Vistusertib (AZD2014)


Vistusertib (AZD2014)化学構造


Vistusertib (AZD2014)は一種の新たなmTOR阻害剤で、無細胞試験でIC50値が2.8 nMになって、多種なPI3K亜型(α/β/γ/δ)に高選択性を表します。臨床2期。

サイズ 価格(税別) 在庫  
JPY 28220.00 あり
JPY 44820.00 あり


  • Murine macrophages were treated with AZD2014 (10 nm) or rapamycin (10 ng/ml) for the time periods indicated. B, immunoblot analysis of whole cell lysate performed using an antibody detecting total ERK and phospho-ERK (Thr202/Tyr204). C, detection of MKP-1. Immunoblot analysis of whole cell lysate performed using an antibody against MKP-1 and β-actin.

    J Biol Chem 2013 288(47), 33966-77. Vistusertib (AZD2014) purchased from Selleck.

    Accumulation of autophagosomes in the cytoplasm after 72 h treatment with WORT, CQ, AZD2014 or TMX or their combination with DOX, was visualized after anti-LC3 antibody labeling.

    Histochem Cell Biol, 2017. Vistusertib (AZD2014) purchased from Selleck.

  • AZD-2014 potentiates resminostat's cytotoxicity against human HCC cells. Established HCC cell lines (HepG2, SMMC-7721 and Hep3B), primary HCC cells (two lines, "HCC-1/-2") or the HL-7702 hepatocytes were treated with resminostat (at applied concentrations) or plus AZD-2014 ("AZD", 10 nM), cells were further cultured and subjected to MTT assay (A, E and F), trypan blue staining assay (B) and proliferation assays (C and D); p-mTOR (Ser-2448) and regular mTOR expression was tested by Western blots (A, upper panel). Data represented the means of three independent experiments ± SD (Same for all figures). For each assay, n = 5 (Same for all figures). "CTRL" indicated untreated control group (Same for all figures). "Veh" indicated vehicle (0.1% DMSO) (AeD). "Rsm" indicated resminostat (E). # indicated statistically significant differences as compared to "CTRL" group. * indicated statistically significant differences as compared to "resminostat" only group.

    Biochem Biophys Res Commun, 2016, 477(4):556-62. Vistusertib (AZD2014) purchased from Selleck.

    Tumor growth inhibition studies were performed in SCID mice. Mice bearing 300 mm3 tumors were randomly divided into two groups and were treated with 5 mg/kg AZD-2014 (PO, QD x 14; n = 10, the dose was based on results from pre-experiments) or vehicle (saline, PO, QD x 14; n = 10). After AZD-2014 administration, tumor tissues were isolated and lysed, activation of Akt and mTORC1/2 was tested by Western blot.

    Biochem Biophys Res Commun, 2014, 443(2): 406-12. Vistusertib (AZD2014) purchased from Selleck.

  • Biochem Biophys Res Commun 2014 443(2), 406-12. Vistusertib (AZD2014) purchased from Selleck.

    Biochem Biophys Res Commun 2014 443(2), 406-12. Vistusertib (AZD2014) purchased from Selleck.

  • Biochem Biophys Res Commun 2014 443(2), 406-12. Vistusertib (AZD2014) purchased from Selleck.

    Biochem Biophys Res Commun 2014 443(2), 406-12. Vistusertib (AZD2014) purchased from Selleck.

  • HT-29 cells were treated with vehicle or AZD-2014 (50 nM) for 72 h, cell cycle distribution was analyzed by FACS.

    Biochem Biophys Res Commun 2014 443, 406-12. Vistusertib (AZD2014) purchased from Selleck.

    HT-29 cells were treated with vehicle ("Ctrl") or different concentrations of AZD-2014 for 72 h.

    Biochem Biophys Res Commun 2014 443, 406-12. Vistusertib (AZD2014) purchased from Selleck.

  • Autophagy in NCI-H460 (C, D) and NCI-H460/R (E, F) cells was assessed by fluorescence microscopy. Cells were stained with acridine orange to detect the presence of acidic autophagosomes (acridin orange shifts its fluorescence emission from green to red when found in acidic compartments). Nuclei were counterstained with Hoechst 33342 (blue). Number of autophagosomes increased in NCI-H460 cells (D) after 18 h of 250 nM ADZ2014 treatment, in comparison with untreated cells (C). NCI-H460/R cells treated with 100 nM AZD2014 for 18 h also showed increased number of autophagosomes in the cytoplasm (F) when compared to untreated cells (E).

    2013 Dr. Milica Pesic from Institute for Biological Research. Vistusertib (AZD2014) purchased from Selleck.

    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).

    2013 Dr. Milica Pesic from Institute for Biological Research. Vistusertib (AZD2014) purchased from Selleck.




製品説明 Vistusertib (AZD2014)は一種の新たなmTOR阻害剤で、無細胞試験でIC50値が2.8 nMになって、多種なPI3K亜型(α/β/γ/δ)に高選択性を表します。臨床2期。
mTOR [1]
(Cell-free assay)
P-Akt (S473) [1]
(Cell-free assay)
pS6 (S235/236) [1]
(Cell-free assay)
2.8 nM 80 nM 200 nM

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]

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HEK293 cells M{PoTmZ2dmO2aX;uJIF{e2G7 M{DEUGlvcGmkaYTpc44hd2ZicnXjc41jcW6jboSgSmxCTy22YXfn[YQhdVSRUjCoNVM3OiC2bzCyOVQ6MSBqdX7rco94diCxcnnnbY4qKGW6cILld5Nm\CCrbjDISWszQTNiY3XscJMtKEmFNUC9Nk45KG6P NH[5TWMzOzN5NUe5Ny=>
human MDA-MB-468 cells NGjOTJhHfW6ldHnvckBie3OjeR?= NIXXcZczKGh? NGnQfmhKdmirYnn0bY9vKG:oIH3UU3JEOiCrbjDoeY1idiCPRFGtUWIuPDZ6IHPlcIx{KGG|c3Xzd4VlKGG|IILl[JVkfGmxbjDv[kBCU1RicHjvd5Bpd3K7bHH0bY9vKGG2IGPldlQ4OyCjZoTldkAzKGi{czygTWM2OD1yLkC4JO69VQ>? NUW0UGVmOjN|N{W3PVM>
human MDA-MB-468 cells MX3GeY5kfGmxbjDhd5NigQ>? MYCyJIg> MnX1TY5pcWKrdHnvckBw\iCvVF;SR|EhcW5iaIXtZY4hVUSDLV3CMVQ3QCClZXzsd{Bie3Onc4Pl[EBieyC{ZXT1Z5Rqd25ib3[gdHM3KHCqb4PwbI9zgWyjdHnvckBifCCVZYKyN|UwOjN4IHHmeIVzKDJiaILzMEBKSzVyPUCuNkDPxE1? MkPiNlM{PzV5OUO=
human MCF7 cells NIriT3VHfW6ldHnvckBie3OjeR?= MkT1TY5pcWKrdHnvckBw\iCvVF;SR|EhcW5iaIXtZY4hVUOINzDj[YxteyC6ZX7v[5Ji\nSnZDDtc5V{\SCjc4Pld5Nm\CCjczDtc4R2dGG2aX;uJJN2[nO2cnH0[S=> NEHmVJYzOzN5NUe5Ny=>


体内試験 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]


溶解度 (25°C)

体外 DMSO 38 mg/mL (82.15 mM)
Water Insoluble
Ethanol Insoluble
体内 順序で溶剤を入れること:
5% DMSO+30% PEG 300+ddH2O

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。


分子量 462.54


CAS No. 1009298-59-2
別名 N/A





マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)


  • マス




貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1



  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):




チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2


マス 濃度 ボリューム 分子量


NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02831257 Recruiting Neurofibromatosis 2|Meningioma Massachusetts General Hospital|AstraZeneca|United States Department of Defense July 2016 Phase 2
NCT02780830 Withdrawn Core: Relapsed or Refractory Diffuse Large B-Cell Lymphoma|Module 1: Non-GCB Diffuse Large B-Cell Lymphoma AstraZeneca June 2016 Phase 1
NCT02813135 Recruiting Children, Adolescents and Young Adults With Refractory or Recurrent Malignancies Gustave Roussy, Cancer Campus, Grand Paris|National Cancer Institute, France June 2016 Phase 1|Phase 2
NCT02730923 Recruiting Endometrial Carcinoma|Metastatic Carcinoma|Hormone Receptor Positive Tumor Centre Leon Berard April 2016 Phase 1|Phase 2
NCT02640755 Active, not recruiting Solid Malignancies AstraZeneca|Quintiles, Inc. January 2016 Phase 1
NCT02599714 Recruiting Advanced and Metastatic Breast Cancer AstraZeneca|SCRI Development Innovations, LLC December 2015 Phase 1|Phase 2



Handling Instructions


  • * 必須


  • 問題1:

    I am looking for a i.p. or i.v. formula of AZD2014. Any suggestion?

  • 回答:

    S2783 AZD2014 can be dissolved in 5% DMSO/30% PEG 300/ddH2O at 5 mg/ml as a clear solution for I.P. use.


mTOR Inhibitors with Unique Features


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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID