Colecalciferol 20,000units/ml oral solution
Requires a prescription from a doctor or prescriber
Vitamin D, in general, is a secosteroid generated in the skin when 7-dehydrocholesterol located there interacts with ultraviolet irradiation - like that commonly found in sunlight [L5689].
Safety information for pregnancy and breastfeeding
Pregnancy
Breastfeeding
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
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Suspected adverse reactions reported for Colecalciferol
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1 branded products available
Part of the Cubicole brand family (generic: Colecalciferol)
MHRA licensed products
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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)
20 microgram
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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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: 15 · Randomised trials: 4 · 2007–2026
Showing the 50 most relevant studies, sorted by most relevant.
Kay‐Tee Khaw, Alistair W. Stewart, Debbie Waayer, et al.
The Lancet Diabetes & Endocrinology, 2017
- Accidental Falls
- Vitamin D
- Proportional Hazards Models
Adrian R. Martineau, Wai Yee James, Richard Hooper, et al.
The Lancet Respiratory Medicine, 2014
- Cholecalciferol
- Respiratory Tract Infections
- Vitamin D
Manoj P, Derwin R, George S
2023
- Hip Fractures
- Cholecalciferol
- Calcium
IntroductionHip fractures have a huge impact in reducing the quality of life and increasing mortality. This review aims to assess the impact of daily oral supplementation of vitamin D3 plus calcium on the incidence of hip fracture in people over 65 years.MethodsPRISMA guidelines were followed and RCTs that evaluated the effectiveness of daily oral supplementation of vitamin D3 plus calcium in preventing hip fracture in adults over 65 years were included in the study. The databases such as Cochrane Library, Embase, Medline, PubMed, CINAHL, Web of Science and Scopus were searched from October 2019- January 2020.The Cochrane risk of bias tool was used to check the quality of the included studies. A meta-analysis with fixed effect model using Review Manager (Revman 5.3) was used to analyse the data.ResultsThe meta-analysis of seven RCTs on vitamin D3 plus calcium supplementation and hip fracture (n = 12,620) identified odds ratio (OR) of 0.75; 95% Confidence interval (CI): 0.64, 0.87; p = .0003. Daily oral supplementation of 800 IU of Vitamin D3 plus 1200 mg of calcium was found more effective (n = 5676 participants; OR = 0.69; 95% CI: 0.58, 0.82; p ConclusionDaily oral supplementation 800 IU of vitamin D3 plus 1200 mg of calcium reduces hip fracture and non-vertebral fracture in older people. Administering vitamin D3 and calcium supplements had no effect in increasing the femoral neck BMD.Implications for practiceEven though it is evident from the review that optimal daily intake of vitamin D3 plus calcium supplementation help in the prevention of fracture, it is only one essential element in fracture prevention. Also, people who are on dietary supplements should be compliant with same for better result. Efforts to prevent bone loss and osteoporosis should begin from an early age. It includes maintaining a healthy lifestyle, optimal intake of calcium and vitamin D3, proper nutrition, adequate exposure to sunlight, exercise etc. Proper education on healthy lifestyle, avoiding risk factors like smoking, caffeine, alcohol and awareness of bone health should continue throughout life with emphasis during menopause when increased bone loss is expected.
Abstract licence: CC BY
Tan L, He R, Zheng X
2024
- Vitamin D
- Accidental Falls
- Dietary Supplements
BackgroundThe association between vitamin D supplementation and the risk of falls in older adults has been controversial. This systematic review and network meta-analysis aims to assess the efficacy of vitamin D, calcium, and combined supplementation in the prevention of falls.MethodsRandomized controlled trials (RCTs) on the efficacy of vitamin D in fall prevention were systematically searched in PubMed, Embase, Cochrane Library, and Web of Science from inception to May 9, 2023. The network meta-analysis was performed using a random effects model in R4.1.3 and Stata15.0. Heterogeneity was evaluated by the I2 statistic, and publication bias was assessed using funnel plots, Begg's test, and Egger's tests. Data were pooled and expressed as relative risk (RR) and 95% confidence interval (CI).ResultsA total of 35 RCTs involving 58,937 participants were included in this study, among which 11 RCTs (31.4%) applied calcium combined with vitamin D. There was low heterogeneity (I2 = 11%) among the included studies. Vitamin D supplementation at 800-1000 International Unit (IU)/d resulted in a lower risk of falls than placebo or no treatment (RR = 0.85, 95%CI: 0.74-0.95). In addition, 800-1000 IU/d of vitamin D with or without calcium were more effective in preventing falls than calcium alone. High-dose vitamin D (> 1000 IU/day) increased the risk of falls compared with 800-1000 IU/d of vitamin D. According to the subgroup analysis, daily administration of 800-1000 IU/d vitamin D was associated with a 22% reduction in the risk of falls (RR = 0.78, 95%CI:0.64-0.92), whereas intermittent vitamin D administration had no preventive effect. Furthermore, 800-1000 IU/d of vitamin D also significantly decreased the risk of falls in old adults with ≤ 50 nmol/L 25-hydroxyvitamin D [25(OH)D] (RR = 0.69, 95%CI:0.52-0.86) but not in individuals with > 50 nmol/L 25(OH)D.ConclusionVitamin D supplementation at 800-1000 IU/d is associated with a lower risk of falls among older adults. 800-1000IU/d of vitamin D has a benefit on prevention of falls in population received daily dose regimens and in population with vitamin D deficiency.
Abstract licence: CC BY
Apivatthakakul A, Jaruvongvanich S, Upala S, et al.
2024
Previous studies found seasonal variations in the incidence of retinal vascular occlusion (RVO), with more occurrence in winter. There is increasing evidence linking vitamin D deficiency and RVO. Therefore, we conducted a meta-analysis to evaluate the association between vitamin D levels and RVO. From inception to February 2024, MEDLINE and EMBASE databases were comprehensively searched. Observational studies comparing 25-hydroxyvitamin D (25(OH)D) levels between adult patients with RVO and non-RVO controls were included. We calculated pooled mean difference (MD) and pooled odds ratio (OR) with 95% confidence intervals (CI) of our data using a random-effects model and generic inverse variance method. Five studies involving 528 patients (228 patients with RVO and 300 controls were included in the meta-analysis. 25(OH)D was significantly lower in patients with RVO (pooled MD of -9.65 (95%CI -13.72 to -5.59, I2 = 92.2%). Vitamin D deficiency (serum 25(OH)D < 20) was significantly associated with RVO with the pooled OR of 14.52 (95%CI 1.72 to 122.59, I2 = 90.5). There was no difference in 25(OH)D levels between patients with central RVO and branched RVO (pooled MD of -0.94 (95%CI -3.91 to 2.03, I2 = 59.1%). In conclusion, our meta-analysis demonstrates that serum vitamin D levels were lower in patients with RVO than non-RVO controls. Clinicians could consider screening for vitamin D deficiency in patients with RVO. Further studies are warranted to determine the correlation between vitamin D levels and disease severity and the role of vitamin D supplements in these populations.
Abstract licence: CC BY
Krajewska M, Witkowska-Sędek E
2025
Obesity-related low-grade inflammation is a significant factor responsible for the development of metabolic syndrome and chronic diseases, which can begin even in early childhood. Recently, there has been growing interest in the impact of vitamin D3 supplementation on inflammatory markers in overweight and obese individuals; however, findings remain inconsistent. Therefore, we aimed to conduct a systematic review to assess the effects of vitamin D3 supplementation on inflammatory markers in overweight and obese children and adolescents, focused exclusively on the analysis of randomized controlled trials (RCTs) identified by searching PubMed, EMBASE, and Cochrane Library. The results of this study were synthesized and reported following the PRISMA statement. A total of 294 citations were identified through electronic literature searches, of which two RCTs were finally included in our systematic review. We found that vitamin D3 supplementation did not affect the changes in C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), but led to a decrease in leptin levels. The small number of studies meeting the inclusion criteria for our systematic review limits the value of the presented results, but also indicates the need for in-depth research on this topic.
Abstract licence: CC BY
Tan CN, Yeo B, Vasanwala RF, et al.
2025
ContextVitamin D deficiency (VDD) is common in paediatric populations, and its relationship with critical care outcomes warrants further investigation.ObjectiveThe aim is to examine the association between VDD and clinical outcomes in children admitted to the Pediatric Intensive Care Unit (PICU).MethodsThis systematic review and meta-analysis investigated the impact of VDD on clinical outcomes in PICU patients. A comprehensive search of Embase, Web of Science, PubMed, and Cochrane databases was conducted. Our primary outcomes were mortality and sepsis incidence, while secondary outcomes included length of stay (LOS), need for inotropic support, and need for and duration of mechanical ventilation. Eligible studies included infants and children aged 1 month to 18 years admitted to the PICU, with baseline 25-hydroxyvitamin D levels measured on admission. Two independent reviewers screened studies, extracted data, and assessed quality. Pooled estimates were obtained using a random-effects model.ResultsOut of 2298 screened studies, 27 met the inclusion criteria, comprising 4682 patients. VDD was defined as 25-hydroxyvitamin D levels ConclusionVDD in critically ill pediatric patients was associated with increased mortality and higher need for inotropic support. Further research is warranted to evaluate the potential benefits of vitamin D supplementation in this high-risk population.
Abstract licence: CC BY
Anto M, Elkashif I, Vithayathil S, et al.
2025
Adolescent idiopathic scoliosis is a common spinal orthopedic condition that is associated with a high prevalence of vitamin D deficiency. Vitamin D is known to affect bone health, and we conducted a systematic review to assess the impact of vitamin D deficiency on patients diagnosed with adolescent idiopathic scoliosis who undergo surgery. We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 checklist for our systematic review, utilizing various databases to conduct a thorough analysis of the current literature. We included specific search terms related to vitamin D deficiency and adolescent idiopathic scoliosis, and considered articles published between 2010 and 2025, focusing on papers with free full-text access. We used the PRISMA flowchart and initially identified 1,286 articles using the keywords for our search strategy across the databases. After removing duplicates, conducting title screening, assessing abstracts, and evaluating quality, we included 12 research papers in this review. Our review focused on the prevalence of vitamin D deficiency in adolescent idiopathic scoliosis patients and the impact of vitamin D deficiency on patients undergoing surgical management. This study was inconclusive in proving how significant the impact of vitamin D deficiency was in surgical adolescent idiopathic scoliosis patients, and we recommended conducting additional research to establish the importance of correcting vitamin D deficiency pre-operatively. However, considering that vitamin D has been linked to poorer surgical outcomes in most of the studies included in our review, we recommend routine screening for vitamin D in adolescent idiopathic scoliosis patients and its correction pre-operatively.
Abstract licence: CC BY
Bokayeva K, Jamka M, Kałużny Ł, et al.
2025
- Phenylketonurias
- beta Carotene
- Vitamin A
Background/Objectives: The impact of dietary adherence and formula intake regularity on fat-soluble vitamin status in phenylketonuria (PKU) is uncertain. This study assessed whether vitamin A, D, E, and beta-carotene levels differ by dietary adherence and regularity of Phe-free formula intake. Methods: A cross-sectional study included 98 individuals (age 6-41 years) with vitamin D measurements. In a subgroup of 68 patients, vitamin A, vitamin E, and beta-carotene levels were determined. Vitamin levels were compared between adherent and non-adherent groups and between participants with regular vs. irregular formula intake. A subsequent systematic review and meta-analysis of six studies (from PubMed, Scopus, Web of Science, and Cochrane; searched in August 2025) pooled standardised mean differences (SMDs) using fixed-effects and random-effects models. Results: The cross-sectional results showed higher vitamin D in adherent (35.60 [30.39-41.65] vs. 32.90 [26.50-40.00] ng/mL, p = 0.034) and regular formula consumers (35.97 [30.03-42.28] vs. 30.20 [26.08-35.06] ng/mL, p = 0.002). Beta-carotene was elevated with regular intake (74.40 [56.70-98.45] vs. 53.20 [34.10-68.60] ng/mL, p = 0.003). Meta-analysis confirmed higher vitamin D in adherent individuals (fixed-effects model, SMD = 0.290, 95% CI: 0.004, 0.576, p = 0.047) and regular consumers (fixed-effects model, SMD = 0.750, 95% CI: 0.382, 1.118, p Conclusions: Adherence to diet and regular formula intake is associated with improved vitamin D status, underscoring the critical role of fortified formulas in PKU management. The very low certainty of evidence necessitates further research, especially for the other fat-soluble vitamins. Nonetheless, clinical practice should emphasise support for adherence and ongoing nutritional monitoring.
Abstract licence: CC BY
Ulla Kampmann, Leif Mosekilde, Claus Bogh Juhl, et al.
Metabolism, 2014
- Insulin Resistance
- Insulin Secretion
- C-Peptide
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
50 days
Mechanism
Most individuals naturally generate adequate amounts of vitamin D through ordina…
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
50 days
Protein binding
50 to 80%
Volume of distribution
237 L
[A176417]…
Metabolism
Elimination
Clearance
2.5 L
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Appropriate levels of vitamin D must be upheld in the body in order to maintain calcium and phosphorus levels in a healthy physiologic range to sustain a variety of metabolic functions, transcription regulation, and bone metabolism [A223, L5689, L1782, L5771, F4027, F4042, F4048]. However, studies are also ongoing to determine whether or not cholecalciferol may also play certain roles in cancer, autoimmune disorders, cardiovascular disease, and other medical conditions that may be associated with vitamin D deficiency [L5689].
Concurrently, as one of the most commonly utilized forms of vitamin D, cholecalciferol is also very frequently used as a supplement in individuals to maintain sufficient vitamin d levels in the body or to treat vitamin D deficiency, as well as various medical conditions that can be associated directly or indirectly with vitamin d insufficiency like osteoporosis and chronic kidney disease, among others [A176041, A176044, F4051].
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 475 interactions
Safety of doses in excess of 400 IU (10mcg) of vitamin D3 daily during pregnancy has not been established [F4027, F4042, F4048].
Maternal hypercalcemia, possibly caused by excessive vitamin D intake during pregnancy, has been associated with hypercalcemia in neonates, which may lead to supravalvular aortic stenosis syndrome, the features of which may include retinopathy, mental or growth retardation, strabismus, and other effects [F4027, F4042, F4048]. Hypercalcemia during pregnancy may also lead to suppression of parathyroid hormone release in the neonate, resulting in hypocalcemia, tetany, and seizures [F4027, F4042, F4048].
Vitamin D is deficient in maternal milk; therefore, breastfed infants may require supplementation. Use of excessive amounts of Vitamin D in nursing mothers may result in hypercalcemia in infants.
Doses of Vitamin D3 in excess of 10 µg daily should not be administered daily to nursing women.
Conversely, vitamin D deficiency can often occur from a combination of insufficient exposure to sunlight, inadequate dietary intake of vitamin D, genetic defects with endogenous vitamin D receptor, or even severe liver or kidney disease [A243]. Such deficiency is known for resulting in conditions like rickets or osteomalacia, all of which reflect inadequate mineralization of bone, enhanced compensatory skeletal demineralization, resultant decreased calcium ion blood concentrations, and increases in the production and secretion of parathyroid hormone [A223]. Increases in parathyroid hormone stimulate the mobilization of skeletal calcium and the renal excretion of phosphorus [A223]. This enhanced mobilization of skeletal calcium leads towards porotic bone conditions [A223].
Ordinarily, while vitamin D3 is made naturally via photochemical processes in the skin, both itself and vitamin D2 can be found in various food and pharmaceutical sources as dietary supplements. The principal biological function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet [A223]. At the liver, vitamin D3 or D2 is hydroxylated to 25-hydroxyvitamin D and then finally to the primary active metabolite 1,25-dihydroxyvitamin D in the kidney via further hydroxylation [A223][A243]. This final metabolite binds to endogenous vitamin d receptors, which results in a variety of regulatory roles - including maintaining calcium balance, the regulation of parathyroid hormone, the promotion of the renal reabsorption of calcium, increased intestinal absorption of calcium and phosphorus, and increased calcium and phosphorus mobilization of calcium and phosphorus from bone to plasma to maintain balanced levels of each in bone and the plasma [A223][A243].
In particular, calcitriol interacts with vitamin D receptors in the small intestine to enhance the efficiency of intestinal calcium and phosphorous absorption from about 10-15% to 30-40% and 60% increased to 80%, respectively [L5689]. Furthermore, calcitriol binds with vitamin D receptors in osteoblasts to stimulate a receptor activator of nuclear factor kB ligand (or RANKL) which subsequently interacts with receptor activator of nuclear factor kB (NFkB) on immature preosteoclasts, causing them to become mature bone-resorbing osteoclasts [L5689]. Such mature osteoclasts ultimately function in removing calcium and phosphorus from bone to maintain blood calcium and phosphorus levels [L5689]. Moreover, calcitriol also stimulates calcium reabsorption from the glomerular filtrate in the kidneys [L5689].
Additionally, it is believed that when calcitriol binds with nuclear vitamin D receptors, that this bound complex itself binds to retinoic acid X receptor (RXR) to generate a heterodimeric complex that consequently binds to specific nucleotide sequences in the DNA called vitamin D response elements [L5689]. When bound, various transcription factors attach to this complex, resulting in either up or down-regulation of the associated gene's activity. It is thought that there may be as much as 200 to 2000 genes that possess vitamin D response elements or that are influenced indirectly to control a multitude of genes across the genome [L5689]. It is in this way that cholecalciferol is believed to function in regulating gene transcription associated with cancer risk, autoimmune disorders, and cardiovascular disease linked to vitamin D deficiency [L5689]. In fact, there has been some research to suggest calcitriol may also be able to prevent malignancies by inducing cellular maturation and inducing apoptosis and inhibiting angiogenesis, exhibit anti-inflammatory effects by inhibiting foam cell formation and promoting angiogenesis in endothelial colony-forming cells in vitro, inhibit immune reactions by enhancing the transcription of endogenous antibiotics like cathelicidin and regulate the activity and differentiation of CD4+ T cells, amongst a variety of other proposed actions [L5689].
How the body processes this drug — absorption, distribution, metabolism, and elimination
In particular, recent studies have determined aspects about the absorption of vitamin D, like the fact that a) the 25-hydroxyvitamin D metabolite of cholecalciferol is absorbed to a greater extent than the nonhydroxy form of cholecalciferol, b) the quantity of fat with which cholecalciferol is ingested does not appear to largely affect its bioavailability, and c) age does not apparently effect vitamin D cholecalciferol .
[A176447]
[L1782]
Moreover, it appears that the half-lives of any particular administration of vitamin d can vary due to variations in vitamin d binding protein concentrations and genotype in particular individuals .
[A32185]
[A176417]
[A176417]
Proteins and enzymes this drug interacts with in the body
PMID:10678179 PMID:15728261 PMID:16913708 PMID:28698609 PMID:37478846
Enters the nucleus upon vitamin D3 binding where it forms heterodimers with the retinoid X receptor/RXR .
PMID:28698609
The VDR-RXR heterodimers bind to specific response elements on DNA and activate the transcription of vitamin D3-responsive target genes .
PMID:28698609
Plays a central role in calcium homeostasis (By similarity). Also functions as a receptor for the secondary bile acid lithocholic acid (LCA) and its metabolites PMID:12016314 PMID:32354638
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
ATC M05BB09
ATC M05BX53
ATC M05BB07
ATC M05BB08
ATC A11CC55
ATC M05BB05
ATC A11CC05
ATC M05BB03
ATC M05BB04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Cholecalciferol
Matched from: Colecalciferol
Additional database identifiers
Drugs Product Database (DPD)
4922
Drugs Product Database (DPD)
703
ChemSpider
4444353
BindingDB
50030475
PDB
VD3
ZINC
ZINC000004474460
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12679
GenAtlas
VDR
GeneCards
VDR
GenBank Gene Database
J03258
GenBank Protein Database
340203
Guide to Pharmacology
605
UniProt Accession
VDR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:20580
GenAtlas
CYP2R1
GeneCards
CYP2R1
GenBank Gene Database
AY323817
GenBank Protein Database
33591222
UniProt Accession
CP2R1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2605
GenAtlas
CYP27A1
GeneCards
CYP27A1
GenBank Gene Database
M62401
GenBank Protein Database
181292
Guide to Pharmacology
1369
UniProt Accession
CP27A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2634
GeneCards
CYP2J2
GenBank Gene Database
U37143
GenBank Protein Database
18254513
Guide to Pharmacology
1332
UniProt Accession
CP2J2_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:2590
GeneCards
CYP11A1
GenBank Gene Database
M14565
GenBank Protein Database
181376
Guide to Pharmacology
1358
UniProt Accession
CP11A_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:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4187
GenAtlas
GC
GeneCards
GC
GenBank Gene Database
L10641
GenBank Protein Database
639896
UniProt Accession
VTDB_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
ATC classifications (Wikidata)
Linked open data from Wikidata (Q139347), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.