AZD-1480
Based on 21 publication(s) in Google Scholar
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.
- Purity: 99.74%
- CAS No.: 935666-88-9
- Formula: C14H14ClFN8
- Molecular Weight:348.77
-
Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year
Publications Citing Use of MedChemExpress (MCE) AZD-1480
More- Nature. 2025 Jun;642(8066):201-211. [Abstract]
- Cancer Res. 2025 Apr 15;85(8):1368-1389. [Abstract]
- Sci Transl Med. 2018 Jul 18;10(450):eaaq1093. [Abstract]
- Neuro Oncol. 2017 Jan;19(1):22-30. [Abstract]
- Leukemia. 2012 Oct;26(10):2233-44. [Abstract]
- Cell Rep Med. 2025 Sep 16;6(9):102324. [Abstract]
- J Exp Med. 2024 Mar 4;221(3):e20232028. [Abstract]
- Clin Cancer Res. 2018 Apr 15;24(8):1917-1931. [Abstract]
- Acta Pharmacol Sin. 2025 Jan;46(1):184-195. [Abstract]
- Biomed Pharmacother. 2017 Nov:95:1799-1808. [Abstract]
- Mol Cancer Ther. 2020 Jan;19(1):231-246. [Abstract]
- J Ethnopharmacol. 2023 Oct 5:314:116633. [Abstract]
- J Biotechnol. 2025 Mar:399:9-18. [Abstract]
- J Biochem Mol Toxicol. 2026 Jan;40(1):e70661. [Abstract]
- STAR Protoc. 2025 Dec 1;6(4):104250. [Abstract]
- bioRxiv. 2026 Jan 22.
- bioRxiv. 2024 Nov 6:2024.11.04.621884. [Abstract]
- bioRxiv. 2024 Apr 30.
- J Pers Med. 2022 Feb 9;12(2):249. [Abstract]
- University of Toronto. 2019 Nov.
- Patent. US20180263995A1.
-
WB
-
WB
-
WB
Biological Activity
|
JAK2 <0.4 nM (IC50) |
JAK1 1.3 nM (IC50) |
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| BaF3 | GI50 |
0.06 μM
Compound: 9e
|
Growth inhibition of mouse BA/F3 cells expressing Tel-JAK2 kinase after 48 hrs by MTS assay
Growth inhibition of mouse BA/F3 cells expressing Tel-JAK2 kinase after 48 hrs by MTS assay
|
[PMID: 21138246] |
| BaF3 | GI50 |
0.7 μM
Compound: 9e
|
Growth inhibition of mouse BA/F3 cells expressing Tel-JAK1 kinase after 48 hrs by MTS assay
Growth inhibition of mouse BA/F3 cells expressing Tel-JAK1 kinase after 48 hrs by MTS assay
|
[PMID: 21138246] |
| BaF3 | GI50 |
2 μM
Compound: 9e
|
Growth inhibition of mouse BA/F3 cells expressing Tel-Tyk2 kinase after 48 hrs by MTS assay
Growth inhibition of mouse BA/F3 cells expressing Tel-Tyk2 kinase after 48 hrs by MTS assay
|
[PMID: 21138246] |
| BaF3 | GI50 |
2.1 μM
Compound: 9e
|
Growth inhibition of mouse BA/F3 cells expressing Tel-JAK3 kinase after 48 hrs by MTS assay
Growth inhibition of mouse BA/F3 cells expressing Tel-JAK3 kinase after 48 hrs by MTS assay
|
[PMID: 21138246] |
| BaF3 | IC50 |
0.046 μM
Compound: 9e
|
Inhibition of Stat5 phosphorylation in mouse Ba/F3 cells expressing TEL-Jak2
Inhibition of Stat5 phosphorylation in mouse Ba/F3 cells expressing TEL-Jak2
|
[PMID: 21138246] |
| HEL | GI50 |
0.39 μM
Compound: 9e
|
Growth inhibition of human HEL cells expressing Jak2 V617F mutant after 48 hrs by MTS assay
Growth inhibition of human HEL cells expressing Jak2 V617F mutant after 48 hrs by MTS assay
|
[PMID: 21138246] |
| HEL | IC50 |
0.041 μM
Compound: 9e
|
Inhibition of Stat5 phosphorylation in human HEL cells after 1 hr by Western blotting
Inhibition of Stat5 phosphorylation in human HEL cells after 1 hr by Western blotting
|
[PMID: 21138246] |
| HEL | IC50 |
0.08 μM
Compound: 9e
|
Inhibition of Stat3 phosphorylation in human HEL cells after 1 hr by Western blotting
Inhibition of Stat3 phosphorylation in human HEL cells after 1 hr by Western blotting
|
[PMID: 21138246] |
| HEL | IC50 |
0.73 μM
Compound: AZD1480
|
Antiproliferative activity against human HEL cells harboring JAK2 V617F mutant assessed as inhibition of cell growth incubated for 72 hrs by MTT assay
Antiproliferative activity against human HEL cells harboring JAK2 V617F mutant assessed as inhibition of cell growth incubated for 72 hrs by MTT assay
|
[PMID: 33689932] |
| MDA-MB-468 | IC50 |
5.87 μM
Compound: AZD1480
|
Antiproliferative activity against human MDA-MB-468 cells overexpressing STAT3 assessed as inhibition of cell growth incubated for 72 hrs by MTT assay
Antiproliferative activity against human MDA-MB-468 cells overexpressing STAT3 assessed as inhibition of cell growth incubated for 72 hrs by MTT assay
|
[PMID: 33689932] |
| SET-2 | GI50 |
0.016 μM
Compound: 9e
|
Growth inhibition of human SET2 cells expressing Jak2 V617F mutant after 48 hrs by MTS assay
Growth inhibition of human SET2 cells expressing Jak2 V617F mutant after 48 hrs by MTS assay
|
[PMID: 21138246] |
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 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.
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
-
CAS No. 935666-88-9
-
Appearance Solid
-
Molecular Weight 348.77
-
Formula C14H14ClFN8
-
Color White to yellow
-
SMILES
ClC1=C(N=C(N=C1)N[C@@H](C)C2=NC=C(C=N2)F)NC3=NNC(C)=C3
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Publications (21)
-
Journal Impact Factor
-
Most Recent
-
Nature
2025 Jun;642(8066):201-211. PMID: 40269158 -
Cancer Res
SMAD4 and KRAS Status Shape Cancer Cell-Stromal Crosstalk and Therapeutic Response in Pancreatic Cancer. [Abstract]2025 Apr 15;85(8):1368-1389. PMID: 39841099 -
Sci Transl Med
PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. [Abstract]2018 Jul 18;10(450):eaaq1093. PMID: 30021885 -
Neuro Oncol
2017 Jan;19(1):22-30. PMID: 27402815
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.
-
Leukemia
Using combination therapy to override stromal-mediated chemoresistance in mutant FLT3-positive AML: synergism between FLT3 inhibitors, dasatinib/multi-targeted inhibitors and JAK inhibitors. [Abstract]2012 Oct;26(10):2233-44. PMID: 22469781 -
Cell Rep Med
2025 Sep 16;6(9):102324. PMID: 40897177 -
J Exp Med
2024 Mar 4;221(3):e20232028. PMID: 38284990 -
Clin Cancer Res
STAT5A/B Blockade Sensitizes Prostate Cancer to Radiation through Inhibition of RAD51 and DNA Repair. [Abstract]2018 Apr 15;24(8):1917-1931. PMID: 29483142
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.
-
Acta Pharmacol Sin
Inhibiting the Otub1/phosphorylated STAT3 axis for the treatment of non-small cell lung cancer. [Abstract]2025 Jan;46(1):184-195. PMID: 39198663 -
Biomed Pharmacother
Effects of apigenin pretreatment against renal ischemia/reperfusion injury via activation of the JAK2/STAT3 pathway. [Abstract]2017 Nov:95:1799-1808. PMID: 28962085
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.
-
Mol Cancer Ther
Enzalutamide-Induced Feed-Forward Signaling Loop Promotes Therapy-Resistant Prostate Cancer Growth Providing an Exploitable Molecular Target for Jak2 Inhibitors. [Abstract]2020 Jan;19(1):231-246. PMID: 31548294 -
J Ethnopharmacol
Fu-Zheng-Tong-Luo formula promotes autophagy and alleviates idiopathic pulmonary fibrosis by controlling the Janus kinase 2/signal transducer and activator of transcription 3 pathway. [Abstract]2023 Oct 5:314:116633. PMID: 37207878 -
J Biotechnol
2025 Mar:399:9-18. PMID: 39824361 -
J Biochem Mol Toxicol
Heme Oxygenase-1 Regulates the JAK/STAT Pathway to Inhibit Ferroptosis in Metabolic Dysfunction-Associated Steatotic Liver Disease. [Abstract]2026 Jan;40(1):e70661. PMID: 41486516 -
STAR Protoc
Protocol for high-content drug screening using tumor organoids on a 384-pillar plate platform. [Abstract]2025 Dec 1;6(4):104250. PMID: 41335519 -
-
bioRxiv
PAIRWISE: Deep Learning-based Prediction of Effective Personalized Drug Combinations in Cancer. [Abstract]2024 Nov 6:2024.11.04.621884. PMID: 39574568 -
-
J Pers Med
2022 Feb 9;12(2):249. PMID: 35207737 -
-
Solvent & Solubility
DMSO : 50 mg/mL (143.36 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
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
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
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
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Please enter the basic information of animal experiments:
-
-
-
-
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
-
%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
-
%+
-
+%Tween-80 + +
-
%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocol
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.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Purity & Documentation
-
Data Sheet (282 KB)
-
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
-
Handling Instructions (2659 KB)
References
[1]. Derenzini E, et al. The JAK inhibitor AZD1480 regulates proliferation and immunity in Hodgkin lymphoma. Blood Cancer J. 2011 Dec;1(12):e46. [Content Brief]
[2]. Scuto A, et al. The novel JAK inhibitor AZD1480 blocks STAT3 and FGFR3 signaling, resulting in suppression of human myeloma cell growth and survival. Leukemia. 2011 Mar;25(3):538-50. [Content Brief]
[3]. McFarland BC, et al. Therapeutic potential of AZD1480 for the treatment of human glioblastoma. Mol Cancer Ther. 2011 Dec;10(12):2384-93. [Content Brief]
[4]. Xin H, et al. Antiangiogenic and antimetastatic activity of JAK inhibitor AZD1480. Cancer Res. 2011 Nov 1;71(21):6601-10. [Content Brief]
[5]. Hedvat M, et al. The JAK2 inhibitor AZD1480 potently blocks Stat3 signaling and oncogenesis in solid tumors. Cancer Cell. 2009 Dec 8;16(6):487-9 [Content Brief]
[6]. Ni J, et al. Tyrosine receptor kinase B is a drug target in astrocytomas. Neuro Oncol. 2017 Jan;19(1):22-30. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.8672 mL | 14.3361 mL | 28.6722 mL | 71.6805 mL |
| 5 mM | 0.5734 mL | 2.8672 mL | 5.7344 mL | 14.3361 mL | |
| 10 mM | 0.2867 mL | 1.4336 mL | 2.8672 mL | 7.1680 mL | |
| 15 mM | 0.1911 mL | 0.9557 mL | 1.9115 mL | 4.7787 mL | |
| 20 mM | 0.1434 mL | 0.7168 mL | 1.4336 mL | 3.5840 mL | |
| 25 mM | 0.1147 mL | 0.5734 mL | 1.1469 mL | 2.8672 mL | |
| 30 mM | 0.0956 mL | 0.4779 mL | 0.9557 mL | 2.3893 mL | |
| 40 mM | 0.0717 mL | 0.3584 mL | 0.7168 mL | 1.7920 mL | |
| 50 mM | 0.0573 mL | 0.2867 mL | 0.5734 mL | 1.4336 mL | |
| 60 mM | 0.0478 mL | 0.2389 mL | 0.4779 mL | 1.1947 mL | |
| 80 mM | 0.0358 mL | 0.1792 mL | 0.3584 mL | 0.8960 mL | |
| 100 mM | 0.0287 mL | 0.1434 mL | 0.2867 mL | 0.7168 mL |