Chlorphenamine 10mg/1ml solution for injection ampoules
Requires a prescription from a doctor or prescriber
A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma.
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 Chlorphenamine
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 Chlorphenamine
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.
8 branded products available
MHRA licensed products
View all licensed products for Chlorphenamine on the MHRA register
Chlorphenamine 10mg/1ml solution for injection ampoules
Chlorphenamine 10mg/1ml solution for injection ampoules
Chlorphenamine 10mg/1ml solution for injection ampoules
Chlorphenamine 10mg/1ml solution for injection ampoules
Chlorphenamine 10mg/1ml solution for injection ampoules
Chlorphenamine 10mg/1ml solution for injection ampoules
Chlorphenamine 10mg/1ml solution for injection ampoules
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)
12 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
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. 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: 3 · Randomised trials: 1 · Trials: 3 · 2005–2026
Showing the 50 most relevant studies, sorted by most relevant.
P. Picon, M. Costa, Rafael da Veiga Picon, et al.
BMC Infectious Diseases, 2013
- Acetaminophen
- Chlorpheniramine
- Common Cold
BackgroundThe common cold and other viral airway infections are highly prevalent in the population, and their treatment often requires the use of medications for symptomatic relief. Paracetamol is as an analgesic and antipyretic; chlorphenamine is an antihistamine; and phenylephrine, a vasoconstrictor and decongestant. This randomized, double-blind, placebo-controlled trial sought to evaluate the efficacy and safety of a fixed-dose combination of paracetamol, chlorphenamine and phenylephrine in the symptomatic treatment of the common cold and flu-like syndrome in adults.MethodsThis study enrolled 146 individuals aged 18 to 60 years who had moderate to severe flu-like syndrome or common cold. After clinical examination and laboratory tests, individuals were randomly assigned to receive the fixed-dose combination (73) or placebo (73), five capsules per day for 48 to 72 hours. The primary efficacy endpoint was the sum of the scores of 10 symptoms on a four-point Likert-type scale. To evaluate treatment safety, the occurrence of adverse events was also measured.ResultsMean age was 33.5 (±9.5) years in the placebo group and 33.8 (±11.5) in the treatment group. There were 55 women and 18 men in the placebo group, and 46 women and 27 men in the treatment group. Comparison of overall symptom scores in the two groups revealed a significantly greater reduction in the treatment group than in the placebo group (p = 0.015). Analysis at the first 13 dose intervals (± 66 h of treatment) showed a greater reduction of symptom scores in the treatment group than in the placebo group (p < 0.05). The number and distribution of adverse events were similar in both groups.ConclusionA fixed-dose combination of paracetamol, chlorphenamine and phenylephrine was safe and more effective than placebo in the symptomatic treatment of the common cold or flu-like syndrome in adults.Trial registrationNCT01389518
Abstract licence: CC BY 2.0
Romain Douhard, Philippe Humbert, Jean-Yves Milon, et al.
Current Medical Research and Opinion, 2024
- Chlorpheniramine
- Common Cold
- Pseudoephedrine
Abstract The common cold is the most frequent upper respiratory viral infection. Although benign, it represents a high socioeconomic burden. Many over-the-counter drugs are available to manage the symptoms of this condition, with antihistamines and vasoconstrictors being the most widely used. This review aimed to compare the potential mechanisms underlying the efficacy and safety of chlorphenamine and pseudoephedrine, the most commonly used agents in these two classes of drugs, and provide a useful perspective to impact appropriate decisions when considering these options for symptomatic common cold treatment. To conduct a comprehensive analysis, we systematically reviewed the use of pseudoephedrine and chlorphenamine using various databases, including MEDLINE, Google Scholar, Scopus, and Embase. We also perused the bibliographies of relevant articles and the EudraVigilance database. The findings suggest that pseudoephedrine may offer specific benefits in rapidly alleviating nasal congestion in the short term. Chlorphenamine appears to exhibit a higher degree of efficacy in alleviating rhinorrhea and other specific cold symptoms compared to pseudoephedrine. Pharmacovigilance data and case report reviews showed that pseudoephedrine may induce a higher incidence of less common but potentially life-threatening adverse effects compared to chlorphenamine. We concluded that antihistamine drugs exhibit a more favorable benefit/risk profile than vasoconstrictors for treating symptomatic common colds.
Abstract licence: CC BY-NC-ND 4.0
Syed A. A. Rizvi, Gustavo Ferrer, Uzzam Ahmed Khawaja, et al.
Current Reviews in Clinical and Experimental Pharmacology, 2022
- Common Cold
- Hypersensitivity
- SARS-CoV-2
Andrew A. Monte, Ryan Chuang, Michael Bodmer
British Journal of Clinical Pharmacology, 2010
- Antitussive Agents
- Chlorpheniramine
- Dextromethorphan
Honggang Lou, Hong Yuan, Zourong Ruan, et al.
Journal of Chromatography B, 2010
- Acetaminophen
- Chromatography, Liquid
- Dextrorphan
Jianhao Lin, Zhiwei Liu, Tian Guan, et al.
Foods, 2024
Gerbino C, Foglietta F, Corsi D, et al.
2025
- Epithelial Cells
- Histamine
- Sodium-Hydrogen Exchanger 3
Objective and designInvestigate the potential role of histamine and its receptors on the functional expression of the sodium/hydrogen (Na+/H+) exchanger (NHE)3.MaterialThe human epithelial kidney (HK-2) cells were used as an in vitro model of the renal proximal tubule.TreatmentHK-2 cells were exposed to histamine 0-1000 nM alone or in combination with chlorphenamine (10 μM) and JNJ-7777120 (1 μM) for 0-48 h. MAPK involvement was determined using the selective inhibitors SB202190 (p38 MAPK), PD98059 (ERK1/2), and SP600125 (SAPK/JNK).MethodsGene and protein expression were evaluated by qPCR and immunoblotting. The activity of NHE3 was measured by the BCECF-AM-based method.ResultsHistamine (100 nM) induced a concentration-dependent NHE3 gene transcription with a peak 16 h after the treatment, followed by protein translation at 48 h after. A Consistent increase in NHE3 activity was observed at 48 h, but also at 60 min, when both p38 MAPK and ERK1/2 were phosphorylated. JNJ-7777120 blunted the activation and expression of NHE3. Chlorpheniramine was effective only on NHE3 activity.ConclusionsHistamine shows early (within 60 min) and late (48 h) effects on NHE3 expression. The histamine H1 and H4 receptors are shown to contribute to these effects differentially. The findings of this study extends the evidence for a direct contribution of histamine on the renal reabsorptive machinery.
Abstract licence: CC BY
Xian Wu, Zhimian Liang, Xuemei Chen
Tropical Journal of Pharmaceutical Research, 2023
Donato Morena, Salvatore Silvio Colonna, Alessandro Santurro, et al.
Therapeutic Advances in Psychopharmacology, 2026
Serotonin syndrome (SS) and hyponatremia are severe, potentially life-threatening adverse reactions to serotonergic medications. Their concurrent manifestation is rare but clinically significant due to overlapping pathophysiological mechanisms. This report describes the fatal outcome of a 30-year-old female who presented to the Emergency Department with agitation following self-administration of duloxetine 60 mg, in addition to ongoing amitriptyline therapy and possible L-tryptophan supplementation. During hospitalization, she was treated with intravenous chlorphenamine for a suspected allergic reaction. Subsequently, she developed severe neurological deterioration, malignant arrhythmia, and profound acute hyponatremia (serum sodium 114 mmol/L), culminating in brain death within 48 h. The synergistic pharmacodynamic and pharmacokinetic interactions between duloxetine, amitriptyline, and chlorphenamine-three agents with serotonin reuptake inhibition properties-were implicated in precipitating SS and syndrome of inappropriate antidiuresis (SIAD)-induced hyponatremia. This combination resulted in extensive cerebral edema and cardiopulmonary arrest. The case highlights the diagnostic challenge posed by overlapping SS and hyponatremia manifestations, particularly when compounded by incomplete pharmacological histories and inappropriate drug administration. Clinicians should maintain high vigilance for SS and hyponatremia in patients receiving serotonergic agents, especially when multiple such drugs are co-administered. Comprehensive medication anamnesis, prompt electrolyte monitoring, and avoidance of pharmacodynamic duplication are essential to prevent similar outcomes.
Abstract licence: CC BY-NC 4.0
Saesiw U, Itharat A, Ruangnoo S, et al.
2025
Background and purposeHa-rak (HR), an equal-proportion combination of roots from Capparis micracantha DC., Clerodendrum petasites S. Moore., Ficus racemosa L., Harrisonia perforata (Blanco) Merr., and Tiliacora triandra (Colebr.) Diels, Piper betle L. (PB), and Garcinia mangostana L. (GM) are commonly used in traditional Thai medicine to treat skin diseases, including atopic dermatitis (AD). Combining three medicines in adjusted proportions can improve efficacy, reduce toxicity, and reduce medication. This study aimed to evaluate the anti-allergic, anti-inflammatory, antimicrobial, and cytotoxic activities of the ethanolic extracts of different combinations to analyze the relationship among elements, medicinal tastes, and biological activities.Experimental approachThe biological activities (anti-allergic, anti-inflammatory, and anti-microbial activities and cell viability) of ethanolic extracts of plants and their combinations in various proportions were evaluated, as well as the chemical content of the developed remedies using the HPLC technique.Findings/resultsHMB-123 was the most significantly effective combination for AD. HMB-123 reduced β-hexosaminidase release from RBL-2H3 cells to a greater extent than chlorpheniramine. HMB-123 significantly inhibited nitric oxide and TNF-α production in LPS-stimulated RAW 264.7 cells. HMB-123 demonstrated antibacterial activity against all tested bacteria and antifungal activity against Candida albicans. For single extract, PB exhibited the highest anti-fungal activity, while GM exhibited the highest anti-bacterial activity.Conclusion and implicationsThe combined extracts showed potential as an optimized remedy for AD. HMB-123 demonstrated the highest anti-allergic, anti-inflammatory, and antimicrobial activities, making it a promising development candidate for AD treatment. To confirm safety and efficacy, further pre-clinical and clinical testing is necessary.
Abstract licence: CC BY-NC-SA
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
15 found
Half-life
21-27 hours
Mechanism
Chlorpheniramine binds to the histamine H1 receptor.
Food interactions
2 warnings
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
21-27 hours
Protein binding
72%
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1318 interactions
Sweet, US Dept. of Health & Human Services: Cincinatti, 2010.]
Also a mild reproductive toxin to women of childbearing age.
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:33828102 PMID:8280179
Through the H1 receptor, histamine mediates the contraction of smooth muscles and increases capillary permeability due to contraction of terminal venules. Also mediates neurotransmission in the central nervous system and thereby regulates circadian rhythms, emotional and locomotor activities as well as cognitive functions (By similarity)
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Essential for serotonin homeostasis in the central nervous system. In the developing somatosensory cortex, acts in glutamatergic neurons to control serotonin uptake and its trophic functions accounting for proper spatial organization of cortical neurons and elaboration of sensory circuits.
In the mature cortex, acts primarily in brainstem raphe neurons to mediate serotonin uptake from the synaptic cleft back into the pre-synaptic terminal thus terminating serotonin signaling at the synapse (By similarity). Modulates mucosal serotonin levels in the gastrointestinal tract through uptake and clearance of serotonin in enterocytes. Required for enteric neurogenesis and gastrointestinal reflexes (By similarity).
Regulates blood serotonin levels by ensuring rapid high affinity uptake of serotonin from plasma to platelets, where it is further stored in dense granules via vesicular monoamine transporters and then released upon stimulation .
PMID:17506858 PMID:18317590
Mechanistically, the transport cycle starts with an outward-open conformation having Na1(+) and Cl(-) sites occupied. The binding of a second extracellular Na2(+) ion and serotonin substrate leads to structural changes to outward-occluded to inward-occluded to inward-open, where the Na2(+) ion and serotonin are released into the cytosol. Binding of intracellular K(+) ion induces conformational transitions to inward-occluded to outward-open and completes the cycle by releasing K(+) possibly together with a proton bound to Asp-98 into the extracellular compartment.
Na1(+) and Cl(-) ions remain bound throughout the transport cycle .
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Additionally, displays serotonin-induced channel-like conductance for monovalent cations, mainly Na(+) ions. The channel activity is uncoupled from the transport cycle and may contribute to the membrane resting potential or excitability (By similarity)
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)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:9260930 PMID:9687576
Functions as a Na(+)-independent, bidirectional uniporter .
PMID:21128598 PMID:9687576
Cation cellular uptake or release is driven by the electrochemical potential, i.e. membrane potential and concentration gradient .
PMID:15212162 PMID:9260930 PMID:9687576
However, may also engage electroneutral cation exchange when saturating concentrations of cation substrates are reached (By similarity). Predominantly expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow .
PMID:15783073
Implicated in monoamine neurotransmitters uptake such as histamine, dopamine, adrenaline/epinephrine, noradrenaline/norepinephrine, serotonin and tyramine, thereby supporting a physiological role in the central nervous system by regulating interstitial concentrations of neurotransmitters .
PMID:16581093 PMID:17460754 PMID:9687576
Also capable of transporting dopaminergic neuromodulators cyclo(his-pro), salsolinol and N-methyl-salsolinol, thereby involved in the maintenance of dopaminergic cell integrity in the central nervous system .
PMID:17460754
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Also transports guanidine and endogenous monoamines such as vitamin B1/thiamine, creatinine and N-1-methylnicotinamide (NMN) .
PMID:12089365 PMID:15212162 PMID:17072098 PMID:24961373 PMID:9260930
Mediates the uptake and efflux of quaternary ammonium compound choline .
PMID:9260930
Mediates the bidirectional transport of polyamine agmatine and the uptake of polyamines putrescine and spermidine .
PMID:12538837 PMID:21128598
Able to transport non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
Also involved in the uptake of xenobiotic 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) .
PMID:12395288 PMID:16394027
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
Involved compounds
ATC R06AB54
ATC R06AB04
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)
Chlorpheniramine
Matched from: Chlorphenamine
Additional database identifiers
Drugs Product Database (DPD)
10259
ChemSpider
2624
BindingDB
35938
Guide to Pharmacology
1213
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:11050
GenAtlas
SLC6A4
GeneCards
SLC6A4
GenBank Gene Database
X70697
GenBank Protein Database
36433
Guide to Pharmacology
928
UniProt Accession
SC6A4_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: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:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10966
GeneCards
SLC22A2
GenBank Gene Database
X98333
GenBank Protein Database
2281942
Guide to Pharmacology
1020
UniProt Accession
S22A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10963
GeneCards
SLC22A1
GenBank Gene Database
X98332
GenBank Protein Database
2511670
Guide to Pharmacology
1019
UniProt Accession
S22A1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q420133), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.