2. Immunology/Inflammation Epigenetics Stem Cell/Wnt JAK/STAT Signaling Protein Tyrosine Kinase/RTK
  3. IFNAR JAK Interleukin Related STAT
  4. Deucravacitinib (hydrochloride)

Deucravacitinib (hydrochloride)  (Synonyms: BMS-986165 (hydrochloride))

Cat. No.: HY-117287A
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Deucravacitinib (BMS-986165) hydrochloride is an orally active allosteric inhibitor of tyrosine kinase 2 (TYK2), with an IC50 of 0.2 nM and a Ki of 0.02 nM against the JH2 domain of TYK2, and it exhibits selectivity over other JAK subtypes and most of the kinome. Deucravacitinib hydrochloride blocks IL-23, IL-12, p-STAT1/3 and Type I IFN signaling, and inhibits Th17/Th1-mediated psoriasis inflammation. Deucravacitinib hydrochloride can be used in research related to moderate-to-severe plaque psoriasis, inflammatory bowel disease and systemic lupus erythematosus.

For research use only. We do not sell to patients.

CAS No. : 1609392-28-0

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Deucravacitinib (hydrochloride) Related Antibodies

Top Publications Citing Use of Products

33 Publications Citing Use of MCE Deucravacitinib (hydrochloride)

WB
Cell Proliferation/Viability Assay
IHC
In Vivo Efficacy Study

    Deucravacitinib (hydrochloride) purchased from MedChemExpress. Usage Cited in: Clin Cancer Res. 2023 Apr 14;29(8):1592-1604.  [Abstract]

    Deucravacitinib (5-80 μM; 0-72 h). The specific TYK2 inhibitor deucravacitinib (BMS-986165) decreases MPNST cell proliferation at lower doses.

    Deucravacitinib (hydrochloride) purchased from MedChemExpress. Usage Cited in: Clin Cancer Res. 2023 Apr 14;29(8):1592-1604.  [Abstract]

    The combination of drugs inhibiting TYK2 and MEK block MPNST tumor growth in mice. Mice with JW23.3 MPNST xenograft tumors were treated daily with 30 mg/kg deucravacitinib (Deucra, BMS-986165), the combination of drugs, or vehicle control for 3 weeks or until tumors reached the maximum allowed volume.

    Deucravacitinib (hydrochloride) purchased from MedChemExpress. Usage Cited in: J Invest Dermatol. 2025 Apr 8:S0022-202X(25)00393-8.  [Abstract]

    BMS-986165 (10 mg/kg; Oral). Representative images of histopathology images taken from each experimental group.

    Deucravacitinib (hydrochloride) purchased from MedChemExpress. Usage Cited in: Nat Chem Biol. 2022 Dec;18(12):1388-1398.  [Abstract]

    Western blots measuring effects of VVD-118313 (5a) and BMS-986165 (BMS) (2 µM, 2 h) on JAK1 phosphorylation (pJAK1).

    Deucravacitinib (hydrochloride) purchased from MedChemExpress. Usage Cited in: Cell Death Differ. 2021 Feb;28(2):748-763.  [Abstract]

    BMS-986165 (0.02-1 μM; 18 h).Cells are treated with the allosteric TYK2 inhibitor BMS-986165 (TYK2 Inh.). BMS-986165 dose-dependently inhibits upregulation of CASP5 in response to LPS in U937 macrophages.

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    Description

    Deucravacitinib (BMS-986165) hydrochloride is an orally active allosteric inhibitor of tyrosine kinase 2 (TYK2), with an IC50 of 0.2 nM and a Ki of 0.02 nM against the JH2 domain of TYK2, and it exhibits selectivity over other JAK subtypes and most of the kinome. Deucravacitinib hydrochloride blocks IL-23, IL-12, p-STAT1/3 and Type I IFN signaling, and inhibits Th17/Th1-mediated psoriasis inflammation. Deucravacitinib hydrochloride can be used in research related to moderate-to-severe plaque psoriasis, inflammatory bowel disease and systemic lupus erythematosus[1][2].

    Application

    1. This compound can be used as a tracer.
    2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.

    In Vitro

    Deucravacitinib hydrochloride potently inhibits TYK2-dependent IFNα-induced STAT5 phosphorylation in human CD3+ T cells, with an IC50 of 2 nM[2].
    Deucravacitinib hydrochloride potently inhibits TYK2-dependent IL-23-induced STAT3 phosphorylation in human CD161+ CD3+ T cells, with an IC50 of 9 nM[2].
    Deucravacitinib hydrochloride potently inhibits TYK2-dependent IFNα-induced STAT5 phosphorylation in human whole blood with an IC50 of 13 nM, while exhibiting high functional selectivity for signaling pathways dependent on JAK2, JAK1 and JAK3[2].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Deucravacitinib (hydrochloride) Related Antibodies
    In Vivo

    Deucravacitinib (7.5-30 mg/kg; p.o.; twice daily; for 9 consecutive days) hydrochloride exhibits dose-dependent efficacy in a mouse IL-23-driven psoriasis model[2].
    Deucravacitinib (50 mg/kg; p.o.; twice daily) hydrochloride almost completely inhibits body weight loss and significantly reduces histological damage in a mouse model of anti-CD40-induced colitis[2].
    Deucravacitinib (30 mg/kg; p.o.; once daily; for 3 consecutive months) hydrochloride is well tolerated in a mouse lupus model and exerts significant efficacy in preventing nephritis[2].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: C57BL/6 (PK studies; IL-23-driven acanthosis psoriasis model)[2]
    Dosage: 7.5 mg/kg; 15 mg/kg; 30 mg/kg
    Administration: p.o.; twice daily; 9 days
    Result: Reduced ear thickness increase relative to vehicle, inhibited epidermal hyperplasia and inflammatory cellular infiltration, and dose-dependently reduced relative gene expression of IL-17a, IL-21, IL-23a, IL-23R, IL-12 (p35), and IL-12 (p40) in skin biopsies at 7.5 mg/kg twice daily.
    Maintained drug levels at or above mouse whole blood IC50 (100 nM) for 19 hours at 7.5 mg/kg twice daily.
    Achieved ear thickness inhibition equivalent to the anti-IL-23 adnectin positive control, reduced epidermal hyperplasia and inflammatory cellular infiltration, showed greater reduction of cytokine gene expression than the 7.5 mg/kg dose, and maintained drug levels at or above mouse whole blood IC50 for 21 hours at 15 mg/kg twice daily.
    Provided greater ear thickness protection than the anti-IL-23 adnectin, more effectively inhibited epidermal hyperplasia and inflammatory cellular infiltration than the positive control, showed the greatest reduction of cytokine gene expression across all doses, and maintained drug levels at or above mouse whole blood IC50 for 24 hours at 30 mg/kg twice daily.
    Animal Model: NZB/W (spontaneous lupus-prone nephritis model; treated for three months)[2]
    Dosage: 30 mg/kg
    Administration: p.o.; once daily; three months
    Result: Was well-tolerated, highly efficacious in protecting against nephritis, inhibited type I IFN-dependent gene expression in whole blood and kidneys, and was at least as effective as a blocking anti-IFNαR antibody control; efficacy correlated with coverage of the whole blood IC50 over dosing intervals.
    Molecular Weight

    461.92

    Formula

    C20H20D3ClN8O3
    CAS No.
    SMILES

    COC1=C(C2=NN(C)C=N2)C=CC=C1NC3=C(N=NC(NC(C4CC4)=O)=C3)C(NC([2H])([2H])[2H])=O.Cl
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    Room temperature in continental US; may vary elsewhere.
    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.
    Purity & Documentation
    References
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    Deucravacitinib (hydrochloride) Related Classifications

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    Help & FAQs
    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

    Keywords:

    Deucravacitinib (hydrochloride)1609392-28-0BMS-986165BMS986165BMS 986165IFNARJAKInterleukin RelatedSTATInterferon-α/β receptorInterferon-alpha/beta receptor Janus kinaseILInhibitorinhibitorinhibit

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