AZ 960

JAKs inhibitor CAS# 905586-69-8

AZ 960

Catalog No. BCC2197----Order now to get a substantial discount!

Product Name & Size Price Stock
AZ 960: 5mg $414 In Stock
AZ 960: 10mg Please Inquire In Stock
AZ 960: 20mg Please Inquire Please Inquire
AZ 960: 50mg Please Inquire Please Inquire
AZ 960: 100mg Please Inquire Please Inquire
AZ 960: 200mg Please Inquire Please Inquire
AZ 960: 500mg Please Inquire Please Inquire
AZ 960: 1000mg Please Inquire Please Inquire
Related Products
  • NVP-BSK805

    Catalog No.:BCC1815
    CAS No.:1092499-93-8
  • LY2784544

    Catalog No.:BCC2200
    CAS No.:1229236-86-5
  • CEP-33779

    Catalog No.:BCC2199
    CAS No.:1257704-57-6
  • BMS-911543

    Catalog No.:BCC2204
    CAS No.:1271022-90-2
  • NSC 33994

    Catalog No.:BCC2441
    CAS No.:82058-16-0

Quality Control of AZ 960

Number of papers citing our products

Chemical structure

AZ 960

3D structure

Chemical Properties of AZ 960

Cas No. 905586-69-8 SDF Download SDF
PubChem ID 25099184 Appearance Powder
Formula C18H16F2N6 M.Wt 354.36
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : ≥ 30 mg/mL (84.66 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 5-fluoro-2-[[(1S)-1-(4-fluorophenyl)ethyl]amino]-6-[(5-methyl-1H-pyrazol-3-yl)amino]pyridine-3-carbonitrile
SMILES CC1=CC(=NN1)NC2=C(C=C(C(=N2)NC(C)C3=CC=C(C=C3)F)C#N)F
Standard InChIKey SUNXHXDJOIXABJ-NSHDSACASA-N
Standard InChI InChI=1S/C18H16F2N6/c1-10-7-16(26-25-10)23-18-15(20)8-13(9-21)17(24-18)22-11(2)12-3-5-14(19)6-4-12/h3-8,11H,1-2H3,(H3,22,23,24,25,26)/t11-/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of AZ 960

DescriptionAZ 960 is a potent, selective and ATP competitive inhibitor of JAK2 with Ki value of 0.45 nM.
TargetsJAK2    
IC500.45 nM (Ki)     

Protocol

Cell Assay [2]
AZ960 is dissolved in 100% DMSO to a 0.01 M. HTLV-1–infected T cells and MOLT-4 cells are cultured with various concentrations of AZ960 (0.03-1 μM) for 2 days in 96-well plates. Peripheral blood lymphocytes are activated by phytohemagglutinin (PHA; 5 ng/mL) for 1 hour, then cultured with various concentrations of AZ960 (0.03–1 μM) for 2 days in 96-well plates. After culture, cell number and viability are evaluated by measuring the mitochondrial-dependent conversion of the MTT to a colored formazan product[2].

References:
[1]. Ikezoe T, et al. Expression of p-JAK2 predicts clinical outcome and is a potential molecular target of acute myelogenous leukemia. Int J Cancer. 2011 Nov 15;129(10):2512-21. [2]. Yang J, et al. AZ960, a novel Jak2 inhibitor, induces growth arrest and apoptosis in adult T-cell leukemia cells. Mol Cancer Ther. 2010 Dec;9(12):3386-95. [3]. Valenciano AL, et al. Discovery and antiparasitic activity of AZ960 as a Trypanosoma brucei ERK8 inhibitor. Bioorg Med Chem. 2016 Oct 1;24(19):4647-51. [4]. Gozgit JM, et al. Effects of the JAK2 inhibitor, AZ960, on Pim/BAD/BCL-xL survival signaling in the human JAK2 V617F cell line SET-2. J Biol Chem. 2008 Nov 21;283(47):32334-43.

AZ 960 Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

AZ 960 Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of AZ 960

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.822 mL 14.1099 mL 28.2199 mL 56.4398 mL 70.5497 mL
5 mM 0.5644 mL 2.822 mL 5.644 mL 11.288 mL 14.1099 mL
10 mM 0.2822 mL 1.411 mL 2.822 mL 5.644 mL 7.055 mL
50 mM 0.0564 mL 0.2822 mL 0.5644 mL 1.1288 mL 1.411 mL
100 mM 0.0282 mL 0.1411 mL 0.2822 mL 0.5644 mL 0.7055 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on AZ 960

AZ960 is a novel inhibitor of janus-associated kinases (JAKs) that exhibits a potent inhibition against janus kinase 2 (JAK2) with the value of inhibition constant of Ki of 0.45 nmol/L. It also exhibits a lesser inhibitory effects against other JAKs family members, including JAK1, JAK3 and TYK2 as well as other kinases, including TrkA, Aurora A and FAK, with 50% inhibition concentration IC50 of around 0.1 μmol/L. In recent studies, AZ960 demonstrates potential anti-cancer activity against adult T-cell leukemia (ATL), an aggressive malignancy of CD4+ T lymphocytes, by effectively inducing growth arrest and apoptosis in human T-cell lumphotropic virus type 1 (HTLV-1) infected T cells.

Reference

Yang J, Ikezoe T, Nishioka C, Furihata M, Yokoyama A. AZ960, a novel Jak2 inhibitor, induces growth arrest and apoptosis in adult T-cell leukemia cells. Mol Cancer Ther. 2010;9(12):3386-3395.

Featured Products
New Products
 

References on AZ 960

Discovery and antiparasitic activity of AZ960 as a Trypanosoma brucei ERK8 inhibitor.[Pubmed:27519462]

Bioorg Med Chem. 2016 Oct 1;24(19):4647-4651.

Human African trypanosomiasis (HAT) is a lethal, vector-borne disease caused by the parasite Trypanosoma brucei. Therapeutic strategies for this neglected tropical disease suffer from disadvantages such as toxicity, high cost, and emerging resistance. Therefore, new drugs with novel modes of action are needed. We screened cultured T. brucei against a focused kinase inhibitor library to identify promising bioactive compounds. Among the ten hits identified from the phenotypic screen, AZ960 emerged as the most promising compound with potent antiparasitic activity (IC50=120nM) and was shown to be a selective inhibitor of an essential gene product, T. brucei extracellular signal-regulated kinase 8 (TbERK8). We report that AZ960 has a Ki of 1.25muM for TbERK8 and demonstrate its utility in establishing TbERK8 as a potentially druggable target in T. brucei.

AZ960, a novel Jak2 inhibitor, induces growth arrest and apoptosis in adult T-cell leukemia cells.[Pubmed:21159615]

Mol Cancer Ther. 2010 Dec;9(12):3386-95.

Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive disease in which the Jak2/Stat5 pathway is constitutively activated. This study found that AZ960, a novel inhibitor of Jak2 kinase, effectively induced growth arrest and apoptosis of human T-cell lymphotropic virus type 1, HTLV-1-infected T cells (MT-1 and MT-2) in parallel with downregulation of the phosphorylated forms of Jak2 and Bcl-2 family proteins including Bcl-2 and Mcl-1. Interestingly, AZ960 increased levels of Bcl-xL in MT-1 and MT-2 cells in association with accumulation of cAMP response element-binding protein bound to the Bcl-xL promoter as measured by chromatin immunoprecipitation assay. Importantly, genetic inhibition of Bcl-xL by a small interfering RNA potentiated antiproliferative effects of AZ960 in MT-1 cells. Taken together, Jak2 is an attractive molecular target for treatment of ATL. Concomitant blockade of Jak2 and Bcl-xL may be a promising treatment strategy for this lethal disease.

Expression of p-JAK2 predicts clinical outcome and is a potential molecular target of acute myelogenous leukemia.[Pubmed:21207414]

Int J Cancer. 2011 Nov 15;129(10):2512-21.

Our study determined if Janus kinase 2 (JAK2) was activated in acute myelogenous leukemia (AML; n = 77, excluding acute promyelocytic leukemia) by immunohistochemistry (IHC) using a phosphor-specific antibody against JAK2. p-JAK2 was detectable in all cases, although its levels varied between patient samples (high levels, n = 31; low levels, n = 46). The quantification of levels of p-JAK2 by IHC was well correlated with that assessed by Western blot analyses and fluorescence-activated cell sorting (FACS). Levels of p-JAK2 were directly correlated with high white blood cell count (52.3 x 10(3) /L in patients with high p-JAK2 vs. 28.3 x 10(3) /L in patients with low p-JAK2, p < 0.01) and were inversely correlated with complete remission rates (45% in patients with high p-JAK2 vs. 78% in patients with low p-JAK2, p < 0.003). In addition, multivariate analysis confirmed that high levels of p-JAK2 remained a significant factor for overall survival (hazard ratio = 2.213; 95% confidence interval, 1.212-4.041, p = 0.023). Moreover, we found that AZ960, a novel and specific inhibitor of the JAK2 kinase, potently inhibited the clonogenic growth and induced apoptosis of freshly isolated AML cells from patients in association with cleavage of caspase 3 and downregulation of anti-apoptotic Bcl-xL proteins. Taken together, JAK2 may be a promising molecular target for treatment of AML.

Effects of the JAK2 inhibitor, AZ960, on Pim/BAD/BCL-xL survival signaling in the human JAK2 V617F cell line SET-2.[Pubmed:18775810]

J Biol Chem. 2008 Nov 21;283(47):32334-43.

The Janus-associated kinase 2 (JAK2) V617F mutation is believed to play a critical role in the pathogenesis of polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis. We have characterized a novel small molecule JAK2 inhibitor, AZ960, and used it as a tool to investigate the consequences of JAK2 V617F inhibition in the SET-2 cell line. AZ960 inhibits JAK2 kinase with a K(i) of 0.00045 microm in vitro and treatment of TEL-JAK2 driven Ba/F3 cells with AZ960 blocked STAT5 phosphorylation and potently inhibited cell proliferation (GI(50)=0.025 microm). AZ960 demonstrated selectivity for TEL-JAK2-driven STAT5 phosphorylation and cell proliferation when compared with cell lines driven by similar fusions of the other JAK kinase family members. In the SET-2 human megakaryoblastic cell line, heterozygous for the JAK2 V617F allele, inhibition of JAK2 resulted in decreased STAT3/5 phosphorylation and inhibition of cell proliferation (GI(50)=0.033 microm) predominately through the induction of mitochondrial-mediated apoptosis. We provide evidence that JAK2 inhibition induces apoptosis by direct and indirect regulation of the anti-apoptotic protein BCL-xL. Inhibition of JAK2 blocked BCL-XL mRNA expression resulting in a reduction of BCL-xL protein levels. Additionally, inhibition of JAK2 resulted in decreased PIM1 and PIM2 mRNA expression. Decreased PIM1 mRNA corresponded with a decrease in Pim1 protein levels and inhibition of BAD phosphorylation at Ser(112). Finally, small interfering RNA-mediated suppression of BCL-xL resulted in apoptotic cell death similar to the phenotype observed following JAK2 inhibition. These results suggest a model in which JAK2 promotes cell survival by signaling through the Pim/BAD/BCL-xL pathway.

Description

AZ960 is a potent and specific inhibitor of the JAK2 kinase with a Ki of 0.45 nM.

Keywords:

AZ 960,905586-69-8,Natural Products,JAK, buy AZ 960 , AZ 960 supplier , purchase AZ 960 , AZ 960 cost , AZ 960 manufacturer , order AZ 960 , high purity AZ 960

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: