Tretinoin 10mg capsules
Requires a prescription from a doctor or prescriber
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Tretinoin
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 Tretinoin
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 Tretinoin
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.
5 branded products available
MHRA licensed products
View all licensed products for Tretinoin on the MHRA register
Tretinoin 10mg capsules
Tretinoin 10mg capsules
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.
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.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 13 · Randomised trials: 14 · 1986–2026
Showing the 50 most relevant studies, sorted by most relevant.
Zoya Siddiqui, A. Zufall, M. Nash, et al.
American Journal of Clinical Dermatology, 2024
Balado-Simó P, Morgado-Carrasco D, Gómez-Armayones S, et al.
2025
Topical tretinoin (all-trans-retinoic acid) is a first-generation vitamin A derivative with well-established efficacy in acne vulgaris and photoaging. Owing to its pleiotropic effects on epidermal differentiation, collagen synthesis, and skin pigmentation, numerous off-label uses have been proposed across dermatology. This narrative review summarizes current evidence on the efficacy and safety of topical tretinoin for multiple dermatological conditions, based on studies published between January 2000 and July 2025. Robust data from randomized clinical trials (RCTs) and systematic reviews support its benefit in acne and photoaging, whereas smaller RCTs and prospective studies indicate potential efficacy for melasma, postinflammatory hyperpigmentation, striae distensae, flat warts, alopecia areata, androgenetic alopecia, hypertrophic scars and keloids, and actinic keratosis and as pretreatment before chemical peels or laser resurfacing. However, high-quality, adequately powered trials with standardized outcome measures are still needed to establish clinical guidelines. Regarding cutaneous oncology, a large RCT demonstrated no preventive effect of tretinoin on keratinocyte carcinomas. Adverse events are typically mild, localized, and transient, and available evidence does not support an association with systemic adverse effects.
Abstract licence: CC BY
Alamri A, Alraddadi RA, Alzahrani D, et al.
2025
BackgroundAcanthosis nigricans (AN) is a skin disorder marked by darkening and thickening of the skin, often linked to metabolic abnormalities. This systematic review of randomized controlled trials (RCTs) assesses the comparative effectiveness and tolerability of different topical treatment options of AN, aiming to determine the most suitable therapeutic strategies.MethodsA comprehensive literature search was conducted across PubMed, Scopus, ClinicalTrials.gov, Web of Science, and the Cochrane Library, yielding 6,407 studies. After screening and a full-text review, seven randomized controlled trials (n = 268) assessed topical urea (10-20%), tretinoin (0.025-0.05%), salicylic acid (10%), and chemical peels such as glycolic acid (35-70%) and trichloroacetic acid (15%) over 8 weeks to 2 months, primarily on the neck and axilla. Outcomes included melanin and erythema indices (M/E), ANASI/ANSC scores, Investigator's and Participant's Global Evaluation (IGE/PGE), and adverse events.ResultsUrea demonstrated significant efficacy in reducing erythema, particularly at higher concentrations (20%), with mild adverse events such as stinging or irritation. Tretinoin was the most effective for reducing dark pigmentation, especially on the neck, and patients were more satisfied with it than with glycolic acid. Salicylic acid (10%) gave results similar to urea, with only mild side effects like dryness or peeling. Trichloroacetic acid (15%) peel was more effective than glycolic acid (35%) peel, both in skin improvement and patient satisfaction after 8 weeks. Overall, side effects with all treatments were mild and went away on their own.ConclusionBoth urea and tretinoin are effective treatments for AN, choice of therapy should be individualized tretinoin for predominant hyperpigmentation, urea for erythema or lower irritation tolerance, salicylic acid as a tolerable alternative, and TCA peel when stronger procedural options are suitable glycolic peel showed more modest effects.Systematic review registrationProspero registration number: (CRD42023444441); https://www.crd.york.ac.uk/PROSPERO/view/CRD42023444441.
Abstract licence: CC BY
M. Weinstock, S. Bingham, J. DiGiovanna, et al.
The Journal of investigative dermatology, 2012
Li ZC, Zhu YF, Song YJ, et al.
2026
- Cicatrix, Hypertrophic
- Tretinoin
- Glucose
BackgroundAbnormal glucose metabolism often contributes to myofibroblast activation and the pathogenesis of skin fibrotic diseases. All-trans retinoic acid (ATRA), the active component of tretinoin cream, can regulate glucose metabolism and activate myofibroblasts. Importantly, investigating the potential of ATRA to inhibit myofibroblast activation by modulating glucose metabolism could reveal the translational significance of ATRA in attenuating hypertrophic scar (HS) formation.MethodsWe first conducted a multicenter, double-blind, randomized controlled trial (RCT) to compare the effects of tretinoin cream with those of the first-line medication, silicone gel. In the mechanistic study, the characteristics of glucose metabolic reprogramming and the activation of hypertrophic scar fibroblasts (HSFs) after ATRA treatment were identified through multi-omics profiling, complemented by glucose metabolism assays and functional validations. Besides, genetic overexpression targeting the potential downstream molecules of ATRA, including hypermethylated in cancer 1 (HIC1), phosphoenolpyruvate carboxykinase (PCK)1, and PCK2, was conducted in vitro in HSFs and in vivo in skin fibroblasts of Col1a2-CreER mice.ResultsOur RCT demonstrated that tretinoin cream is non-inferior to silicone gel in preventing HS formation, with the absolute risk difference of incidence rates [-8.65% 90% two-sided confidence interval (CI) -23.03 to 5.74] and in decreasing scar thickness [(2856.20±211.83) μm vs. (1664.57±273.50) μm], attributing to the reduction in HSF proliferation and the proportion of myofibroblasts. Moreover, tretinoin cream effectively mitigated HS formation in both mice and rabbits without impeding normal wound healing. Mechanistically, HSFs underwent glucose reprogramming, characterized by increased aerobic glycolysis, which facilitated the transition of HSFs to myofibroblasts and their proliferation. However, ATRA upregulated HIC1, PCK1, and PCK2 expression through retinoic acid receptor alpha (RARα) activation, thereby inhibiting the fibrotic phenotypes of HSFs by suppressing aerobic glycolysis and facilitating gluconeogenesis. The fibroblast-specific overexpression of HIC1, PCK1, or PCK2 in Col1a2-CreER mice significantly reduced myofibroblast activation and hypertrophic scarring.ConclusionsOur study not only substantiated that topical tretinoin cream could serve as an effective strategy to prevent HSs in clinical settings, but also established ATRA as a regulator of glucose metabolism. Importantly, ATRA/RARα-mediated glucose reprogramming was identified as a potential therapeutic target for attenuating HS formation.Trial registrationChiCTR, ChiCTR2500097242. Registered on 14 Feb, 2025. Available from https://www.chictr.org.cn/bin/project/edit?pid=220146.
Abstract licence: CC BY
Grove GL, Karmisholt KE, Philipsen PA, et al.
2026
- Tretinoin
- Keratolytic Agents
- Striae Distensae
Mature striae distensae, called striae albae, are common but treatment-resistant dermal scars. Fractional radiofrequency (FRF) can potentially act as transdermal permeation enhancer for topical tretinoin (TT). This study investigated FRF and TT as a combination treatment for striae albae. Twenty patients were included, each with four anatomically comparable areas that were randomized to (i) TT (ii) FRF (iii) combination FRF + TT and (iv) untreated control. Three treatment sessions were performed one month apart, and TT was also applied in-between. The change in striae from baseline to 20-week follow-up (Δ) was assessed using the Patient Observer Scar Assessment Scale (POSAS, SUM: 6-60). At baseline, patients assessed the striae as moderate-severe (POSAS-PT: SUM medians 24-25) and at follow-up, they reported an improvement (POSAS-PT: ΔSUM 5-10 points), but only the combination treatment improved significantly better (FRF + TT vs. control p = 0.029). A blinded dermatologist confirmed a tendency towards treatment improvement (POSAS-OBS: ΔSUM: 0-2 point, all treatments vs control p≥0.269). A subtle tendency was observed in objective measures with 3D photographs. Combination treatment with FRF and TT was tolerable and improved patient-reported striae compared to control. Striae albae remain challenging, but the findings highlight a potential for future combination treatment approaches.Trial registration number: NCT05461755Date of registration: 15.07.2022.
Abstract licence: CC BY
R. Warrell, S. Frankel, W. Miller, et al.
The New England journal of medicine, 1991
A. Kligman, G. Grove, R. Hirose, et al.
Journal of the American Academy of Dermatology, 1986
J. Weiss, C. Ellis, J. Headington, et al.
JAMA, 1988
C. E. Griffiths, A. Russman, G. Majmudar, et al.
The New England journal of medicine, 1993
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
0.5 to 2 hours
Mechanism
The exact mechanism of action of tretinoin in skin conditions and acute promyelo…
Food interactions
1 warning
Human targets
16 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
28 days
[A257684][A257699]
…
Half-life
0.5 to 2 hours
[L45349]
Protein binding
95%
[A257689][L45349]
…
Volume of distribution
0.12 L/kg
Metabolism
Elimination
2.75 mg
[L13083]
Following administration of radiolabeled tretinoin at doses of 2.75…
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L45349]
Topical tretinoin is also indicated alone [L45389] or in combination with [benzoyl peroxide] [L34869] or [clindamycin] [L45384] for the treatment of acne vulgaris. It is also used in prescription and over-the-counter for treating various skin conditions such as melasma,[L45394] hyperpigmentation,[A257474] and photoaging [A258180] alone or in combination with other drugs.
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 996 interactions
[L45409]
Reversible signs of hypervitaminosis A, such as headache, nausea, vomiting, and mucocutaneous symptoms, are expected to appear in tretinoin overdose. Overdosage with other retinoids has been associated with transient headache, facial flushing, cheilosis, abdominal pain, dizziness and ataxia: these symptoms have quickly resolved without apparent residual effects. here is no specific treatment in the case of an overdose and it is advised to treat patients experiencing tretinoin overdose in a special hematological unit.
[L45349]
Acne is associated with abnormal follicular formation from excessive keratinization of epithelial cells. Tretinoin promotes cornified cell detachment and enhances keratinocyte shedding. It also stimulates mitotic activity and loosely-adherent corneocyte turnover to expel comedo contents, reducing microcomedo precursor lesions of acne vulgaris.[A257474][L34869] Tretinoin may reduce epidermal melanin and pigmentation by increasing keratinocyte turnover and reducing tyrosinase activity.[A257609][A258180]
RAR-alpha and -beta have also been implicated in APL.[A257724] APL is characterized by a t(15;17) chromosomal translocation, which fuses the promyelocytic myeloid leukemia (PML) gene with the RAR-alpha gene.[A257689][A257694] The resulting PML-RAR-alpha fusion protein plays a role in the pathogenesis of APL by aberrating promyelocyte differentiation. The PML-RAR-alpha fusion protein is found to be predominant in leukemic cells, exerting a dominant negative effect on RAR, RXR and PML function.[A257689] Tretinoin induces terminal differentiation in hemopoietic precursor cell lines and APL cells.[A257694] Tretinoin is believed to promote caspase-mediated cleavage and proteasome-dependent degradation to cause apoptosis and degradation of the PML-RAR-alpha fusion protein.[A257474] It may also convert the fusion protein from a transcription repressor to an activator.[A257474]
Tretinoin exhibits antineoplastic activities when given orally.[L45349] Tretinoin was shown to induce differentiation in tumour cells.[A257694] It induced cytodifferentiation and decreased acute promyelocytic leukemia (APL) cell proliferation in culture and in vivo. In patients with APL, tretinoin promoted the initial maturation of the primitive promyelocytes derived from the leukemic clone, followed by a repopulation of the bone marrow and peripheral blood by normal, polyclonal hematopoietic cells in patients achieving complete remission.[L45349]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A257684][A257699]
In one study, the topical application of radiolabelled tretinoin for 28 days was associated with a total percutaneous absorption of 2%.
[A257684]
The extent of absorption was examined after a once-daily application of 1.9 g of the combination product with [benzoyl peroxide] for 14 days. On Day 14, at steady-state, the mean Cmax was 0.15-0.19 ng/mL for tretinoin, 0.27-0.34 ng/mL for the metabolite 4-keto 13-cis retinoic acid, and 0.13-0.28 ng/mL for 13-cis retinoic acid, respectively. The Cmax varied across different age groups (children, adolescents, and adults).
The corresponding ranges for the mean AUC0-24 were 0.63-2.06, 2.39-2.89, and 0.96-1.99 ng\*h/mL.
[L34869]
Following oral administration, the absolute bioavailability of tretinoin was approximately 50%.
[L45349]
While the effect of food on tretinoin is unclear, food increases the oral absorption of retinoids, as a class.
[L45349][L13083]
When the oral dose of 22.5 mg/m2 tretinoin was administered twice daily, the mean ± SD Cmax was 394 ± 89 ng/mL after the first dose and 138 ± 139 ng/mL after one week of continuous treatment. The area under the curve (AUC) was 537 ± 191 ng·h/mL after the first dose and 249 ± 185 ng·h/mL after one week of continuous treatment. The Tmax was between one and two hours.
[L45349]
[L45349]
[A257689][L45349]
Plasma protein binding remains constant over the 10 to 500 ng/mL concentration range.
[L45349]
[A257689]
[A257689]
Tretinoin is metabolized by several CYP enzymes, including CYP3A4, CYP2C8, and CYP2E. It also undergoes glucuronidation by UGT2B7.
The metabolites 4-oxo retinoic acid and 4-oxo trans retinoic acid glucuronide have one-third of the pharmacological activity of the parent compound.
[A14890][L45349]
When the plasma concentrations decreased to one-third of their day-one concentrations after one week of continuous therapy, tretinoin induced its own metabolism.
[A257689][L45349]
[L13083]
Following administration of radiolabeled tretinoin at doses of 2.75 mg and 50 mg - which are 0.53 to 9.6 times the approved recommended dosage based on 1.7 m2, respectively - approximately 63% of the radioactivity was recovered in the urine within 72 hours, and 31% appeared in the feces within six days.
[L45349]
Proteins and enzymes this drug interacts with in the body
PMID:16417524 PMID:19850744 PMID:20215566 PMID:21152046 PMID:37478846
Retinoic acid receptors bind as heterodimers to their target response elements in response to their ligands, all-trans or 9-cis retinoic acid, and regulate gene expression in various biological processes .
PMID:21152046 PMID:28167758 PMID:37478846
The RXR/RAR heterodimers bind to the retinoic acid response elements (RARE) composed of tandem 5'-AGGTCA-3' sites known as DR1-DR5 .
PMID:19398580 PMID:28167758
In the absence of ligand, the RXR-RAR heterodimers associate with a multiprotein complex containing transcription corepressors that induce histone deacetylation, chromatin condensation and transcriptional suppression .
PMID:16417524
On ligand binding, the corepressors dissociate from the receptors and associate with the coactivators leading to transcriptional activation .
PMID:19850744 PMID:20215566 PMID:37478846 PMID:9267036
Formation of a complex with histone deacetylases might lead to inhibition of RARE DNA element binding and to transcriptional repression .
PMID:28167758
Transcriptional activation and RARE DNA element binding might be supported by the transcription factor KLF2 .
PMID:28167758
RARA plays an essential role in the regulation of retinoic acid-induced germ cell development during spermatogenesis (By similarity). Has a role in the survival of early spermatocytes at the beginning prophase of meiosis (By similarity). In Sertoli cells, may promote the survival and development of early meiotic prophase spermatocytes (By similarity).
In concert with RARG, required for skeletal growth, matrix homeostasis and growth plate function (By similarity). Together with RXRA, positively regulates microRNA-10a expression, thereby inhibiting the GATA6/VCAM1 signaling response to pulsatile shear stress in vascular endothelial cells .
PMID:28167758
In association with HDAC3, HDAC5 and HDAC7 corepressors, plays a role in the repression of microRNA-10a and thereby promotes the inflammatory response PMID:28167758
In the absence or presence of hormone ligand, acts mainly as an activator of gene expression due to weak binding to corepressors .
PMID:12554770
The RXRA/RARB heterodimer can act as a repressor on the DR1 element and as an activator on the DR5 element .
PMID:29021580
In concert with RARG, required for skeletal growth, matrix homeostasis and growth plate function (By similarity)
In the absence of ligand, acts mainly as an activator of gene expression due to weak binding to corepressors. Required for limb bud development. In concert with RARA or RARB, required for skeletal growth, matrix homeostasis and growth plate function (By similarity)
The high affinity ligand for RXRs is 9-cis retinoic acid (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Involved compounds
Involved compounds
ATC L01XF01
ATC D10AD51
ATC D10AD01
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)
Tretinoin
Additional database identifiers
Drugs Product Database (DPD)
5054
ChemSpider
392618
BindingDB
323588
PDB
REA
ZINC
ZINC000012358651
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9864
GenAtlas
RARA
GeneCards
RARA
GenBank Gene Database
X06614
GenBank Protein Database
36157
Guide to Pharmacology
590
UniProt Accession
RARA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9865
GenAtlas
RARB
GeneCards
RARB
GenBank Gene Database
X07282
GenBank Protein Database
35883
Guide to Pharmacology
591
UniProt Accession
RARB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9866
GenAtlas
RARG
GeneCards
RARG
GenBank Gene Database
M24857
GenBank Protein Database
306887
Guide to Pharmacology
592
UniProt Accession
RARG_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10478
GenAtlas
RXRB
GeneCards
RXRB
GenBank Gene Database
X63522
GenBank Protein Database
30448
Guide to Pharmacology
611
UniProt Accession
RXRB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10479
GenAtlas
RXRG
GeneCards
RXRG
GenBank Gene Database
U38480
GenBank Protein Database
1053069
Guide to Pharmacology
612
UniProt Accession
RXRG_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10477
GenAtlas
RXRA
GeneCards
RXRA
GenBank Gene Database
X52773
GenBank Protein Database
35885
Guide to Pharmacology
610
UniProt Accession
RXRA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2338
GenAtlas
CRABP1
GeneCards
CRABP1
GenBank Gene Database
S74445
GenBank Protein Database
241542
UniProt Accession
RABP1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9867
GenAtlas
RARRES1
GeneCards
RARRES1
GenBank Gene Database
U27185
GenBank Protein Database
942585
UniProt Accession
TIG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:402
GenAtlas
ALDH1A1
GeneCards
ALDH1A1
GenBank Gene Database
M31994
GenBank Protein Database
178372
UniProt Accession
AL1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15472
GenAtlas
ALDH1A2
GeneCards
ALDH1A2
GenBank Gene Database
AB015226
GenBank Protein Database
3970842
UniProt Accession
AL1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9836
GenAtlas
GPRC5A
GeneCards
GPRC5A
GenBank Gene Database
AF095448
GenBank Protein Database
4063890
UniProt Accession
RAI3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6525
GeneCards
LCN1
UniProt Accession
LCN1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:23380
GeneCards
OBP2A
UniProt Accession
OBP2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9922
GenAtlas
RBP4
GeneCards
RBP4
GenBank Gene Database
X00129
GenBank Protein Database
35897
Guide to Pharmacology
2549
UniProt Accession
RET4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8812
GeneCards
PDK4
GenBank Gene Database
U54617
GenBank Protein Database
1399197
Guide to Pharmacology
2144
UniProt Accession
PDK4_HUMAN
GenBank Gene Database
Z21818
UniProt Accession
Q14081_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: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:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_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:2610
GenAtlas
CYP2A6
GeneCards
CYP2A6
GenBank Gene Database
X13897
Guide to Pharmacology
1321
UniProt Accession
CP2A6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2620
GeneCards
CYP2C18
GenBank Gene Database
M61853
Guide to Pharmacology
1327
UniProt Accession
CP2CI_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:2642
GenAtlas
CYP4A11
GeneCards
CYP4A11
GenBank Gene Database
L04751
GenBank Protein Database
181397
Guide to Pharmacology
1341
UniProt Accession
CP4AB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12554
GeneCards
UGT2B7
GenBank Gene Database
J05428
GenBank Protein Database
340080
UniProt Accession
UD2B7_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:2603
GenAtlas
CYP26A1
GeneCards
CYP26A1
GenBank Gene Database
AF005418
Guide to Pharmacology
1366
UniProt Accession
CP26A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2338
GenAtlas
CRABP1
GeneCards
CRABP1
GenBank Gene Database
S74445
GenBank Protein Database
241542
UniProt Accession
RABP1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2339
GenAtlas
CRABP2
GeneCards
CRABP2
GenBank Gene Database
M68867
GenBank Protein Database
181026
UniProt Accession
RABP2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72