Deucravacitinib 6mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
6mg
Oral
Deucravacitinib is a novel oral selective tyrosine kinase 2 (TYK2) inhibitor.
Active ingredients:
Deucravacitinib
No active safety alerts
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Sotyktu 6mg tablets
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WHO defined daily dose (DDD)
6 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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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
Deucravacitinib
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(2)
Deucravacitinib for treating moderate to severe plaque psoriasis (TA907)
TA907
Technology appraisal
Updated Jun 2023Psoriasis: assessment and management (CG153)
CG153
Clinical guideline
Updated Sept 2017Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF 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
10 hours
Mechanism
Tyrosine kinase 2 (TYK2) is a member of the Janus kinase (JAK) family of kinases…
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
3 mg
Following oral administration, deucravacitinib plasma Cmax and AUC increased proportionally over a dose range from 3 mg to 36 mg (0.5…
Half-life
10 hours
The terminal half-life of deucravacitinib was 10 hours.
[L43150]
[L43150]
Protein binding
82 to 90%
Protein binding of deucravacitinib was 82 to 90% and the blood-to-plasma concentration ratio was 1.26.
[L43150]
[L43150]
Volume of distribution
140 L
The volume of distribution of deucravacitinib at steady state is 140 L.
[L43150]
[L43150]
Metabolism
20%
Deucravacitinib undergoes N-demethylation mediated by cytochrome P-450 (CYP) 1A2 to form major metabolite BMT-153261, which has a comparable pharmacological activity to the parent drug.…
Elimination
13%
After a single dose of radiolabeled deucravacitinib, approximately 13% and 26% of the dose was recovered as unchanged in urine and feces, respectively.…
Clearance
27 to 54 mL/min
The renal clearance of deucravacitinib ranged from 27 to 54 mL/minute.
[L43150]
[L43150]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Deucravacitinib is a novel oral selective tyrosine kinase 2 (TYK2) inhibitor. Unlike other Janus kinase 1/2/3 inhibitors that bind to the conserved active domain of these non-receptor tyrosine kinases, deucravacitinib binds to the regulatory domain of TYK2 with high selectivity to this therapeutic target.[A246938][A246943] This selectivity towards TYK2 may lead to an improved safety profile of deucravacitinib, as nonselective JAK inhibitors are associated with a range of adverse effects such as altered cholesterol and triglyceride levels and liver and kidney dysfunction.[A246943]
Deucravacitinib was first approved by the FDA in September 2022 to treat moderate-to-severe plaque psoriasis.[L43150] It was later approved by Health Canada in November 2022 [L44216] and by the European Medicines Agency in March 2023.[L45788]
Deucravacitinib was first approved by the FDA in September 2022 to treat moderate-to-severe plaque psoriasis.[L43150] It was later approved by Health Canada in November 2022 [L44216] and by the European Medicines Agency in March 2023.[L45788]
Properties:
solid
Avg. mass: 425.47 Da
DrugBank indication
Deucravacitinib is a tyrosine kinase 2 (TYK2) inhibitor indicated for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy. It is not recommended for use in combination with other potent immunosuppressants.
[L43150][L44216][L45778]
[L43150][L44216][L45778]
Also known as(68)
Deucravacitinib
2.7.10.2
1.14.14.1
Cholesterol 25-hydroxylase
CYPIA2
Cytochrome P(3)450
Cytochrome P450 4
Cytochrome P450-P3
Dosage forms(5)
Tablet (Oral) — 6 mg
Tablet (Oral) — 6.000 mg
Tablet, film coated (Oral) — 6 mg/1
Tablet, film coated (Oral) — 6 mg
Tablet, coated (Oral) — 6 mg
Molecular properties(19)
Drug interactions(384)
Known interactions with other medications. Always consult a healthcare professional.
Acetaminophen
Unknown severity
The serum concentration of Acetaminophen can be increased when it is combined with Deucravacitinib.
Propacetamol
Unknown severity
The serum concentration of Propacetamol can be increased when it is combined with Deucravacitinib.
Salmon calcitonin
Moderate
The therapeutic efficacy of Salmon calcitonin can be decreased when used in combination with Deucravacitinib.
Thyrotropin alfa
Moderate
The therapeutic efficacy of Thyrotropin alfa can be decreased when used in combination with Deucravacitinib.
Follitropin
Moderate
The therapeutic efficacy of Follitropin can be decreased when used in combination with Deucravacitinib.
Liothyronine
Moderate
The therapeutic efficacy of Liothyronine can be decreased when used in combination with Deucravacitinib.
Carbimazole
Moderate
The therapeutic efficacy of Carbimazole can be decreased when used in combination with Deucravacitinib.
Levothyroxine
Moderate
The therapeutic efficacy of Levothyroxine can be decreased when used in combination with Deucravacitinib.
Propylthiouracil
Moderate
The therapeutic efficacy of Propylthiouracil can be decreased when used in combination with Deucravacitinib.
Methimazole
Moderate
The therapeutic efficacy of Methimazole can be decreased when used in combination with Deucravacitinib.
The therapeutic efficacy of Liotrix can be decreased when used in combination with Deucravacitinib.
3,5-Diiodotyrosine
Moderate
The therapeutic efficacy of 3,5-Diiodotyrosine can be decreased when used in combination with Deucravacitinib.
Tiratricol
Moderate
The therapeutic efficacy of Tiratricol can be decreased when used in combination with Deucravacitinib.
Parathyroid hormone
Moderate
The therapeutic efficacy of Parathyroid hormone can be decreased when used in combination with Deucravacitinib.
Teriparatide
Moderate
The therapeutic efficacy of Teriparatide can be decreased when used in combination with Deucravacitinib.
Potassium Iodide
Moderate
The therapeutic efficacy of Potassium Iodide can be decreased when used in combination with Deucravacitinib.
Dibromotyrosine
Moderate
The therapeutic efficacy of Dibromotyrosine can be decreased when used in combination with Deucravacitinib.
Thyroid, porcine
Moderate
The therapeutic efficacy of Thyroid, porcine can be decreased when used in combination with Deucravacitinib.
Potassium perchlorate
Moderate
The therapeutic efficacy of Potassium perchlorate can be decreased when used in combination with Deucravacitinib.
Protirelin
Moderate
The therapeutic efficacy of Protirelin can be decreased when used in combination with Deucravacitinib.
The therapeutic efficacy of 3,5-diiodothyropropionic acid can be decreased when used in combination with Deucravacitinib.
Methylthiouracil
Moderate
The therapeutic efficacy of Methylthiouracil can be decreased when used in combination with Deucravacitinib.
The therapeutic efficacy of Elcatonin can be decreased when used in combination with Deucravacitinib.
Benzylthiouracil
Moderate
The therapeutic efficacy of Benzylthiouracil can be decreased when used in combination with Deucravacitinib.
Thyrotropin
Moderate
The therapeutic efficacy of Thyrotropin can be decreased when used in combination with Deucravacitinib.
The risk or severity of adverse effects can be increased when Denosumab is combined with Deucravacitinib.
Etanercept
Unknown severity
The risk or severity of adverse effects can be increased when Etanercept is combined with Deucravacitinib.
Peginterferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2a is combined with Deucravacitinib.
Interferon alfa-n1
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n1 is combined with Deucravacitinib.
Interferon alfa-n3
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n3 is combined with Deucravacitinib.
Peginterferon alfa-2b
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2b is combined with Deucravacitinib.
The risk or severity of adverse effects can be increased when Anakinra is combined with Deucravacitinib.
Interferon gamma-1b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon gamma-1b is combined with Deucravacitinib.
Interferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-2a is combined with Deucravacitinib.
Aldesleukin
Unknown severity
The risk or severity of adverse effects can be increased when Aldesleukin is combined with Deucravacitinib.
Adalimumab
Unknown severity
The risk or severity of adverse effects can be increased when Adalimumab is combined with Deucravacitinib.
Gemtuzumab ozogamicin
Unknown severity
The risk or severity of adverse effects can be increased when Gemtuzumab ozogamicin is combined with Deucravacitinib.
Pegaspargase
Unknown severity
The risk or severity of adverse effects can be increased when Pegaspargase is combined with Deucravacitinib.
Infliximab
Unknown severity
The risk or severity of adverse effects can be increased when Infliximab is combined with Deucravacitinib.
Interferon beta-1b
Unknown severity
The risk or severity of adverse effects can be increased when Interferon beta-1b is combined with Deucravacitinib.
Interferon alfacon-1
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfacon-1 is combined with Deucravacitinib.
Trastuzumab
Unknown severity
The risk or severity of neutropenia can be increased when Trastuzumab is combined with Deucravacitinib.
The risk or severity of adverse effects can be increased when Rituximab is combined with Deucravacitinib.
Basiliximab
Unknown severity
The risk or severity of adverse effects can be increased when Basiliximab is combined with Deucravacitinib.
The risk or severity of adverse effects can be increased when Muromonab is combined with Deucravacitinib.
Ibritumomab tiuxetan
Unknown severity
The risk or severity of adverse effects can be increased when Ibritumomab tiuxetan is combined with Deucravacitinib.
Tositumomab
Unknown severity
The risk or severity of adverse effects can be increased when Tositumomab is combined with Deucravacitinib.
Alemtuzumab
Unknown severity
The risk or severity of adverse effects can be increased when Alemtuzumab is combined with Deucravacitinib.
Cyclosporine
Moderate
Deucravacitinib may increase the immunosuppressive activities of Cyclosporine.
The risk or severity of adverse effects can be increased when Alefacept is combined with Deucravacitinib.
Showing 50 of 384 interactions
Food & lifestyle interactions
Advice
Take with or without food. Food has no clinically significant effect on drug absorption and exposure.
Toxicity & overdose
No information regarding the acute toxicity profile and LD50 of deucravacitinib is available. There is no experience regarding human overdosage with deucravacitinib. There is no known antidote for deucravacitinib overdose and hemodialysis is unlikely to be effective, as the extent of deucravacitinib elimination by hemodialysis is small (5.4% of dose per dialysis treatment).
[L43150]
[L43150]
How it works
Mechanism of action
Tyrosine kinase 2 (TYK2) is a member of the Janus kinase (JAK) family of kinases, which are intracellular tyrosine kinases that activate the JAK–signal transducer and activator of the transcription pathway. Unlike other members of the JAK family that promote broader immune and extra-immune pathways, such as lipid metabolism, the TYK2 signalling pathway is responsible for selected immune pathways.[A246938] TYK2 mediates the signalling of inflammatory cytokines of both adaptive (e.g., interleukin (IL) 12 and IL-23) and innate (e.g., type I interferons) immune responses.[A246948] IL-23 has been implicated in the pathogenesis of immune-mediated disorders such as psoriasis and psoriatic arthritis.[A246938] It activates and promotes the proliferation of Th17 cells: subsequently, Th17 cells secrete inflammatory mediators, such as IL-17 and tumour necrosis factor-alpha, that stimulate epidermal cells to produce cytokines and chemokines that attract and activate innate immune system cells.[A246938][A246943] Enhanced activity of Th17 cells leads to sustained inflammatory responses in the skin and joints as manifested in psoriatic arthritis.[A246938]
Deucravacitinib inhibits TYK2 via an allosteric mechanism: it binds to the enzyme's regulatory domain - also known as the pseudokinase (JH2) domain - instead of the catalytic domain. This binding activity allows high selectivity towards TYK2 over other tyrosine kinase enzymes. In in vitro cellular assays, deucravacitinib showed a 100-fold to 2000-fold selectivity for TYK2 over JAK 1/2/3 and demonstrated minimal or no activity against JAK 1/2/3. Upon binding to TYK2, deucravacitinib induces a conformational change and locks the regulatory domain of TYK2 into an inhibitory confirmation with the catalytic domain, trapping TYK2 in an inactive state.[A246938][A246943] Inhibiting TYK2 leads to the downregulation of the IL-23/TH17 pathway, IL-12 signalling, type 1 interferon pathway, and keratinocyte activation.[A246948]
Deucravacitinib inhibits TYK2 via an allosteric mechanism: it binds to the enzyme's regulatory domain - also known as the pseudokinase (JH2) domain - instead of the catalytic domain. This binding activity allows high selectivity towards TYK2 over other tyrosine kinase enzymes. In in vitro cellular assays, deucravacitinib showed a 100-fold to 2000-fold selectivity for TYK2 over JAK 1/2/3 and demonstrated minimal or no activity against JAK 1/2/3. Upon binding to TYK2, deucravacitinib induces a conformational change and locks the regulatory domain of TYK2 into an inhibitory confirmation with the catalytic domain, trapping TYK2 in an inactive state.[A246938][A246943] Inhibiting TYK2 leads to the downregulation of the IL-23/TH17 pathway, IL-12 signalling, type 1 interferon pathway, and keratinocyte activation.[A246948]
Pharmacodynamics
Deucravacitinib is a tyrosine kinase 2 (TYK2) inhibitor that works to suppress the immune signaling pathways in inflammatory disorders, such as plaque psoriasis. In clinical studies comprising patients with psoriasis, deucravacitinib reduced psoriasis-associated gene expression in psoriatic skin in a dose dependent manner, including reductions in IL-23-pathway and type I IFN pathway regulated genes. Following 16 weeks of once-daily treatment, deucravacitinib reduced inflammatory markers such as IL-17A, IL-19 and beta-defensin by 47 to 50%, 72%, and 81 to 84%, respectively.[L43150] Deucravacitinib does not affect with JAK2-dependent hematopoietic functions.[A252310]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Following oral administration, deucravacitinib plasma Cmax and AUC increased proportionally over a dose range from 3 mg to 36 mg (0.5 to 6 times the approved recommended dosage) in healthy subjects. The steady state Cmax and AUC24 of deucravacitinib following administration of 6 mg once daily were 45 ng/mL and 473 ng x hr/mL, respectively. The steady state Cmax and AUC24 of the active deucravacitinib metabolite, BMT-153261, following administration of 6 mg once daily were 5 ng/mL and 95 ng x hr/mL, respectively.
The absolute oral bioavailability of deucravacitinib was 99% and the median Tmax ranged from two to three hours.
[L43150]
A high-fat, high-calorie meal decreased Cmax and AUC of deucravacitinib by 24% and 11%, respectively, and prolonged Tmax by one hour; however, this has clinically significant effects on drug absorption and exposure.
[L43150]
The absolute oral bioavailability of deucravacitinib was 99% and the median Tmax ranged from two to three hours.
[L43150]
A high-fat, high-calorie meal decreased Cmax and AUC of deucravacitinib by 24% and 11%, respectively, and prolonged Tmax by one hour; however, this has clinically significant effects on drug absorption and exposure.
[L43150]
Half-life
The terminal half-life of deucravacitinib was 10 hours.
[L43150]
[L43150]
Protein binding
Protein binding of deucravacitinib was 82 to 90% and the blood-to-plasma concentration ratio was 1.26.
[L43150]
[L43150]
Volume of distribution
The volume of distribution of deucravacitinib at steady state is 140 L.
[L43150]
[L43150]
Metabolism
Deucravacitinib undergoes N-demethylation mediated by cytochrome P-450 (CYP) 1A2 to form major metabolite BMT-153261, which has a comparable pharmacological activity to the parent drug. However, the circulating exposure of BMT-153261 accounts for approximately 20% of the systemic exposure of the total drug-related components. Deucravacitinib is also metabolized by CYP2B6, CYP2D6, carboxylesterase (CES) 2, and uridine glucuronyl transferase (UGT) 1A9.
[L43150]
[L43150]
Route of elimination
After a single dose of radiolabeled deucravacitinib, approximately 13% and 26% of the dose was recovered as unchanged in urine and feces, respectively. Approximately 6% and 12% of the dose was detected as BMT-153261 in urine and feces, respectively.
[L43150]
[L43150]
Clearance
The renal clearance of deucravacitinib ranged from 27 to 54 mL/minute.
[L43150]
[L43150]
Drug targets(1)
Proteins and enzymes this drug interacts with in the body
Non-receptor tyrosine-protein kinase TYK2
TYK2
inhibitory allosteric modulator
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(5)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP1A2Cytochrome P450 1A2
substrate
CYP2B6Cytochrome P450 2B6
substrate
CYP2D6Cytochrome P450 2D6
substrate
CES2Cocaine esterase
substrate
UGT1A9UDP-glucuronosyltransferase 1A9
substrate
Transporters(4)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
substrate
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
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
substrate
inhibitor
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Broad substrate specificity ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes a wide variety of physiological compounds, dietary toxins and xenobiotics from cells .
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Solute carrier family 22 member 1
SLC22A1
substrate
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
Solute carrier organic anion transporter family member 1B3
SLCO1B3
inhibitor
Specific functionbile acid transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Mediates the Na(+)-independent uptake of organic anions .
PMID:10779507 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (17-beta-glucuronosyl estradiol, dehydroepiandrosterone sulfate (DHEAS), and estrone 3-sulfate), as well as eicosanoid leukotriene C4, prostaglandin E2 and L-thyroxine (T4) .
PMID:10779507 PMID:11159893 PMID:12568656 PMID:15159445 PMID:17412826 PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
Shows a pH-sensitive substrate specificity towards sulfated steroids, taurocholate and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Involved in the clearance of bile acids and organic anions from the liver .
PMID:22232210
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins) such as pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:15159445
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver PMID:16624871 PMID:16627748
PMID:10779507 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (17-beta-glucuronosyl estradiol, dehydroepiandrosterone sulfate (DHEAS), and estrone 3-sulfate), as well as eicosanoid leukotriene C4, prostaglandin E2 and L-thyroxine (T4) .
PMID:10779507 PMID:11159893 PMID:12568656 PMID:15159445 PMID:17412826 PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
Shows a pH-sensitive substrate specificity towards sulfated steroids, taurocholate and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Involved in the clearance of bile acids and organic anions from the liver .
PMID:22232210
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins) such as pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:15159445
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver PMID:16624871 PMID:16627748
Scientific references(4)
Mease P.J., Deodhar A.A., van der Heijde D., Behrens F., Kivitz A.J., Neal J., Kim J., Singhal S., Nowak M., Banerjee S.
Efficacy and safety of selective TYK2 inhibitor, deucravacitinib, in a phase II trial in psoriatic arthritis. Ann Rheum Dis. 2022 Mar 3. pii: annrheumdis-2021-221664.
doi: 10
1136/annrheumdis-2021-221664
Chimalakonda A., Burke J., Cheng L., Catlett I., Tagen M., Zhao Q., Patel A., Shen J., Girgis I.G., Banerjee S., Throup J.
Selectivity Profile of the Tyrosine Kinase 2 Inhibitor Deucravacitinib Compared with Janus Kinase 1/2/3 Inhibitors.
Dermatology Therapeutics (Heidelb)
2021 Oct11(5):1763-1776. doi: 10.1007/s13555-021-00596-8. Epub 2021 Aug 30
Catlett I.M., Hu Y., Gao L., Banerjee S., Gordon K., Krueger J.G.
Molecular and clinical effects of selective tyrosine kinase 2 inhibition with deucravacitinib in psoriasis. J Allergy Clin Immunol. 2021 Nov 10. pii: S0091-6749(21)01690-0. doi: 10.1016/j.jaci.2021.
11
001
Le A.M., Puig L., Torres T.
Deucravacitinib for the Treatment of Psoriatic Disease. Am J Clin Dermatol. 2022 Aug 12. pii: 10.1007/s40257-022-00720-0.
doi: 10
1007/s40257-022-00720-0
ATC classification(1 code)
ATC L04AF07
Salt forms(1)
Deucravacitinib hydrochloride(DBSALT003167)
Commercial products(10)
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)
Deucravacitinib
Additional database identifiers
Drugs Product Database (DPD)
23806
ChemSpider
72380005
BindingDB
50507816
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:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_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:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1864
GeneCards
CES2
Guide to Pharmacology
3298
UniProt Accession
EST2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12541
GeneCards
UGT1A9
GenBank Gene Database
S55985
GenBank Protein Database
7690346
UniProt Accession
UD19_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:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_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:10961
GeneCards
SLCO1B3
GenBank Gene Database
AJ251506
GenBank Protein Database
9187497
Guide to Pharmacology
1221
UniProt Accession
SO1B3_HUMAN
Patent information
3 active patents
11021475
United States
Approved 1 Jun 2021 · Expires 7 Nov 2033
7y 7m
RE47929
United States
Approved 7 Apr 2020 · Expires 7 Nov 2033
7y 7m
10000480
United States
Approved 19 Jun 2018 · Expires 7 Nov 2033
7y 7m
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)