Delgocitinib 20mg/g cream
Requires a prescription from a doctor or prescriber
Delgocitinib is a pan-Janus kinase (JAK) inhibitor.
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Anzupgo 20mg/g cream
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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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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: 7 · 2019–2026
Showing the 50 most relevant studies, sorted by most relevant.
Sandesh Raja, Adarsh Raja, Muhammad Hamza Shuja, et al.
Archives of Dermatological Research, 2024
de Moraes-Souza R, Bornia MJP, Chater RC, et al.
2026
- Eczema
- Hand Dermatoses
- Heterocyclic Compounds, 3-Ring
Chronic hand eczema (CHE) is associated with substantial functional impairment and reduced quality of life. Delgocitinib, a pan-Janus kinase (JAK) inhibitor, has emerged as a promising topical treatment for CHE. A systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to assess the efficacy and safety of topical delgocitinib 20-30 mg/g compared with vehicle in patients with CHE. PubMed, Embase, Cochrane Library, ClinicalTrials.gov, EU CTR, and WHO ICTRP were searched up to 15 February 2026. The primary outcome was treatment success at week 16, defined as clear or almost clear skin with a ≥ 2-point improvement on the Investigator's or Physician's Global Assessment (IGA/PGA). Secondary outcomes included treatment success at weeks 4 and 8, changes in Hand Eczema Symptom Diary (HESD) itch and pain scores, and safety outcomes. Relative risks (RRs) and mean differences (MDs) with 95% confidence intervals (CIs) were calculated using random-effects models. Three publications reporting four RCTs involving 1154 patients were included, with 752 receiving delgocitinib and 402 receiving vehicle. At week 16, treatment success was significantly higher with delgocitinib (RR 3.17; 95% CI 1.78-5.65; p < 0.01), corresponding to an absolute risk difference of 16.9% and a number needed to treat (NNT) of 6 (95% CI 3-16). Similar results at weeks 4 and 8. Delgocitinib also led to significantly greater improvements in HESD itch and pain scores. No significant differences were found in overall adverse events (AEs), treatment-related AEs, or serious AEs. Discontinuation due to AEs was lower in the delgocitinib group. Delgocitinib 20-30 mg/g demonstrated greater efficacy than vehicle and a favourable safety profile, supporting its use as a topical treatment for CHE.
Abstract licence: CC BY-NC-ND 4.0
Chia Siang Kow, Syed Shahzad Hasan, Kaeshaelya Thiruchelvam
Proceedings of Singapore Healthcare, 2025
Background: Chronic hand eczema (CHE) is a persistent inflammatory skin condition that is often difficult to manage and associated with substantial functional impairment and reduced quality of life. Delgocitinib, a topical pan-Janus kinase inhibitor, has emerged as a potential nonsteroidal therapeutic option for CHE. Purpose: The purpose of this study was to evaluate the efficacy and safety of delgocitinib in adult patients with chronic hand eczema using evidence from randomized controlled trials. Research Design: This study was conducted as a systematic review and meta-analysis of randomized controlled trials. Study Sample: The study sample comprised individual randomized controlled trials that enrolled adult patients diagnosed with chronic hand eczema and compared topical delgocitinib with vehicle control. Data Collection and/or Analysis: A comprehensive literature search was performed to identify eligible randomized controlled trials. Data on treatment efficacy and adverse events were extracted and pooled using random-effects meta-analysis, with results expressed as odds ratios and 95% confidence intervals. Results: Pooled analysis demonstrated that delgocitinib significantly improved treatment outcomes compared with vehicle controls. The odds ratio for treatment success at week 8 was 3.53 (95% CI: 2.28–5.45), and at week 16 was 3.56 (95% CI: 1.93–6.57), indicating sustained efficacy over time. There was no significant increase in adverse events associated with delgocitinib use, with an odds ratio of 1.03 (95% CI: 0.79–1.60). Conclusions: Delgocitinib demonstrates significant and sustained efficacy in improving clinical outcomes in adult patients with chronic hand eczema, without an associated increase in adverse event risk. These findings support delgocitinib as an effective and well-tolerated nonsteroidal treatment option for chronic hand eczema.
Abstract licence: CC BY-NC 4.0
Shanshal M, Uthayakumar A
2026
BackgroundThe lichen planus spectrum includes cutaneous, scalp, pigmentary, and nail phenotypes. Topical Janus kinase inhibitors offer targeted treatment with limited systemic exposure.ObjectiveTo map and critically appraise clinical, safety, and molecular evidence for topical Janus kinase inhibitors across lichen planus phenotypes.MethodsWe performed a PRISMA-guided systematic review (PROSPERO CRD420251155683) searching MEDLINE, Embase, Scopus, trial registries, and other sources to 1 November 2025. Human studies of topical JAK inhibitors for cutaneous lichen planus (LP), lichen planopilaris, frontal fibrosing alopecia (FFA), lichen planus pigmentosus (LPPig), or nail lichen planus were included. Risk of bias was assessed, certainty of evidence was graded, and findings were synthesized narratively.ResultsThirteen studies (n = 118 patients) and one registry trial were included. In FFA, a phase 2 double-blind, vehicle-controlled trial of delgocitinib 2% cream in 30 patients met its molecular primary endpoint and showed greater clinical improvements than vehicle over 12 weeks. Two cohorts reported improvement with topical tofacitinib 2% and topical ruxolitinib 1.5% in scarring alopecia. In cutaneous LP (n = 12), an open-label study showed improvement in lesion severity and symptoms with topical ruxolitinib. Evidence for LPPig and nail LP was limited to case reports. Topical JAK inhibitors were well tolerated with infrequent local irritation and no serious adverse events.ConclusionsTopical Janus kinase inhibitors appear promising, well tolerated, and potentially steroid-sparing, particularly in lichen planopilaris and FFA. However, the evidence remains limited, and well-designed vehicle-controlled trials are needed before routine use can be justified.
Abstract licence: CC BY
R. de Moraes-Souza, Rubiana Sarto, Yasmin Luz Lima de Mesquita, et al.
Journal of the American Academy of Dermatology, 2025
Abdelaziz A. Awad, B. El-Khalifa, Esraa Awad, et al.
Archives of Dermatological Research, 2026
Padro Nina, Rachael Gigliotti, Suzanne Rose, et al.
2025
Gupta AK, Bamimore MA, Talukder M
2025
- Eczema
- Hand Dermatoses
- Dermatologic Agents
IntroductionChronic hand eczema (CHE) is a highly prevalent dermatology-related occupational hazard. This condition, which is a distinct diagnosis from atopic dermatitis (AD), can be quite symptomatic with implications for one's personal and professional life. Many therapeutic interventions exist for CHE, and the current study determined-through network meta-analyses (NMAs)-the relative efficacy of the newer treatments for CHE.MethodsData for eligible studies were identified after systematically reviewing the literature in PubMed and Scopus. Eligible studies were those that had an arm investigating the impact of monotherapy on 12- or 16-week changes in Hand Eczema Severity Index (HECSI) scores. We conducted sensitivity analyses where network meta-regressions were performed to (ecologically) adjust for variation due to age and sex. Base and sensitivity analyses were adjusted for disease severity at baseline.ResultsWe identified 5 eligible studies-across which there were 10 active comparators. Among the active comparators were two treatments approved by the Food and Drug Administration (FDA) and European Medicines Agency (EMA) for the treatment of CHE, namely, alitretinoin 30 mg once daily (oral) and delgocitinib 20 mg/g twice daily (topical). We estimated pairwise relative effects using the mean difference (i.e., mean reduction) in the respective HECSI scores; furthermore, efficacy was ranked with Surface Under the Cumulative Ranking Curve (SUCRA) values.ConclusionsWe attempted to contribute to the existing CHE literature by producing comparative information on its treatments' relative efficacy; moreover, we found no published NMA study on available treatments for CHE before the conduct of our work. Our results can guide clinical decision-making.
Abstract licence: CC BY
Ryan Pulleyblank, R. Eyben, Daniela Goncalvez-Bradley, et al.
Value in Health, 2025
Margitta Worm, Jacob P. Thyssen, Sibylle Schliemann, et al.
British Journal of Dermatology, 2022
- Janus Kinase Inhibitors
- Dermatitis, Atopic
- Eczema
Background Chronic hand eczema (CHE) is a burdensome disease, and new well-documented, safe and efficacious treatments are warranted. In a recent CHE phase IIa trial, the pan-Janus kinase (JAK) inhibitor delgocitinib in an ointment formulation was found to be efficacious and well tolerated. Objectives This trial assessed the dose response, efficacy and safety of delgocitinib cream in CHE. Methods In this double-blind, phase IIb dose-ranging trial, adults with CHE and a recent history of inadequate response or contraindication to topical corticosteroids were randomized to delgocitinib cream 1, 3, 8, 20 mg g–1 or vehicle treatment twice daily for 16 weeks. The primary endpoint was the Investigator’s Global Assessment for CHE (IGA-CHE) treatment success [0 (clear) or 1 (almost clear) with a ≥ two-point improvement from baseline to week 16]. Secondary endpoints were the time to IGA-CHE treatment success and changes in Hand Eczema Severity Index (HECSI); other endpoints were itch and pain numerical rating scale (NRS) scores, and Patient’s Global Assessment (PaGA) at week 16. Results Patients (n = 258) were randomized 1 : 1 : 1 : 1 : 1 to delgocitinib cream 1, 3, 8, 20 mg g–1 or vehicle. A significant dose–response relationship was established for IGA-CHE (P < 0.025). IGA-CHE treatment success at week 16 was achieved in 21.2% (1 mg g–1), 7.8% (3 mg g–1), 36.5% (8 mg g–1), 37.7% (20 mg g–1) and 8.0% (vehicle) of patients. Delgocitinib 8 and 20 mg g–1 showed a treatment effect against vehicle (P < 0.001). Similarly, there were improvements in HECSI, itch and pain NRS scores, and PaGA. Delgocitinib cream was well tolerated with the majority of adverse events being mild or moderate and considered unrelated to treatment. The most frequently reported adverse events were nasopharyngitis (17.3–29.4% in delgocitinib groups vs. 40% in vehicle group), eczema (5.8–11.3% in delgocitinib groups vs. 16.0% in vehicle group) and headache (3.8–11.5% in delgocitinib groups vs. 4.0% in vehicle group). Conclusions In this trial, delgocitinib cream showed a dose–response relationship in terms of efficacy and was well tolerated.
Abstract licence: CC BY-NC 4.0
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
20.3 hours
Mechanism
Delgocitinib is a pan Janus kinase (JAK) inhibitor that targets the activity of…
Food interactions
None known
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
22 to 69 years
Half-life
20.3 hours
[L51589]
Protein binding
22 to 29%
[L51589]
Metabolism
[L51589]
Elimination
70-80%
[L51589]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L51589][L53503]
[L51589]
There is no information regarding the LD50 of delgocitinib.
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L51589]
The geometric mean (GSD) maximum plasma concentration (Cmax) and area under the concentrationcurve from time 0 to 12 hours (AUC0-12) on Day 8 was 0.46 ng/mL (1.74) and 3.7 ng x h/mL (1.74), respectively. Steady state was reached by Day 8.
The systemic exposure (AUC and Cmax) between Day 1 and Day 8 were similar. Following twice daily application of delgocitinib 20 mg/g cream in DELTA 2, the geometric mean plasma concentration observed 2-6 hours after application at Day 113 was 48% lower than that at Day 8 (0.11 ng/mL and 0.21 ng/mL, respectively). The relative bioavailability of delgocitinib following topical application is approximately 0.6% compared to administration via oral tablets.
[L51589]
[L51589]
[L51589]
[L51589]
[L51589]
Proteins and enzymes this drug interacts with in the body
PMID:16239216 PMID:28111307 PMID:32750333 PMID:7615558 PMID:8232552
Kinase partner for the interleukin (IL)-2 receptor PMID:11909529 as well as interleukin (IL)-10 receptor .
PMID:12133952
Kinase partner for the type I interferon receptor IFNAR2 .
PMID:16239216 PMID:28111307 PMID:32750333 PMID:7615558 PMID:8232552
In response to interferon-binding to IFNAR1-IFNAR2 heterodimer, phosphorylates and activates its binding partner IFNAR2, creating docking sites for STAT proteins .
PMID:7759950
Directly phosphorylates STAT proteins but also activates STAT signaling through the transactivation of other JAK kinases associated with signaling receptors PMID:16239216 PMID:32750333 PMID:8232552
PMID:15690087 PMID:7615558 PMID:9657743 PMID:15899890
Following ligand-binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins .
PMID:15690087 PMID:9618263
Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor.
Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription. For example, cell stimulation with erythropoietin (EPO) during erythropoiesis leads to JAK2 autophosphorylation, activation, and its association with erythropoietin receptor (EPOR) that becomes phosphorylated in its cytoplasmic domain .
PMID:9657743
Then, STAT5 (STAT5A or STAT5B) is recruited, phosphorylated and activated by JAK2. Once activated, dimerized STAT5 translocates into the nucleus and promotes the transcription of several essential genes involved in the modulation of erythropoiesis.
Part of a signaling cascade that is activated by increased cellular retinol and that leads to the activation of STAT5 (STAT5A or STAT5B) .
PMID:21368206
In addition, JAK2 mediates angiotensin-2-induced ARHGEF1 phosphorylation .
PMID:20098430
Plays a role in cell cycle by phosphorylating CDKN1B .
PMID:21423214
Cooperates with TEC through reciprocal phosphorylation to mediate cytokine-driven activation of FOS transcription. In the nucleus, plays a key role in chromatin by specifically mediating phosphorylation of 'Tyr-41' of histone H3 (H3Y41ph), a specific tag that promotes exclusion of CBX5 (HP1 alpha) from chromatin .
PMID:19783980
Up-regulates the potassium voltage-gated channel activity of KCNA3 PMID:25644777
Following ligand binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins. Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor. Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription.
For example, upon IL2R activation by IL2, JAK1 and JAK3 molecules bind to IL2R beta (IL2RB) and gamma chain (IL2RG) subunits inducing the tyrosine phosphorylation of both receptor subunits on their cytoplasmic domain. Then, STAT5A and STAT5B are recruited, phosphorylated and activated by JAK1 and JAK3. Once activated, dimerized STAT5 translocates to the nucleus and promotes the transcription of specific target genes in a cytokine-specific fashion
PMID:10542297 PMID:10995743 PMID:7657660 PMID:7813427 PMID:8232552
Plays both structural and catalytic roles in numerous interleukins and interferons (IFN-alpha/beta) signaling .
PMID:10542297
Associates with heterodimeric cytokine receptor complexes and activates STAT family members including STAT1, STAT3, STAT4 or STAT6 .
PMID:10542297 PMID:7638186
The heterodimeric cytokine receptor complexes are composed of (1) a TYK2-associated receptor chain (IFNAR1, IL12RB1, IL10RB or IL13RA1), and (2) a second receptor chain associated either with JAK1 or JAK2 .
PMID:10542297 PMID:25762719 PMID:7526154 PMID:7813427
In response to cytokine-binding to receptors, phosphorylates and activates receptors (IFNAR1, IL12RB1, IL10RB or IL13RA1), creating docking sites for STAT members .
PMID:7526154 PMID:7657660
In turn, recruited STATs are phosphorylated by TYK2 (or JAK1/JAK2 on the second receptor chain), form homo- and heterodimers, translocate to the nucleus, and regulate cytokine/growth factor responsive genes .
PMID:10542297 PMID:25762719 PMID:7657660
Negatively regulates STAT3 activity by promototing phosphorylation at a specific tyrosine that differs from the site used for signaling PMID:29162862
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
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:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
ATC D11AH11
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)
Delgocitinib
Additional database identifiers
ChemSpider
59718502
PDB
FHX
ZINC
ZINC000117625213
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6190
GeneCards
JAK1
Guide to Pharmacology
2047
UniProt Accession
JAK1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6192
GenAtlas
JAK2
GeneCards
JAK2
GenBank Gene Database
AF058925
Guide to Pharmacology
2048
UniProt Accession
JAK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6193
GenAtlas
JAK3
GeneCards
JAK3
GenBank Gene Database
U57096
Guide to Pharmacology
2049
UniProt Accession
JAK3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12440
GeneCards
TYK2
GenBank Gene Database
X54637
GenBank Protein Database
37504
Guide to Pharmacology
2269
UniProt Accession
TYK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_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:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
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