AZD2014

AZD2014 is a novel mTOR inhibitor with IC50 of 2.8 nM; highly selective against multiple PI3K isoforms (α/β/γ/δ). Phase 2.

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AZD2014 Chemical Structure

AZD2014 Chemical Structure
Molecular Weight: 462.54

Validation & Quality Control

Customer Reviews(4)

Quality Control & MSDS

Related Compound Libraries

AZD2014 is available in the following compound libraries:

Product Information

  • Inhibition Profile
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  • Research Area

Product Description

Biological Activity

Description AZD2014 is a novel mTOR inhibitor with IC50 of 2.8 nM; highly selective against multiple PI3K isoforms (α/β/γ/δ). Phase 2.
Targets mTOR
IC50 2.8 nM [1]
In vitro AZD2014 is a close analogue of AZD8055 and a selective inhibitor of mTOR kinase. AZD2014 has greater inhibitory activity against mTORC1 compared to rapamycin: AZD2014 decreases p4EBP1 Thr37/46, inhibits the translation initiation complex and decreases overall protein synthesis while rapamycin has no effect. AZD2014 also inhibits the mTORC2 biomarkers pAKTSer473 and pNDRG1Thr346. AZD2014 has broad antiproliferative activity across multiple tumour cell lines. In particular, AZD2014 induces growth inhibition and cell death in breast cancer cell lines, including ER+ cell lines with acquired resistance to hormone therapy. [1]
In vivo AZD2014 induces tumour growth inhibition against several xenograft models including a human primary explant model of ER+ breast cancer refractory to tamoxifen. The antitumour activity is associated with modulation of both mTORC1 and mTORC2 substrates. [1]
Features

Protocol(Only for Reference)

1

References

Clinical Trial Information( data from http://clinicaltrials.gov)

NCT Number Recruitment Conditions Sponsor
/Collaborators
Start Date Phases
NCT01026402 Recruiting Advanced Solid Malignancies AstraZeneca 2009-12 Phase 1
NCT01597388 Recruiting Advanced Metastatic Breast Cancer AstraZeneca 2012-05 Phase 1
NCT01793636 Recruiting Metastatic Clear Cell Renal Carcinoma Queen Mary University of London|AstraZeneca|Cancer Research UK 2013-02 Phase 2

Chemical Information

Download AZD2014 SDF
Molecular Weight (MW) 462.54
Formula

C25H30N6O3

CAS No. 1009298-59-2
Storage 3 years -20℃Powder
6 months-80℃in DMSO
Syonnyms N/A
Solubility (25°C) * In vitro DMSO 38 mg/mL (82 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 30% PEG400/0.5% Tween80/5% propylene glycol, 30 mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Chemical Name 3-(2,4-bis((S)-3-methylmorpholino)pyrido[2,3-d]pyrimidin-7-yl)-N-methylbenzamide

Preparing Stock Solutions

Stock Solution (1ml DMSO) 1mM 10mM 20mM 30mM
Mass(mg) 0.46254 4.6254 9.2508 13.8762

Research Area

Customer Reviews (4)


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Rating
Source Dr Milica Pesic from Institute for Biological Research. AZD2014 purchased from Selleck
Method Western blot
Cell Lines NCI-H460 cells /NCI-H460/R cells
Concentrations 100/250 nM
Incubation Time 18 h
Results Concentration-dependent cell growth inhibition induced by AZD2014 did not differ between sensitive (NCI-H460) and multi-drug resistant (NCI-H460/R) human non-small cell lung carcinoma cell lines (A). AZD2014 cell growth inhibition efficacy decreased in multi-drug resistant colorectal carcinoma cell line DLD1-TxR in comparison to its sensitive counterpart DLD1 (B). The results were obtained by the Sulforhodamine B assay. All values represent average ?SD obtained from two independent experiments, n = 5. (DLD1 possesses mutated p53, while its resistant counterpart DLD1-TxR additionally acquired the LOH in PTEN gene during the course of resistance induction.)

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Rating
Source Biochem Biophys Res Commun. 2014 Jan 10;443(2):406-12. AZD2014 purchased from Selleck
Method FACS
Cell Lines HT-29 cells
Concentrations 50 nM
Incubation Time 72 h
Results HT-29 cells were treated with vehicle or AZD-2014 (50 nM) for 72 h, cell cycle distribution was analyzed by FACS. AZD-2014 could arrest cells in G2 and G0/G1 phases.

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Rating
Source Biochem Biophys Res Commun. 2014 Jan 10;443(2):406-12. AZD2014 purchased from Selleck
Method MTT
Cell Lines HT-29 cells
Concentrations 1-100 nM
Incubation Time 72 h
Results HT-29 cells were treated with vehicle ("Ctrl") or different concentrations of AZD-2014 for 72 h. AZD-2014 dose-dependently inhibited HT-29 cell growth.

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Rating
Source Dr Milica Pesic from Institute for Biological Research. AZD2014 purchased from Selleck
Method
Cell Lines Sea urchin embryo
Concentrations
Incubation Time 24 h
Results The effects of SelleckChem inhibitors on sea urchin embryo development evaluated 24 h after fertilization. All compounds were added to embryos suspension 20 min after fertilization. The relative presence of late gastrula, swimming blastula, undeveloped embryos and dead embryos was compared next to untreated control embryos (A). Fertilized egg, swimming blastula and late gastrula are illustrated (B). The embryonic development was relatively synchronized in untreated control samples after 24 h (A, E). GSK690693 treatment sustained the development of embryos. Swimming blastulas kept normal motility regardless the deformities in their shape. Tipifarnib treatment induced significant toxicity due to occurrence of dead fragmented embryos. Some abnormal blastulas kept the motility. AZD2014 treatment sustained the development of embryos. Some developed gastrulas and blastulas were less motile in comparison with control (A, C). WZ811 was the least toxic compound. Significant number of gastrulas and blastulas was developed. However, their motility was considerably suppressed (A, D). In contrast to SelleckChem inhibitors, classic anticancer agent – cisplatin was extremely toxic to sea urchin embryos (A). Cisplatin killed many embryos, while a small amount of survived embryos was stopped at early phases of development: immediately after fertilization or after first and second division (A, F).

Product Citations (3)

Tech Support & FAQs

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