Ergocalciferol 4,500units/5ml oral solution
Requires a prescription from a doctor or prescriber
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Suspected adverse reactions reported for Ergocalciferol
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1 branded products available
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.
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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: 35 · Randomised trials: 9 · 2000–2026
Showing the 50 most relevant studies, sorted by most relevant.
Heike A. Bischoff‐Ferrari, Bess Dawson‐Hughes, Hannes B. Staehelin, et al.
BMJ, 2009
- Dietary Supplements
- Accidental Falls
- Calcium
Philippe Autier
Archives of Internal Medicine, 2007
- Dietary Supplements
- Cardiovascular Diseases
- Diabetes Mellitus
Kow CS, Ramachandram DS, Hasan SS, et al.
2024
- Vitamin D
- Dietary Supplements
- COVID-19
Junmei Lai, Xiaofan Yu, K. Prabahar, et al.
Nutrition reviews, 2025
- Calcium
- Phosphorus
- Ergocalciferols
Ranjbar M, Rahimlou M, Fallah M, et al.
2025
BackgroundRheumatoid arthritis (RA) is known as an inflammatory illness. Evidence shows that Vitamin D modulates immunologic function and inflammation by affecting various immunological cells. We decided to run a systematic review and meta-analysis to investigate the relationship between vitamin D supplementation and the outcomes of adult patients suffering from RA.MethodsWe searched electronic databases, using specific search terms in PubMed, Scopus, and ISI Web of Science, until May 2024. Clinical studies involving patients with RA were included if they compared the effects of vitamin D supplementation to either a placebo or standard care. The results from the selected studies were presented as weighted mean differences (WMD) along with a 95 % confidence interval (CI).ResultsInclusion criteria have been met by 11 studies and presented as part of this analysis. The results indicate a major influence of vitamin D supplementation on the Disease Activity Score 28 (DAS-28) (WMD: -0.83, 95 % CI: -1.38 to -0.28, p-value ConclusionTo improve DAS-28, CRP, ESR, and serum vitamin D in RA patients, vitamin D supplements may be beneficial, although the optimal dosage and length of treatment are still unknown.
Abstract licence: CC BY
Khansa F, Ichwan C, Ghifari MH, et al.
2024
BackgroundChildren with one functional ventricle might receive the Fontan procedure as palliative management to prolong their lives. However, the heart remains functionally univentricular, which may result in disrupted absorption of nutrients, including Vitamin D. Individuals with Fontan circulation have limited physical activity and sun exposure, which might further contribute to Vitamin D deficiency.ObjectiveThis study aimed to estimate the prevalence of Vitamin D deficiency among individuals with Fontan circulation and analyze probable contributing factors to it through meta-regression analysis.MethodsA predetermined search strategy was applied on PubMed, Scopus, Scilit, Web of Science, Europe PMC, and Google Scholar to identify relevant literature as of July 2024. In general, studies reporting the prevalence or incidence of Vitamin D deficiency (ResultsSix studies were included, comprising 255 individuals with the Fontan circulation. The prevalence of Vitamin D deficiency was 51% (95% confidence interval: 35%- 67%) with noticeable heterogeneity (I 2 = 84.38%; p-Het P = 0.003) was the main contributor to the heterogeneity.ConclusionVitamin D deficiency is highly prevalent among individuals with Fontan palliation, highlighting the need for active monitoring and investigation into the benefits of Vitamin D supplementation.PROSPERO registration: CRD42024574724.
Abstract licence: CC BY-NC-SA
Georgescu B, Cristea AE, Oprea D, et al.
2024
BackgroundOsteoarthritis is a common chronic disease that affects quality of life and increases public health costs. Knee osteoarthritis is a frequent form, marked by joint degeneration, pain, stiffness, and functional restrictions. Factors such as age, genetics, joint injuries, obesity, and vitamin D deficiency can affect knee osteoarthritis progression. While the exact link between vitamin D and osteoarthritis is still being studied, recent research indicates that low vitamin D levels might influence the articular cartilage's structure and function, potentially accelerating osteoarthritis. This review aims to analyze the last decade of research on vitamin D's role in osteoarthritis.MethodsA systematic review of the literature was conducted in accordance with the PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). Relevant studies from the last ten years were included to evaluate the association between vitamin D levels and knee osteoarthritis. The inclusion criteria were studies examining the role of vitamin D in cartilage health and osteoarthritis progression and the potential clinical implications for disease management.ResultsThis review identified a variety of studies exploring the connection between vitamin D and osteoarthritis, with mixed findings.ConclusionsThe relationship between vitamin D and knee osteoarthritis remains inconclusive, highlighting the need for further research. An updated evaluation of the literature is crucial for osteoarthritis management strategies and to potentially include vitamin D supplementation in therapeutic protocols.
Abstract licence: CC BY
Martinekova P, Obeidat M, Topala M, et al.
2025
- Liver Diseases
- Vitamin D Deficiency
- Vitamins
ContextVitamin D deficiency is highly prevalent in chronic liver disease. Although international societies recommend vitamin D supplementation in cases of proven deficiency, the impact of vitamin D on chronic liver disease remains uncertain.ObjectiveOur aim was to evaluate the effects of vitamin D supplementation in patients with chronic liver disease by conducting a systematic review and meta-analysis of randomized controlled trials (RCTs).Data sourcesWe systematically searched PubMed, EMBASE and the Cochrane Library on July 2, 2024.Data extractionOur primary outcomes involved survival, controlled attenuation parameter (CAP), liver stiffness measurement (LSM), and effects on changes in liver enzymes. Secondary outcomes included lipid profile and homeostasis model assessment of insulin resistance (HOMA-IR), among others. The pooled risk ratio (RR), mean difference (MD), and corresponding 95% CIs were calculated using the random-effects model.Data analysisForty-six RCTs were included, comprising 4084 patients. When we compared the vitamin D group with the control, the RR for overall survival was 1.14 (95% CI, 0.85-1.54; 4 RCTs) at 6 months and 0.99 (95% CI, 0.83-1.17; 4 RCTs) at the 12-month follow-up. Vitamin D supplementation did not result in a lower CAP (MD, -23.50 dB/m; 95% CI, -81.72 to 34.72; 3 RCTs) and LSM (MD, -0.65 kPa; 95% CI, -1.98 to 0.68; 3 RCTs). A significant reduction in HOMA-IR was observed in the vitamin D group (MD, -0.31; 95% CI, -0.62 to -0.01; 15 RCTs). Alanine aminotransferase (ALT) (MD, -4.98 IU/L; 95% CI, -8.28 to -1.68; 24 RCTs), aspartate aminotransferase (AST) (MD, -3.33 IU/L; 95% CI, -6.25 to -0.40; 23 RCTs), gamma-glutamyl transferase (GGT) (MD, -5.14 IU/L; -6.40; -3.88; 11 RCTs), triglycerides (MD, -7.59 mg/dL; 95% CI, -15.09 to -0.81), and insulin (MD -0.79 μIU/L; 95% CI, -1.36 to -0.21) were significantly reduced in the patients with vitamin D supplementation.ConclusionOur results showed significantly reduced ALT, AST, GGT, triglycerides, insulin, and HOMA-IR in the vitamin D-supplemented group; however, the effect was modest. In addition, there were no differences in survival, CAP, or LSM. Further RCTs with adequate power are warranted to clarify the results.Systematic review registrationPROSPERO registration No. CRD42022370312.
Abstract licence: CC BY
Maai N, Frank FA, Meuris A, et al.
2025
It is generally accepted that the maintenance of the health of the musculoskeletal system is highly dependent on vitamin D. However, the relationship between vitamin D levels and the incidence of musculoskeletal injuries is still uncertain. This systematic review aimed to summarize the available information on the association between vitamin D levels and musculoskeletal injuries. Seven electronic databases were searched using Boolean operators to link MeSH (Medical Subject Headings) terms and free text phrases. This improved the sensitivity and specificity of the search results. Studies investigating the association between vitamin D status and musculoskeletal damage were included. Twelve studies met the inclusion criteria. The majority of studies reported an increased prevalence amongst individuals with low vitamin D levels and musculoskeletal symptoms or injury. This underlines the important role of vitamin D screening and supplementation. Some studies have associated certain vitamin D metabolites with injury occurrence, suggesting that levels and balance of these metabolites may influence injury risk. However, there have been conflicting results on the effect of vitamin D supplementation on muscle function and exercise-induced muscle injury, with some studies failing to find any significant changes. Consistent evidence has demonstrated the benefits of vitamin D supplementation in reducing the incidence of stress fractures in athletes. One study suggests that genetic variations may influence how vitamin D is related to musculoskeletal health. The reviewed studies revealed a complex relationship between the vitamin D status and musculoskeletal injuries. While low vitamin D levels were consistently observed, the effects of supplementation on various musculoskeletal outcomes varied. These findings emphasize the need for further research to better understand the underlying mechanisms and to develop targeted interventions for specific populations, considering factors such as vitamin D metabolites, supplementation dosage, and genetic variations.
Abstract licence: CC BY
Liu S, Lin T, Pan Y
2025
- Tuberculosis
- Vitamin D
- Dietary Supplements
Vitamin D plays an important role in immune regulation, prompting interest in its potential for preventing tuberculosis. However, clinical findings regarding its protective effects against tuberculosis infection and disease remain inconsistent. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to assess the impact of vitamin D supplementation on the prevention of tuberculosis infection and the progression to active tuberculosis. We searched PubMed, Embase, Cochrane Library, and Web of Science databases through January 2025. Eligible studies involved participants without active tuberculosis at baseline and reported outcomes related to tuberculosis. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a random-effects model. Subgroup and sensitivity analyses were conducted, and the certainty of evidence was evaluated using the GRADE approach. Six RCTs, involving 15,677 participants, met our inclusion criteria. Compared to placebo, vitamin D supplementation did not significantly reduce the risk of tuberculosis infection (5 RCTs; OR: 0.95; 95% CI: 0.79-1.14; p = 0.55) or the development of active tuberculosis (4 RCTs; OR: 0.77; 95% CI: 0.56-1.05; p = 0.10). The certainty of evidence was moderate for both outcomes. Subgroup analyses based on baseline vitamin D levels and duration of follow-up yielded consistent results. The incidence of serious adverse events was comparable between the vitamin D and placebo groups (OR: 1.02; 95% CI: 0.76-1.38; p = 0.87), and none of the serious events were attributed to vitamin D supplementation. In conclusion, vitamin D supplementation does not significantly reduce the risk of tuberculosis infection or progression to active tuberculosis, although it is safe and well tolerated.
Abstract licence: CC BY
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
1-2 days
Mechanism
For its activity, ergocalciferol is required to be transformed to its major acti…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
1-2 days
Protein binding
70-90%
Volume of distribution
Metabolism
Elimination
Clearance
31 ml/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ergocalciferol is considered the first vitamin D analog and is differentiated from [cholecalciferol] by the presence of a double bond between C22 and C23 and the presence of a methyl group at C24. These modifications reduce the affinity of ergocalciferol for the vitamin D binding protein resulting in faster clearance, limits its activation, and alters its catabolism.[A177637]
The first approved product containing ergocalciferol under the FDA records was developed by US Pharm Holdings and was FDA approved in 1941.[L6058]
Hypoparathyroidism is the result of inadequate parathyroid hormone production that occurs due to the presence of damage or removal of the parathyroid glands. This condition produces decreased calcium and increased phosphorus levels.
[L6082]
Rickets is a condition produced due to a deficiency in vitamin D, calcium or phosphorus. However, this condition can also be related to renal diseases.
It is characterized to present weak or soft bones.
[A177664]
Familial hypophosphatemia is characterized by the impaired transport of phosphate and an altered vitamin D metabolism in the kidneys. The presence of this condition can derive in the presence of osteomalacia, bone softening and rickets.
[L6085]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 145 interactions
[L6094]
Once an overdose state is registered, immediate withdrawal of vitamin D is required along with a calcium diet, generous intake of fluids and symptomatic treatment. The administration of loop diuretics is an option to increase renal calcium excretion. On the other hand, dialysis and administration of citrates, sulfates, phosphates, corticosteroids, EDTA and mithramycin are recommended.
[L6094]
There haven't been long term studies analyzing the carcinogenic and mutagenic potential of ergocalciferol or its effects in fertility.
The activation of the vitamin D receptor is part of the vitamin D endocrine system and it is described by the production of a change in the transcription rates of the vitamin D receptor target genes.T580 The target genes in the DNA affected by the presence of ergocalciferol are called vitamin D response elements which are dependent on co-modulators.[A177637]
The vitamin D receptor is a transcription factor and member of the steroid hormone nuclear receptor family. It presents a DNA binding domain (VDRE) that, when activated, recruits coregulatory complexes to regulate the genomic activity.[A177637]
Additionally, ergocalciferol presents nongenomic effects such as the stimulation of intestinal calcium transport via transcaltachia.[A177637]
Some other effects known to be produced due to the presence of vitamin D are osteoblast formation, fetus development, induction of pancreatic function, induction of neural function, improvement of immune function, cellular growth and cellular differentiation.T580
When compared to its vitamin D counterpart [cholecalciferol], ergocalciferol has been shown to present a reduced induction of calcidiol and hence, it is less potent.[A177529]
Ergocalciferol supplementation in patients with end-stage renal disease has been shown to generate a significant benefit in lab parameters of bone and mineral metabolism as well as improvement in glycemic control, serum albumin levels and reduced levels of inflammatory markers.[A177526]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L6088]
[A177670]
[A177637]
As part of the minor metabolism, ergocalciferol is transformed into 25-hydroxyvitamin D in the liver by the activity of D-25-hydroxylase and CYP2R1. As well, the formation of 24(R),25dihydroxyvitamin D is performed mainly in the kidneys by the action of 25-(OH)D-1-hydroxylase and 25-(OH)D-24-hydroxylase.T580
Additionally, there are reports indicating significant activity of 3-epimerase in the metabolism of ergocalciferol which modifies the hydroxy group in C3 from the alpha position to a beta. The epimers formed seemed to have a reduced affinity for the vitamin D plasma proteins and to the vitamin D receptor.
[A177637]
An alternative activation metabolic pathway has been reported and this process is characterized by the activity of CYP11A1 and its hydroxylation in the C-20.
This 20-hydroxylated vitamin D seems to have similar biological activity than calcitriol.
[A177637]
[L6091]
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
A particularity of this type of channels is an opening at quite negative potentials, and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes.
Gates in voltage ranges similar to, but higher than alpha 1G or alpha 1H
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
ATC A11CC01
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)
Ergocalciferol
Additional database identifiers
Drugs Product Database (DPD)
4924
Drugs Product Database (DPD)
703
ChemSpider
4444351
BindingDB
50247883
PDB
D2V
ZINC
ZINC000004629876
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:1405
GenAtlas
CACNG1
GeneCards
CACNG1
GenBank Gene Database
L07738
GenBank Protein Database
306473
UniProt Accession
CCG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1406
GeneCards
CACNG2
UniProt Accession
CCG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1407
GeneCards
CACNG3
UniProt Accession
CCG3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1408
GeneCards
CACNG4
UniProt Accession
CCG4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1409
GeneCards
CACNG5
UniProt Accession
CCG5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13625
GeneCards
CACNG6
UniProt Accession
CCG6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13626
GeneCards
CACNG7
UniProt Accession
CCG7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13628
GeneCards
CACNG8
UniProt Accession
CCG8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1399
GenAtlas
CACNA2D1
GeneCards
CACNA2D1
GenBank Gene Database
M76559
GenBank Protein Database
179762
UniProt Accession
CA2D1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1400
GenAtlas
CACNA2D2
GeneCards
CACNA2D2
GenBank Gene Database
AJ251368
UniProt Accession
CA2D2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15460
GeneCards
CACNA2D3
GenBank Gene Database
AJ272268
GenBank Protein Database
7105926
UniProt Accession
CA2D3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:20202
GeneCards
CACNA2D4
UniProt Accession
CA2D4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1390
GenAtlas
CACNA1C
GeneCards
CACNA1C
GenBank Gene Database
M92270
Guide to Pharmacology
529
UniProt Accession
CAC1C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1391
GenAtlas
CACNA1D
GeneCards
CACNA1D
GenBank Gene Database
M76558
GenBank Protein Database
179764
Guide to Pharmacology
530
UniProt Accession
CAC1D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1393
GenAtlas
CACNA1F
GeneCards
CACNA1F
GenBank Gene Database
AJ006216
GenBank Protein Database
3183953
Guide to Pharmacology
531
UniProt Accession
CAC1F_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1397
GenAtlas
CACNA1S
GeneCards
CACNA1S
GenBank Gene Database
U30707
GenBank Protein Database
1698403
Guide to Pharmacology
528
UniProt Accession
CAC1S_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1401
GenAtlas
CACNB1
GeneCards
CACNB1
GenBank Gene Database
M92303
GenBank Protein Database
179806
UniProt Accession
CACB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1402
GenAtlas
CACNB2
GeneCards
CACNB2
GenBank Gene Database
S60415
GenBank Protein Database
300417
UniProt Accession
CACB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1403
GenAtlas
CACNB3
GeneCards
CACNB3
GenBank Gene Database
X76555
GenBank Protein Database
435135
UniProt Accession
CACB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1404
GenAtlas
CACNB4
GeneCards
CACNB4
GenBank Gene Database
U95020
GenBank Protein Database
2058727
UniProt Accession
CACB4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1389
GenAtlas
CACNA1B
GeneCards
CACNA1B
GenBank Gene Database
M94172
GenBank Protein Database
179758
Guide to Pharmacology
533
UniProt Accession
CAC1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1388
GenAtlas
CACNA1A
GeneCards
CACNA1A
GenBank Gene Database
AF004884
GenBank Protein Database
2213913
UniProt Accession
CAC1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1392
GeneCards
CACNA1E
Guide to Pharmacology
534
UniProt Accession
CAC1E_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1394
GenAtlas
CACNA1G
GenBank Gene Database
AF134986
GenBank Protein Database
6625659
Guide to Pharmacology
535
UniProt Accession
CAC1G_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1395
GenAtlas
CACNA1H
GeneCards
CACNA1H
GenBank Gene Database
AF051946
GenBank Protein Database
14670397
Guide to Pharmacology
536
UniProt Accession
CAC1H_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1396
GenAtlas
CACNA1I
GeneCards
CACNA1I
GenBank Gene Database
AF129133
GenBank Protein Database
5565888
Guide to Pharmacology
537
UniProt Accession
CAC1I_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10293
GeneCards
RPE
UniProt Accession
RPE_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:2602
GenAtlas
CYP24A1
GeneCards
CYP24A1
GenBank Gene Database
L13286
GenBank Protein Database
306704
Guide to Pharmacology
1365
UniProt Accession
CP24A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2606
GenAtlas
CYP27B1
GeneCards
CYP27B1
GenBank Gene Database
AF027152
GenBank Protein Database
2612976
Guide to Pharmacology
1370
UniProt Accession
CP27B_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:20580
GenAtlas
CYP2R1
GeneCards
CYP2R1
GenBank Gene Database
AY323817
GenBank Protein Database
33591222
UniProt Accession
CP2R1_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
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ATC classifications (Wikidata)
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