1. Epigenetics Stem Cell/Wnt Protein Tyrosine Kinase/RTK JAK/STAT Signaling
  2. JAK
  3. AZD-1480


Cat. No.: HY-10193 Purity: 99.56%
COA Handling Instructions

AZD-1480 est un inhibiteur de JAK1 et de JAK2 qui est l'ATP-compétitif avec des IC50s de 1,3 nM et < 0,4 nM, respectivement.

AZD-1480 is an ATP-competitive inhibitor of JAK1 and JAK2 with IC50s of 1.3 nM and <0.4 nM, respectively.

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

AZD-1480 Chemical Structure

AZD-1480 Chemical Structure

CAS No. : 935666-88-9

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Solid + Solvent
10 mM * 1 mL in DMSO
ready for reconstitution
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10 mM * 1 mL in DMSO USD 73 In-stock
5 mg USD 66 In-stock
10 mg USD 106 In-stock
50 mg USD 264 In-stock
100 mg USD 475 In-stock
200 mg USD 858 In-stock
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Customer Review

Based on 13 publication(s) in Google Scholar

Top Publications Citing Use of Products

    AZD-1480 purchased from MedChemExpress. Usage Cited in: Clin Cancer Res. 2018 Apr 15;24(8):1917-1931.  [Abstract]

    Jak2 is inhibited by lentiviral expression of Jak2 shRNA or control shRNA in CWR22Pc and CWR22Rv1 cells. Alternatively, cells are treated with Jak2 inhibitors AZD1480 (0.8 μM) and INCB018424 (0.4 μM) (72 h), followed by Western blot analysis of Jak2 and active Stat5a/b.

    AZD-1480 purchased from MedChemExpress. Usage Cited in: Neuro Oncol. 2017 Jan;19(1):22-30.  [Abstract]

    AZD1480 and RXDX-101 decrease pSTAT3 levels in a dose- and time-dependent manner. (A) Ink4a-/-/Arf-/-/NTRK2-TEL astrocytes are treated with different concentrations of AZD1480 (upper panel) or RXDX-101 (lower panel) for 1 h. (B) Cells are treated with 0.5 μM AZD1480 (upper panel) or 0.05 μM RXDX-101 (lower panel) for the indicated times. Western blot analyses are then performed with the indicated antibodies.

    AZD-1480 purchased from MedChemExpress. Usage Cited in: Biomed Pharmacother. 2017 Nov;95:1799-1808.  [Abstract]

    The expression of Bcl-2, Bax, pro-Caspase-3 and cleaved-Caspase-3 by western blotting. Representative western blots showing the effects of apigenin and AZD1480 on Bax, Bcl-2, pro-Caspase-3 and cleaved-Caspase-3 expression levels.

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    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review


    AZD-1480 is an ATP-competitive inhibitor of JAK1 and JAK2 with IC50s of 1.3 nM and <0.4 nM, respectively[1].

    IC50 & Target[1]


    <0.4 nM (IC50)


    1.3 nM (IC50)

    In Vitro

    AZD-1480 (5μM) induces G2/M arrest and cell death by inhibiting Aurora kinases[1].
    ? AZD-1480 is a potent JAK2 inhibitor that can suppress growth, survival, as well as FGFR3 and STAT3 signaling and downstream targets including Cyclin D2 in human multiple myeloma cells. At low micromolar concentrations, AZD-1480 blocks cell proliferation and induces apoptosis of myeloma cell lines[2].
    ? AZD-1480 effectively blocks constitutive and stimulus-induced JAK1, JAK2, and STAT-3 phosphorylation in both human and murine glioma cells, and leads to a decrease in cell proliferation and induction of apoptosis[3].
    ? AZD-1480 is a potent, competitive small-molecule inhibitor of JAK1/2 kinase, and that it is capable of inhibiting STAT3 phosphorylation and tumor growth in a STAT3-dependent manner. AZD-1480 inhibits tumor angiogenesis and metastasis in part by affecting the tumor microenvironment[4].

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

    In Vivo

    AZD-1480 inhibits the STAT3 phosphorylation in an xenograft model of human solid tumors and multiple myeloma[1].
    ? In vivo, AZD-1480 inhibits the growth of subcutaneous tumors and increases survival of mice bearing intracranial glioblastoma (GBM) tumors by inhibiting STAT-3 activity, indicating that pharmacologic inhibition of the JAK/STAT-3 pathway by AZD-1480 should be considered for study in the treatment of patients with GBM tumors[3].
    ? AZD-1480 blocks lung infiltration of myeloid cells and formation of pulmonary metastases in both mouse syngeneic experimental and spontaneous metastatic models. Furthermore, AZD-1480 reduces angiogenesis and metastasis in a human xenograft tumor model[4].
    ? AZD-1480 suppresses the growth of human solid tumor xenografts harboring persistent Stat3 activity[5].

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

    Clinical Trial
    Molecular Weight






    CAS No.



    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 2 years
    -20°C 1 year
    Solvent & Solubility
    In Vitro: 

    DMSO : 50 mg/mL (143.36 mM; Need ultrasonic)

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.8672 mL 14.3361 mL 28.6722 mL
    5 mM 0.5734 mL 2.8672 mL 5.7344 mL
    10 mM 0.2867 mL 1.4336 mL 2.8672 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

      Solubility: ≥ 2.5 mg/mL (7.17 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

      Solubility: ≥ 2.5 mg/mL (7.17 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    90% Corn Oil

      Solubility: ≥ 2.5 mg/mL (7.17 mM); Clear solution

    *All of the co-solvents are available by MedChemExpress (MCE).
    Purity & Documentation

    Purity: 99.56%

    Kinase Assay

    Inhibition studies of AZD1480 are performed using recombinant Jak1, Jak2, or Jak3 under buffer conditions of 50 mM HEPES pH 7.3, 1 mM DTT, 0.01% Tween-20, 50 mM/mL BSA, and 10 mM MgCl2. Jak3 enzyme is expressed as N-terminal GST fusion in insect cells and purified by glutathione-affinity and size-exclusion chromatographies. Enzymes are assayed in the presence of AZD1480 (10 point dose response, in triplicate, from 8.3 μM to 0.3 nM in half-log dilution steps) using 1.5 μM peptide substrate (Jak1: FITC-C6-KKHTDDGYMPMSPGVA-NH2, Jak2 and Jak3: FAM-SRCtide) and screened under their respective ATP Km (Jak1: 55 μM, Jak2: 15 μM, Jak3: 3 μM) and approximated physiological ATP concentration of 5 mM. Phosphorylated and unphosphorylated peptides are separated and quantified by a Caliper LC3000 system for calculating percent inhibition.

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

    Cell Assay

    Renca or 786-O cells are suspended in DMEM medium with 5% FBS, and seeded in 96-well plates (5×103 per well) to allow adhesion and then treated with DMSO or AZD1480 for 48 hours. Cell viability is determined by MTS assay. Absorbance at 490 nm is measured with Mikrotek Laborsysteme. Mouse endothelial cells and splenic CD11b+/c- myeloid cells are enriched from tumor-bearing mice,and cultured in 5% FBS RPMI-1640 medium. HUVECs are cultured on collagen 1-coated plates in complete medium. All cells are treated with DMSO and AZD1480 at various doses for 24 hours. Cell viability is determined by counting cell number manually. All the experiments are repeated 3 times.

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

    Animal Administration

    For subcutaneous (s.c.) tumor model, 2.5×106 Renca or 786-O cells suspended in 100 μL PBS are injected into the flank of BALB/c or nude mice, respectively. When average tumor volume reaches approximately 100-150 mm3, AZD1480 or vehicle is administered by oral gavage either once a day at the dose of 50 mg/kg, or twice daily at 30 mg/kg, as indicated. Tumor size is measured by caliper every other day. For experimental lung metastasis model, 0.1×106 Renca or 1×106 786-O cells suspended in 500 μL PBS are injected via tail vein to BALB/c or nude mice, respectively. Three days later, mice are orally treated with AZD1480 (50 mg/kg/d) or vehicle for 21 days for Renca tumors and 60 days for 786-O tumors respectively. For the Calu-6 model, 3×106 tumor cells in matrigel are implanted s.c. into the flanks of nude mice, randomized into vehicle (twice daily, BID) and drug treatment (AZD1480, 30 mg/kg BID) groups, and dosed orally daily for 19 days. For spontaneous lung metastasis model, 2×105 4T1 cells suspended in 100 μL PBS are injected in the mammary gland of female BALB/c mice by gently penetrating the skin. AZD1480 (50 mg/kg/d) or vehicle is given orally for 21 days.

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

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    • 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.

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