A187730]…
Half-life
5 hours
Protein binding
10%
Volume of distribution
0.8-0.9 L/kg
Metabolism
[A187730]…
Elimination
0.5%
Clearance
0.078 L/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
The caffeine citrate injection, used for apnea of the premature newborn, was initially approved by the FDA in 1999.[L9863] According to an article from 2017, more than 15 million babies are born prematurely worldwide. This correlates to about 1 in 10 births. Premature birth can lead to apnea and bronchopulmonary dysplasia, a condition that interferes with lung development and may eventually cause asthma or early onset emphysema in those born prematurely.[A187694] Caffeine is beneficial in preventing and treating apnea and bronchopulmonary dysplasia in newborns, improving the quality of life of premature infants.T716
[L9899]
Caffeine has a broad range of over the counter uses, and is found in energy supplements, athletic enhancement products, pain relief products, as well as cosmetic products.[T716,L9854,L9872]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 678 interactions
Caffeine overdose
In the case of caffeine overdose, seizures may occur, as caffeine is a central nervous system stimulant. It should be used with extreme caution in those with epilepsy or other seizure disorders.
[L9851]
Symptoms of overdose may include nausea, vomiting, diarrhea, and gastrointestinal upset. Intoxication with caffeine is included in the World Health Organization’s International Classification of Diseases (ICD-10). Agitation, anxiety, restlessness, insomnia, tachycardia, tremors, tachycardia, psychomotor agitation, and, in some cases, death can occur, depending on the amount of caffeine consumed. Overdose is more likely to occur in individuals who do not consume caffeine regularly but consume energy drinks.
[A187721]
Overdose management
For a mild caffeine overdose, offer symptomatic treatment.
In the case of a severe overdose, intubation for airway protection from changes in mental status or vomiting may be needed. Activated charcoal and hemodialysis can prevent further complications of an overdose and prevent absorption and metabolism. Benzodiazepine drugs can be administered to prevent or treat seizures. IV fluids and vasopressors may be necessary to combat hypotension associated with caffeine overdose.
In addition, magnesium and beta blocking drugs can be used to treat arrhythmias that may occur, with defibrillation and resuscitation if the arrhythmias are lethal. Follow local ACLS protocols.T716
General and cellular actions
Caffeine exerts several actions on cells, but the clinical relevance is poorly understood. One probable mechanism is the inhibition of nucleotide phosphodiesterase enzymes, adenosine receptors, regulation of calcium handling in cells, and participates in adenosine receptor antagonism.[A187721][L9857] Phosphodiesterase enzymes regulate cell function via actions on second messengers cAMP and cGMP.[A187724] This causes lipolysis through activation of hormone-sensitive lipases, releasing fatty acids and glycerol.T722
Respiratory
The exact mechanism of action of caffeine in treating apnea related to prematurity is unknown, however, there are several proposed mechanisms, including respiratory center stimulation in the central nervous system, a reduced threshold to hypercapnia with increased response, and increased consumption of oxygen, among others.[L9851] The blocking of the adenosine receptors enhances respiratory drive via an increase in brain medullary response to carbon dioxide, stimulating ventilation and respiratory drive, while increasing contractility of the diaphragm.T716
Central nervous system
Caffeine demonstrates antagonism of all 4 adenosine receptor subtypes (A1, A2a, A2b, A3) in the central nervous system.[T716,L9851] Caffeine's effects on alertness and combatting drowsiness are specifically related to the antagonism of the A2a receptor.T716
Renal system
Caffeine has diuretic effects due to is stimulatory effects on renal blood flow, increase in glomerular filtration, and increase in sodium excretion.T716
Cardiovascular system
Adenosine receptor antagonism at the A1 receptor by caffeine stimulates inotropic effects in the heart. Blocking of adenosine receptors promotes catecholamine release, leading to stimulatory effects occurring in the heart and the rest of the body. In the blood vessels, caffeine exerts direct antagonism of adenosine receptors, causing vasodilation. It stimulates the endothelial cells in the blood vessel wall to release nitric oxide, potentiating blood vessel relaxation. Catecholamine release, however, antagonizes this and exerts inotropic and chronotropic effects on the heart, ultimately leading to vasoconstriction. Finally, caffeine is shown to raise systolic blood pressure measurements by 5 to 10 mmHg when it is not taken regularly, versus no effect in those who consume it regularly.T716 The vasoconstricting effects of caffeine are beneficial in migraines and other types of headache, which are normally caused by vasodilation in the brain.[A187709][L9872]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A187730]
After oral administration, onset of action takes place within 45 to 1 hour.
[L9827]
Food may delay caffeine absorption. The peak plasma level for caffeine ranges from 6-10mg/L.
[L9851]
The absolute bioavailability is unavailable in neonates[L9851], but reaches about 100% in adults.T716
The half-life in newborns is prolonged to about 8 hours at full-term and 100 hours in premature infants, likely due to reduced ability to metabolize it. Liver disease or drugs that inhibit CYP1A2 can increase caffeine half-life.[T716,T722]
[L9851]
[A187730]
The products of caffeine metabolism include paraxanthine, theobromine, and theophylline. The first step of caffeine metabolism is demethylation, yielding paraxanthine (a major metabolite), followed by theobromine, and theophylline, which are both minor metabolites. They are then excreted in urine as urates after additional metabolism.[A187730,T716,L9851] The enzymes xanthine oxidase and N-acetyltransferase 2 (NAT2) also participate in the metabolism of caffeine.
[A187730]
Proteins and enzymes this drug interacts with in the body
PMID:15260978 PMID:8855339 PMID:9419816
Has a preference for cGMP as a substrate PMID:9419816
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
ATC D11AX26
ATC R03DA20
ATC V04CG30
ATC N06BC01
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)
Caffeine
Matched from: Caffeine citrate
Additional database identifiers
Drugs Product Database (DPD)
9358
Drugs Product Database (DPD)
9357
ChemSpider
2424
BindingDB
10849
PDB
CFF
Guide to Pharmacology
407
ZINC
ZINC000000001084
HUGO Gene Nomenclature Committee (HGNC)
HGNC:262
GenAtlas
ADORA1
GeneCards
ADORA1
GenBank Gene Database
S45235
GenBank Protein Database
256155
Guide to Pharmacology
18
UniProt Accession
AA1R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:263
GenAtlas
ADORA2A
GeneCards
ADORA2A
GenBank Gene Database
M97370
GenBank Protein Database
177892
Guide to Pharmacology
19
UniProt Accession
AA2AR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:264
GenAtlas
ADORA2B
GeneCards
ADORA2B
GenBank Gene Database
M97759
GenBank Protein Database
178150
Guide to Pharmacology
20
UniProt Accession
AA2BR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:268
GenAtlas
ADORA3
GeneCards
ADORA3
GenBank Gene Database
L20463
GenBank Protein Database
349449
Guide to Pharmacology
21
UniProt Accession
AA3R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8783
GenAtlas
PDE4D
GeneCards
PDE4D
GenBank Gene Database
L20970
GenBank Protein Database
347130
Guide to Pharmacology
1303
UniProt Accession
PDE4D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8779
GenAtlas
PDE3B
GeneCards
PDE3B
GenBank Gene Database
U38178
GenBank Protein Database
1145302
Guide to Pharmacology
1299
UniProt Accession
PDE3B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8784
GenAtlas
PDE5A
GeneCards
PDE5A
GenBank Gene Database
AF043731
GenBank Protein Database
3420185
Guide to Pharmacology
1304
UniProt Accession
PDE5A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8775
GenAtlas
PDE1B
GeneCards
PDE1B
GenBank Gene Database
U56976
Guide to Pharmacology
1295
UniProt Accession
PDE1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8021
GenAtlas
NT5E
GeneCards
NT5E
GenBank Gene Database
X55740
GenBank Protein Database
23897
Guide to Pharmacology
1232
UniProt Accession
5NTD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8781
GenAtlas
PDE4B
GeneCards
PDE4B
GenBank Gene Database
L20966
GenBank Protein Database
347122
Guide to Pharmacology
1301
UniProt Accession
PDE4B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10483
GenAtlas
RYR1
GeneCards
RYR1
GenBank Gene Database
J05200
GenBank Protein Database
337722
UniProt Accession
RYR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8780
GenAtlas
PDE4A
GeneCards
PDE4A
GenBank Gene Database
L20965
GenBank Protein Database
347120
Guide to Pharmacology
1300
UniProt Accession
PDE4A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8781
GenAtlas
PDE4B
GeneCards
PDE4B
GenBank Gene Database
L20966
GenBank Protein Database
347122
Guide to Pharmacology
1301
UniProt Accession
PDE4B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8782
GenAtlas
PDE4C
GeneCards
PDE4C
GenBank Gene Database
Z46632
GenBank Protein Database
727223
Guide to Pharmacology
1302
UniProt Accession
PDE4C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8783
GenAtlas
PDE4D
GeneCards
PDE4D
GenBank Gene Database
L20970
GenBank Protein Database
347130
Guide to Pharmacology
1303
UniProt Accession
PDE4D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8792
GenAtlas
PDE7B
GeneCards
PDE7B
GenBank Gene Database
AB038040
GenBank Protein Database
8439497
Guide to Pharmacology
1306
UniProt Accession
PDE7B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8772
GenAtlas
PDE10A
GeneCards
PDE10A
GenBank Gene Database
AB020593
GenBank Protein Database
4958858
Guide to Pharmacology
1310
UniProt Accession
PDE10_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8777
GenAtlas
PDE2A
GeneCards
PDE2A
GenBank Gene Database
U67733
GenBank Protein Database
2108052
Guide to Pharmacology
1297
UniProt Accession
PDE2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8778
GenAtlas
PDE3A
GeneCards
PDE3A
GenBank Gene Database
M91667
GenBank Protein Database
38201493
Guide to Pharmacology
1298
UniProt Accession
PDE3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8779
GenAtlas
PDE3B
GeneCards
PDE3B
GenBank Gene Database
U38178
GenBank Protein Database
1145302
Guide to Pharmacology
1299
UniProt Accession
PDE3B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8784
GenAtlas
PDE5A
GeneCards
PDE5A
GenBank Gene Database
AF043731
GenBank Protein Database
3420185
Guide to Pharmacology
1304
UniProt Accession
PDE5A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8787
GeneCards
PDE6C
Guide to Pharmacology
1314
UniProt Accession
PDE6C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8773
GeneCards
PDE11A
GenBank Gene Database
AB036704
GenBank Protein Database
10716052
Guide to Pharmacology
1311
UniProt Accession
PDE11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8774
GeneCards
PDE1A
GenBank Gene Database
U40370
GenBank Protein Database
1151109
Guide to Pharmacology
1294
UniProt Accession
PDE1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8775
GenAtlas
PDE1B
GeneCards
PDE1B
GenBank Gene Database
U56976
Guide to Pharmacology
1295
UniProt Accession
PDE1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8776
GeneCards
PDE1C
Guide to Pharmacology
1296
UniProt Accession
PDE1C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8791
GenAtlas
PDE7A
GeneCards
PDE7A
GenBank Gene Database
L12052
GenBank Protein Database
5566609
Guide to Pharmacology
1305
UniProt Accession
PDE7A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8793
GeneCards
PDE8A
GenBank Gene Database
AF388183
GenBank Protein Database
16417190
Guide to Pharmacology
1307
UniProt Accession
PDE8A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8794
GeneCards
PDE8B
GenBank Gene Database
AY129948
GenBank Protein Database
32261241
Guide to Pharmacology
1308
UniProt Accession
PDE8B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8795
GenAtlas
PDE9A
GeneCards
PDE9A
GenBank Gene Database
AF048837
Guide to Pharmacology
1309
UniProt Accession
PDE9A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8785
GeneCards
PDE6A
Guide to Pharmacology
1312
UniProt Accession
PDE6A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8786
GeneCards
PDE6B
UniProt Accession
PDE6B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9413
GenAtlas
PRKDC
GeneCards
PRKDC
GenBank Gene Database
U47077
Guide to Pharmacology
2800
UniProt Accession
PRKDC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8977
GenAtlas
PIK3CD
GeneCards
PIK3CD
GenBank Gene Database
Y10055
Guide to Pharmacology
2155
UniProt Accession
PK3CD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8975
GenAtlas
PIK3CA
GeneCards
PIK3CA
GenBank Gene Database
Z29090
Guide to Pharmacology
2153
UniProt Accession
PK3CA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8976
GenAtlas
PIK3CB
GeneCards
PIK3CB
GenBank Gene Database
S67334
Guide to Pharmacology
2154
UniProt Accession
PK3CB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6180
GeneCards
ITPR1
UniProt Accession
ITPR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6181
GeneCards
ITPR2
UniProt Accession
ITPR2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6182
GeneCards
ITPR3
UniProt Accession
ITPR3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:795
GeneCards
ATM
Guide to Pharmacology
1934
UniProt Accession
ATM_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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_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:2597
GenAtlas
CYP1B1
GeneCards
CYP1B1
GenBank Gene Database
U03688
GenBank Protein Database
501031
Guide to Pharmacology
1320
UniProt Accession
CP1B1_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:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Molecular structure

ATC classifications (Wikidata)
Linked open data from Wikidata (Q60235), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. Molecular structure images from Wikimedia Commons.