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Cat. No. M1666
AZD8055 Structure
Size Price Availability Quantity
Free Sample 0.5 mg  USD 0 In stock
10mM*1mL in DMSO USD 44  USD44 In stock
5mg USD 40  USD40 In stock
10mg USD 60  USD60 In stock
25mg USD 110  USD110 In stock
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Quality Control
Biological Activity

AZD8055 is a novel ATP-competitive inhibitor of mTOR kinase (both complexes mTORC1 and mTORC2) with an IC50 of 0.8 nM.Particularly,AZD8055 fully inhibited multisite eIF4E-binding protein1 phosphorylation,subsequently blocking protein translation, which was in contrast to the effects of rapamycin. In addition, the mTORC1-dependent PI3K/Akt feedback activation was fully abrogated in AZD8055-treated AML cells. Significantly, AZD8055 decreased AML blast cell proliferation and cell cycle progression, reduced the clonogenic growth of leukemic progenitors and induced caspase-dependent apoptosis in leukemic cells but not in normal immature CD34+ cells.

Product Citations
Customer Product Validations & Biological Datas
Source Cell Death & Disease (2018). Figure 2. AZD8055 (Abmole Bioscience)
Method colony formation assays
Cell Lines MDA-MB-231, MDA-MB-157, and MDA-MB-468 cells
Concentrations 1 μM
Incubation Time 24 h
Results The results showed that AZD8055 or BEZ235 in combination with ABT263 strongly inhibited cell proliferation in different TNBC cell lines.
Source Cell Death & Disease (2018). Figure 1. AZD8055 (Abmole Bioscience)
Method Immunoblotting analysis
Cell Lines TNBC cell lines
Concentrations 1 μM
Incubation Time 24 h
Results We found the mTOR inhibitors, especially the BEZ235 and AZD8055, could significantly inhibit the phosphorylation of AKT and 4EBP1 and efficiently led to decreasing MCL-1 expression.
Source Proc Natl Acad Sci U S A. (2015). Figure 3. ABT-263 and AZD8055 were purchased from Active Biochemicals (Hong Kong, China) and Abmole Bioscience (Houston, TX)
Method FACS analysis(Apoptosis), Western blotting, Immunoprecipitation (IP),Traditional human cell-line xenograft experiments
Cell Lines SCLC H82 and H1048 cells
Concentrations 500 nM AZD8055, 1 μM ABT-263
Incubation Time 2,16, 72h
Results Combination treatment with ABT-263 and the TORC1/2 inhibitor AZD8055 leads to robust apoptosis and antitumor activity in vivo.
Source Proc Natl Acad Sci U S A. (2015). Figure 2. ABT-263 and AZD8055 were purchased from Active Biochemicals (Hong Kong, China) and Abmole Bioscience (Houston, TX)
Method FACS analysis(Apoptosis),quantitative (q)RT-PCR, Western blotting, Immunoprecipitation (IP)
Cell Lines SCLC SW1271 and H1048 cells
Concentrations 1µM
Incubation Time 6,48,72h
Results BIM and MCL-1 mediate ABT-263–induced apoptosis in SCLC, and the ratio of BIM to MCL-1 expression predicts the magnitude of apoptosis in SCLC cell lines.
Source Proc Natl Acad Sci U S A. (2015). Figure 1. ABT-263 and AZD8055 were purchased from Active Biochemicals (Hong Kong, China) and Abmole Bioscience (Houston, TX)
Method quantitative (q)RT-PCR
Cell Lines SCLC cell lines
Concentrations 1µM
Incubation Time 72h
Results we found a modest, but significant, correlation between BIM expression and sensitivity to ABT-263.ABT-263 across both data sets (SI Appendix, Fig. S1 B and C). However, the ratio of BIM to MCL-1 predicted sensitivity to ABT-263 more effectively than the expression of either biomarker alone. SCLC lines have increased BIM expression compared with other solid tumor types along with enhanced sensitivity to ABT-263 compared with other solid tumor types across a large panel of cancer cell lines.
Cell Experiment
Cell lines H838 and A549 cells line
Preparation method Growth inhibition and autophagy analysis. For growth inhibition and acridine staining, cells were exposed to increasing concentrations of AZD8055 for 72 to 96 h and stained for cell nuclei (0.03 mg/mL Hoechst 33342) and acidic vesicles (1 μg/mL acridine orange). Images were captured at 450 and 536 nm on an ArrayScan II (Cellomics) platform, and the percentage of acidic vesicles and the number of cells were quantified. For LC3 assessment, cells were exposed to e64d/pepstatin (10 μg/mL) for 30 to 90 min before incubation with AZD8055. Cells were lysed on ice and analyzed by immunoblotting.
Concentrations 0–3 μmol/L
Incubation time 72~96 h
Animal Experiment
Animal models Mice bearing U87-MG xenografts or A549 xenografts
Formulation dissolved in captisol (CyDex) and diluted to a final captisol concentration of 30% (w/v)
Dosages 0.1 mL/10 g of body weight once or twice daily
Administration oral gavage
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

Chemical Information
Molecular Weight 465.54
Formula C25H31N5O4
CAS Number 1009298-09-2
Purity 99.45%
Solubility DMSO 50 mg/mL
Storage at -20°C

[1] Asahina et al. Invest New Drugs. Safety and tolerability of AZD8055 in Japanese patients with advanced solid tumors; a dose-finding phase I study.

[2] Holt et al. Cancer Res. Enhanced apoptosis and tumor growth suppression elicited by combination of MEK (selumetinib) and mTOR kinase inhibitors (AZD8055).

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Keywords: AZD8055 supplier, mTOR, inhibitors

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