Abrocitinib 50mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
50mg
Oral
Abrocitinib is an oral small-molecule inhibitor of Janus kinase 1 (JAK1).
Active ingredients:
Abrocitinib
No active safety alerts
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Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
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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.
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Abrocitinib 100mg tablets
Tablet
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Abrocitinib 200mg tablets
Tablet
200mg
Same therapeutic group
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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Clinical guidelines and formulary information
British National Formulary
Abrocitinib
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(3)
Abrocitinib, tralokinumab or upadacitinib for treating moderate to severe atopic dermatitis (TA814)
TA814
Technology appraisal
Updated Aug 2022Lebrikizumab for treating moderate to severe atopic dermatitis in people 12 years and over (TA986)
TA986
Technology appraisal
Updated Jul 2024Nemolizumab for treating moderate to severe atopic dermatitis in people 12 years and over (TA1077)
TA1077
Technology appraisal
Updated Jul 2025Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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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 codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
Not available
Mechanism
Janus kinases (JAKs) are a family consisting of four receptor-associated kinases…
Food interactions
1 warning
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
91%
Abrocitinib is absorbed with over 91% extent of oral absorption and absolute oral bioavailability of approximately 60%.…
Half-life
The mean elimination half-lives of abrocitinib and its two active metabolites, M1 and M2, range from three to five hours.
[L39769]
[L39769]
Protein binding
64%
Approximately 64%, 37% and 29% of circulating abrocitinib and its active metabolites M1 and M2, respectively, are bound to plasma proteins.…
Volume of distribution
100 L
After intravenous administration, the volume of distribution of abrocitinib was approximately 100 L.
[L39769]
[L39769]
Metabolism
53%
Abrocitinib undergoes CYP-mediated oxidative metabolism. CYP2C19 is the predominant enzyme, accounting for about 53% of drug metabolism.…
Elimination
1%
Abrocitinib is eliminated primarily by metabolic clearance mechanisms, with less than 1% of the dose being excreted in urine as an unchanged parent drug.…
Clearance
There is no information available.
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Abrocitinib is an oral small-molecule inhibitor of Janus kinase 1 (JAK1). Janus kinases are intracellular enzymes involved in transduction pathways that regulate hematopoiesis and immune cell function.[L39774] The Janus kinase (JAK)–signal transducer and activator of transcription (STAT) signalling pathway plays a central role in the pathogenesis of a variety of autoimmune and inflammatory diseases, including atopic dermatitis, a chronic inflammatory skin disease with complex pathogenesis. Atopic dermatitis is characterized by epidermal hyperplasia, skin barrier dysfunction, and the aberrant activation of immune cells. Patients with moderate-to-severe atopic dermatitis report reduced quality of life and often face limited treatment options. JAK inhibitors recently attracted more attention as potential treatments for inflammatory disorders, as JAK inhibition is associated with rapid and sustained anti-inflammatory efects.[A244549]
Abrocitinib was approved by the European Commission on December 10, 2021, for the treatment of moderate-to-severe atopic dermatitis (AD) in adults who are candidates for systemic therapy.[L39784] On January 14, 2022, the FDA approved abrocitinib for the treatment of refractory, moderate-to-severe AD in adults whose disease is not adequately controlled with other systemic drug products, including biologics, or when the use of those therapies is inadvisable.[L39779] Health Canada also approved the use of abrocitinib in pediatric patients 12 years and older.[L42395]
Abrocitinib was approved by the European Commission on December 10, 2021, for the treatment of moderate-to-severe atopic dermatitis (AD) in adults who are candidates for systemic therapy.[L39784] On January 14, 2022, the FDA approved abrocitinib for the treatment of refractory, moderate-to-severe AD in adults whose disease is not adequately controlled with other systemic drug products, including biologics, or when the use of those therapies is inadvisable.[L39779] Health Canada also approved the use of abrocitinib in pediatric patients 12 years and older.[L42395]
Properties:
solid
Avg. mass: 323.42 Da
DrugBank indication
Abrocitinib is indicated for the treatment of moderate-to-severe atopic dermatitis in adults who are candidates for systemic therapy.
[L39774]
In the US, it is indicated to treat refractory, moderate-to-severe atopic dermatitis whose disease is not adequately controlled with other systemic drug products, including biologics, or when the use of those therapies is inadvisable.
[L39769]
Abrocitinib is not recommended for use in combination with other JAK inhibitors, biologic immunomodulators, or other immunosuppressants.
[L39769]
[L39774]
In the US, it is indicated to treat refractory, moderate-to-severe atopic dermatitis whose disease is not adequately controlled with other systemic drug products, including biologics, or when the use of those therapies is inadvisable.
[L39769]
Abrocitinib is not recommended for use in combination with other JAK inhibitors, biologic immunomodulators, or other immunosuppressants.
[L39769]
Also known as(70)
Abrocitinib
PF-04965842
2.7.10.2
JAK-3
Janus kinase 3
L-JAK
Leukocyte janus kinase
2.7.10.2
Dosage forms(12)
Tablet (Oral) — 100 mg
Tablet (Oral) — 200 mg
Tablet (Oral) — 50 mg
Tablet, film coated (Oral) — 100 mg/1
Tablet, film coated (Oral) — 100 mg
Tablet, film coated (Oral) — 200 mg
Tablet, film coated (Oral) — 200 mg/1
Tablet, film coated (Oral) — 50 mg/1
Molecular properties(19)
Drug interactions(568)
Known interactions with other medications. Always consult a healthcare professional.
The serum concentration of Afatinib can be increased when it is combined with Abrocitinib.
The serum concentration of Bosutinib can be increased when it is combined with Abrocitinib.
Brentuximab vedotin
Unknown severity
The serum concentration of Brentuximab vedotin can be increased when it is combined with Abrocitinib.
Colchicine
Unknown severity
The serum concentration of Colchicine can be increased when it is combined with Abrocitinib.
The serum concentration of Edoxaban can be increased when it is combined with Abrocitinib.
Ledipasvir
Unknown severity
The serum concentration of Ledipasvir can be increased when it is combined with Abrocitinib.
The serum concentration of Naloxegol can be increased when it is combined with Abrocitinib.
The serum concentration of Pazopanib can be increased when it is combined with Abrocitinib.
Prucalopride
Unknown severity
The serum concentration of Prucalopride can be increased when it is combined with Abrocitinib.
Ranolazine
Unknown severity
The serum concentration of Ranolazine can be increased when it is combined with Abrocitinib.
The excretion of Silodosin can be decreased when combined with Abrocitinib.
The serum concentration of Topotecan can be increased when it is combined with Abrocitinib.
Dabrafenib
Moderate
The metabolism of Abrocitinib can be increased when combined with Dabrafenib.
Everolimus
Unknown severity
The serum concentration of Everolimus can be increased when it is combined with Abrocitinib.
The serum concentration of Rifaximin can be increased when it is combined with Abrocitinib.
Luliconazole
Unknown severity
The serum concentration of Abrocitinib can be increased when it is combined with Luliconazole.
Vincristine
Unknown severity
The serum concentration of Vincristine can be increased when it is combined with Abrocitinib.
Doxorubicin
Unknown severity
The serum concentration of Doxorubicin can be increased when it is combined with Abrocitinib.
Lumacaftor
Unknown severity
The serum concentration of Abrocitinib can be decreased when it is combined with Lumacaftor.
Fluvoxamine
Moderate
The metabolism of Abrocitinib can be decreased when combined with Fluvoxamine.
Ticlopidine
Unknown severity
The risk or severity of bleeding and thrombocytopenia can be increased when Ticlopidine is combined with Abrocitinib.
Chloramphenicol
Moderate
The metabolism of Abrocitinib can be decreased when combined with Chloramphenicol.
Lansoprazole
Moderate
The metabolism of Abrocitinib can be decreased when combined with Lansoprazole.
Imipramine
Moderate
The metabolism of Abrocitinib can be decreased when combined with Imipramine.
Fluoxetine
Moderate
The metabolism of Abrocitinib can be decreased when combined with Fluoxetine.
Zafirlukast
Moderate
The metabolism of Abrocitinib can be decreased when combined with Zafirlukast.
Delavirdine
Moderate
The metabolism of Abrocitinib can be decreased when combined with Delavirdine.
The metabolism of Abrocitinib can be decreased when combined with Isoniazid.
Miconazole
Moderate
The metabolism of Abrocitinib can be decreased when combined with Miconazole.
Gemfibrozil
Moderate
The metabolism of Abrocitinib can be decreased when combined with Gemfibrozil.
Clomipramine
Moderate
The metabolism of Abrocitinib can be decreased when combined with Clomipramine.
Stiripentol
Moderate
The metabolism of Abrocitinib can be decreased when combined with Stiripentol.
The metabolism of Abrocitinib can be decreased when combined with Efavirenz.
Sertraline
Moderate
The metabolism of Abrocitinib can be decreased when combined with Sertraline.
Armodafinil
Moderate
The metabolism of Abrocitinib can be decreased when combined with Armodafinil.
Eslicarbazepine acetate
Moderate
The metabolism of Abrocitinib can be decreased when combined with Eslicarbazepine acetate.
Troglitazone
Moderate
The metabolism of Abrocitinib can be decreased when combined with Troglitazone.
Valproic acid
Moderate
The metabolism of Abrocitinib can be decreased when combined with Valproic acid.
The metabolism of Abrocitinib can be decreased when combined with Nabilone.
The metabolism of Abrocitinib can be decreased when combined with Imatinib.
Mifepristone
Moderate
The metabolism of Abrocitinib can be decreased when combined with Mifepristone.
The serum concentration of Quinidine can be increased when it is combined with Abrocitinib.
The metabolism of Abrocitinib can be decreased when combined with Felbamate.
Amiodarone
Moderate
The metabolism of Abrocitinib can be decreased when combined with Amiodarone.
Sulfinpyrazone
Unknown severity
The risk or severity of bleeding and thrombocytopenia can be increased when Sulfinpyrazone is combined with Abrocitinib.
Iproniazid
Moderate
The metabolism of Abrocitinib can be decreased when combined with Iproniazid.
Medical Cannabis
Moderate
The metabolism of Abrocitinib can be decreased when combined with Medical Cannabis.
Fluconazole
Moderate
The metabolism of Abrocitinib can be decreased when combined with Fluconazole.
Floxuridine
Moderate
The metabolism of Abrocitinib can be decreased when combined with Floxuridine.
Nicardipine
Moderate
The metabolism of Abrocitinib can be decreased when combined with Nicardipine.
Showing 50 of 568 interactions
Food & lifestyle interactions
Advice
Take at the same time every day. Administer with or without food, as it has no clinically relevant effect on abrocitinib exposures.
Toxicity & overdose
There is no experience regarding human overdosage with abrocitinib.
[L39769]
In clinical trials, there were no specific toxicities observed when abrocitinib was administered in single oral doses of 800 mg and 400 mg daily for 28 days. An overdose should be responded with symptomatic and supportive treatment, as there is no specific antidote for overdose with abrocitinib.
[L39774]
[L39769]
In clinical trials, there were no specific toxicities observed when abrocitinib was administered in single oral doses of 800 mg and 400 mg daily for 28 days. An overdose should be responded with symptomatic and supportive treatment, as there is no specific antidote for overdose with abrocitinib.
[L39774]
How it works
Mechanism of action
Janus kinases (JAKs) are a family consisting of four receptor-associated kinases - JAK1, JAK2, JAK3, and tyrosine kinase 2 (TYK2). Upon ligand binding and subsequent dimerization of cytokine and hormone receptors, receptor-associated JAKs are activated and phosphorylated. This allows the binding of Signal Transducers and Activators of Transcription (STATs), which are transcription factors. STAT binds to the receptor, and JAK phosphorylates and activates STAT to create a STAT dimer. The STAT dimer translocates to the nucleus to upregulate the gene transcription of pro-inflammatory cytokines and growth factors implicated in atopic dermatitis.[A183188][A244549] Blocking the JAK-STAT pathway is advantageous, as it is an intracellular signalling pathway where many pro-inflammatory pathways converge.[A244554]
Each JAK plays a role in the signalling and regulation of different cytokines and immune cells. In atopic dermatitis, JAK1 is the therapeutic target of focus as it is involved in the signalling of the γc family of cytokines involved in immune responses and disease pathophysiology, including IL-2, IL-4, IL-7, IL-9, and IL-15.[A244549] Abrocitinib reversibly inhibits JAK1 by blocking the adenosine triphosphate (ATP) binding site. Biochemical assays demonstrate that abrocitinib is selective for JAK1 over JAK2 (28-fold), JAK3 (>340-fold), and tyrosine kinase (TYK) 2 (43-fold), as well as the broader kinome.[L39769] Similarly, in cellular settings, abrocitinib preferentially inhibited cytokine-induced STAT phosphorylation by signalling pairs involving JAK1, while sparing signalling by JAK2/JAK2, or JAK2/TYK2 pairs.[L39774] The relevance of inhibition of specific JAK enzymes to the drug's therapeutic effectiveness is currently unknown.[L39769]
Each JAK plays a role in the signalling and regulation of different cytokines and immune cells. In atopic dermatitis, JAK1 is the therapeutic target of focus as it is involved in the signalling of the γc family of cytokines involved in immune responses and disease pathophysiology, including IL-2, IL-4, IL-7, IL-9, and IL-15.[A244549] Abrocitinib reversibly inhibits JAK1 by blocking the adenosine triphosphate (ATP) binding site. Biochemical assays demonstrate that abrocitinib is selective for JAK1 over JAK2 (28-fold), JAK3 (>340-fold), and tyrosine kinase (TYK) 2 (43-fold), as well as the broader kinome.[L39769] Similarly, in cellular settings, abrocitinib preferentially inhibited cytokine-induced STAT phosphorylation by signalling pairs involving JAK1, while sparing signalling by JAK2/JAK2, or JAK2/TYK2 pairs.[L39774] The relevance of inhibition of specific JAK enzymes to the drug's therapeutic effectiveness is currently unknown.[L39769]
Pharmacodynamics
Abrocitinib mediates anti-inflammatory effects by blocking the signalling of pro-inflammatory cytokines implicated in atopic dermatitis.[A244554] It dose-dependently reduces the serum markers of inflammation in atopic dermatitis, including high sensitivity C-reactive protein (hsCRP), interleukin-31 (IL-31), and thymus and activation regulated chemokine (TARC). These changes returned to near baseline within four weeks following drug discontinuation.[L39769] At two weeks of treatment, the mean absolute lymphocyte count increased, which returned to baseline by nine months of treatment. Treatment with abrocitinib was associated with a dose-related increase in B cell counts and a dose-related decrease in NK cell counts: the clinical significance of these changes is unknown.[L39774]
Treatment with 200 mg abrocitinib once-daily was associated with a transient, dose-dependent decrease in platelet count with the nadir occurring at a median of 24 days. Recovery of platelet count (~40% recovery by 12 weeks) occurred without discontinuation of the treatment.[L39769]
Treatment with 200 mg abrocitinib once-daily was associated with a transient, dose-dependent decrease in platelet count with the nadir occurring at a median of 24 days. Recovery of platelet count (~40% recovery by 12 weeks) occurred without discontinuation of the treatment.[L39769]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Abrocitinib is absorbed with over 91% extent of oral absorption and absolute oral bioavailability of approximately 60%. The peak plasma concentrations of abrocitinib are reached within one hour. Steady-state plasma concentrations of abrocitinib are achieved within 48 hours after once-daily administration.
Both Cmax and AUC of abrocitinib increased dose proportionally up to 200 mg.
[L39769]
A high-fat meal, high-calorie meal increased AUC by 26% and Cmax by 29%, and prolongs Tmax by two hours; however, there are ultimately no clinically relevant effect on abrocitinib exposures.
[L39769]
Both Cmax and AUC of abrocitinib increased dose proportionally up to 200 mg.
[L39769]
A high-fat meal, high-calorie meal increased AUC by 26% and Cmax by 29%, and prolongs Tmax by two hours; however, there are ultimately no clinically relevant effect on abrocitinib exposures.
[L39769]
Half-life
The mean elimination half-lives of abrocitinib and its two active metabolites, M1 and M2, range from three to five hours.
[L39769]
[L39769]
Protein binding
Approximately 64%, 37% and 29% of circulating abrocitinib and its active metabolites M1 and M2, respectively, are bound to plasma proteins. Abrocitinib and its active metabolites M1 and M2 bind predominantly to albumin and distribute equally between red blood cells and plasma.
[L39769]
[L39769]
Volume of distribution
After intravenous administration, the volume of distribution of abrocitinib was approximately 100 L.
[L39769]
[L39769]
Metabolism
Abrocitinib undergoes CYP-mediated oxidative metabolism. CYP2C19 is the predominant enzyme, accounting for about 53% of drug metabolism. CYP2C9 is responsible for 30% of drug metabolism.
About 11% and 6% of the drug is metabolized by CYP3A4 and CYP2B6, respectively. In a human radiolabeled study, the parent drug was the most prevalent circulating species. Polar mono-hydroxylated metabolites of abrocitinib - M1 (3-hydroxypropyl; PF-06471658), M2 (2-hydroxypropyl; PF-07055087), and M4 (pyrrolidinone pyrimidine; PF-07054874) - were also identified in the systemic circulation.
[L39769][L39774]
M2 has a chiral center, thus has an enantiomer M3 (PF-07055090).
[A244544]
At steady state, M2 and M4 are major metabolites and M1 is a minor metabolite.
[L39774]
M2 has a pharmacological activity comparable to abrocitinib while M1 is less pharmacologically active than abrocitinib.
M3 and M4 are inactive metabolites. The pharmacologic activity of abrocitinib is attributable to the unbound exposures of the parent molecule (~60%) as well as M1 (~10%) and M2 (~30%) in the systemic circulation. The sum of unbound exposures of abrocitinib, M1 and M2, each expressed in molar units and adjusted for relative potencies, is referred to as the abrocitinib active moiety.
[L39774]
About 11% and 6% of the drug is metabolized by CYP3A4 and CYP2B6, respectively. In a human radiolabeled study, the parent drug was the most prevalent circulating species. Polar mono-hydroxylated metabolites of abrocitinib - M1 (3-hydroxypropyl; PF-06471658), M2 (2-hydroxypropyl; PF-07055087), and M4 (pyrrolidinone pyrimidine; PF-07054874) - were also identified in the systemic circulation.
[L39769][L39774]
M2 has a chiral center, thus has an enantiomer M3 (PF-07055090).
[A244544]
At steady state, M2 and M4 are major metabolites and M1 is a minor metabolite.
[L39774]
M2 has a pharmacological activity comparable to abrocitinib while M1 is less pharmacologically active than abrocitinib.
M3 and M4 are inactive metabolites. The pharmacologic activity of abrocitinib is attributable to the unbound exposures of the parent molecule (~60%) as well as M1 (~10%) and M2 (~30%) in the systemic circulation. The sum of unbound exposures of abrocitinib, M1 and M2, each expressed in molar units and adjusted for relative potencies, is referred to as the abrocitinib active moiety.
[L39774]
Route of elimination
Abrocitinib is eliminated primarily by metabolic clearance mechanisms, with less than 1% of the dose being excreted in urine as an unchanged parent drug. The metabolites of abrocitinib are excreted predominantly in urine.
[L39769]
Pharmacokinetics data up to and including a single oral dose of 800 mg in healthy adult volunteers indicate that more than 90% of the administered dose is expected to be eliminated within 48 hours.
[L39774]
[L39769]
Pharmacokinetics data up to and including a single oral dose of 800 mg in healthy adult volunteers indicate that more than 90% of the administered dose is expected to be eliminated within 48 hours.
[L39774]
Clearance
There is no information available.
Drug targets(4)
Proteins and enzymes this drug interacts with in the body
Tyrosine-protein kinase JAK3
JAK3
inhibitor
Specific functionATP binding
Cellular location
Endomembrane system
General function & pharmacology
Non-receptor tyrosine kinase involved in various processes such as cell growth, development, or differentiation. Mediates essential signaling events in both innate and adaptive immunity and plays a crucial role in hematopoiesis during T-cells development. In the cytoplasm, plays a pivotal role in signal transduction via its association with type I receptors sharing the common subunit gamma such as IL2R, IL4R, IL7R, IL9R, IL15R and IL21R.
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
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
Tyrosine-protein kinase JAK2
JAK2
inhibitor
Specific functionacetylcholine receptor binding
Cellular location
Endomembrane system
General function & pharmacology
Non-receptor tyrosine kinase involved in various processes such as cell growth, development, differentiation or histone modifications. Mediates essential signaling events in both innate and adaptive immunity. In the cytoplasm, plays a pivotal role in signal transduction via its association with type I receptors such as growth hormone (GHR), prolactin (PRLR), leptin (LEPR), erythropoietin (EPOR), thrombopoietin receptor (MPL/TPOR); or type II receptors including IFN-alpha, IFN-beta, IFN-gamma and multiple interleukins .
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
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
Tyrosine-protein kinase JAK1
JAK1
inhibitor
Specific functionATP binding
Cellular location
Endomembrane system
General function & pharmacology
Tyrosine kinase of the non-receptor type, involved in the IFN-alpha/beta/gamma signal pathway .
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: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
Non-receptor tyrosine-protein kinase TYK2
TYK2
inhibitor
Specific functionATP binding
General function & pharmacology
Tyrosine kinase of the non-receptor type involved in numerous cytokines and interferons signaling, which regulates cell growth, development, cell migration, innate and adaptive immunity .
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
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
Metabolizing enzymes(4)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP2C19Cytochrome P450 2C19
substrate
CYP2C9Cytochrome P450 2C9
substrate
CYP3A4Cytochrome P450 3A4
substrate
CYP2B6Cytochrome P450 2B6
substrate
Transporters(3)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
inhibitor
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
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: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
Solute carrier family 22 member 1
SLC22A1
inhibitor
Specific function(R)-carnitine transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Electrogenic voltage-dependent transporter that mediates the transport of a variety of organic cations such as endogenous bioactive amines, cationic drugs and xenobiotics .
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
Organic anion transporter 3
SLC22A8
substrate
Specific functionorganic anion transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Functions as an organic anion/dicarboxylate exchanger that couples organic anion uptake indirectly to the sodium gradient .
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)
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)
Carriers(1)
Proteins that carry this drug through the body
Albumin
ALB
binder
Specific functionantioxidant activity
Cellular location
Secreted
General function & pharmacology
Binds water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs (Probable). Its main function is the regulation of the colloidal osmotic pressure of blood (Probable). Major zinc transporter in plasma, typically binds about 80% of all plasma zinc .
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
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
Scientific references(4)
Tripathy S., Wentzel D., Wan X.K., Kavetska O.
Validation of enantioseparation and quantitation of an active metabolite of abrocitinib in human plasma.
Bioanalysis
2021 Oct13(19):1477-1486. doi: 10.4155/bio-2021-0128. Epub 2021 Oct 4
He H., Guttman-Yassky E.
JAK Inhibitors for Atopic Dermatitis: An Update.
American Journal Clinical Dermatology
2019 Apr20(2):181-192. doi: 10.1007/s40257-018-0413-2
Roskoski R Jr
Janus kinase (JAK) inhibitors in the treatment of inflammatory and neoplastic diseases.
Pharmacology Research
2016 Sep111:784-803. doi: 10.1016/j.phrs.2016.07.038. Epub 2016 Jul 26
Crowley E.L., Nezamololama N., Papp K., Gooderham M.J.
Abrocitinib for the treatment of atopic dermatitis.
Expert Review Clinical Immunology
2020 Oct16(10):955-962. doi: 10.1080/1744666X.2021.1828068. Epub 2020 Oct 8
ATC classification(1 code)
ATC D11AH08
Affected organisms(1)
Humans and other mammals
Commercial products(24)
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)
Abrocitinib
Additional database identifiers
Drugs Product Database (DPD)
23751
ChemSpider
58824300
BindingDB
159748
PDB
D7D
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:6192
GenAtlas
JAK2
GeneCards
JAK2
GenBank Gene Database
AF058925
Guide to Pharmacology
2048
UniProt Accession
JAK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6190
GeneCards
JAK1
Guide to Pharmacology
2047
UniProt Accession
JAK1_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:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_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:10963
GeneCards
SLC22A1
GenBank Gene Database
X98332
GenBank Protein Database
2511670
Guide to Pharmacology
1019
UniProt Accession
S22A1_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
Patent information
3 active patents
9549929
United States
Approved 24 Jan 2017 · Expires 19 Feb 2034
7y 10m
9545405
United States
Approved 17 Jan 2017 · Expires 19 Feb 2034
7y 10m
9035074
United States
Approved 19 May 2015 · Expires 19 Feb 2034
7y 10m
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated about 1 month ago(4 Mar 2026)