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    InvivoChem Cat #: V0611
    CAS #: 1356962-20-3Purity ≥98%

    Description: AZD-3463 (AZD3463) is a novel, potent and selective ALK/IGF1R inhibitor with potential anticancer activity. It is able to overcome multiple mechanisms of acquired resistance to crizotinib. AZD3463 inhibits neuroblastoma growth by overcoming crizotinib resistance and inducing apoptosis. AZD3463 showed significant antitumor efficacy against neuroblastoma tumors with WT and F1174L oncogenic mutant ALK in orthotopic xenograft mouse models.

    References: Sci Rep. 2016 Jan 20;6:19423; PLoS One. 2015 Nov 16;10(11):e0142704.

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    Name: AZD-3463
    CAS#: 1356962-20-3
    Chemical Formula: C24H25ClN6O
    Exact Mass: 448.17784
    Molecular Weight: 448.95
    Elemental Analysis: C, 64.21; H, 5.61; Cl, 7.90; N, 18.72; O, 3.56
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Technical InformationSynonym: AZD 3463; AZD-3463;AZD3463;  
    Chemical Name: N-(4-(4-aminopiperidin-1-yl)-2-methoxyphenyl)-5-chloro-4-(1H-indol-3-yl)pyrimidin-2-amine.
    InChi Code: InChI=1S/C24H25ClN6O/c1-32-22-12-16(31-10-8-15(26)9-11-31)6-7-21(22)29-24-28-14-19(25)23(30-24)18-13-27-20-5-3-2-4-17(18)20/h2-7,12-15,27H,8-11,26H2,1H3,(H,28,29,30)

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    In Vitro

    In vitro activity: AZD3463 is potent in ALK-driven preclinical models and in a variety of crizotinib-resistant models. AZD3463 inhibits ALK in cells as demonstrated by its ability to decrease ALK autophosphorylation in tumor cell lines containing ALK fusions including DEL (ALCL NPM-ALK), H3122 (NSCLC EML4-ALK) and H2228 (NSCLC EML4-ALK). Inhibition of ALK is associated with perturbations in downstream signaling including ERK, AKT and STAT3 pathways leading to preferential inhibition of proliferation in the ALK fusion containing cell lines in vitro. AZD3463 retains good activity against a number of clinically relevant crizotinib resistant mutations including the gatekeeper mutant L1196M where equivalent potency to wild type ALK is observed in vitro and in vivo in EML4-ALK containing BAF3 cell lines. To further assess the potential ability of AZD3463 to overcome additional resistance mechanisms, antiproliferative activity is assessed in multiple crizotinib resistant cell lines independently derived in vitro from H3122 cells as well as a patient derived crizotinib relapsed model. These resistant cell lines contain multiple resistance mechanisms including the L1196M gatekeeper and T115Ins mutations, ALK amplification and/or secondary drivers including EGFR and IGF1R. AZD3463 retains antiproliferative potency within 4 fold of parental H3122 cells for 10 out of 12 of these acquired resistance models in vitro.

    Kinase Assay: ZD-3463 is an ALK/IGF1R inhibitor which overcomes multiple mechanisms of acquired resistance to crizotinib. 

    In VivoAZD3463 (15 mg/kg, i.p. injection) showed significant therapeutic efficacy on the growth of the neuroblastoma tumors with WT and F1174L oncogenic mutant ALK in orthotopic xenograft mouse models
    Animal modelMice
    Formulation & Dosage15 mg/kg, i.p. 

    Sci Rep. 2016 Jan 20;6:19423; PLoS One. 2015 Nov 16;10(11):e0142704.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    AZD3463 shows cytotoxic effects on NB cell lines.  2016 Jan 20;6:19423. 


    AZD3463 suppresses anchorage-independent growth of NB cells.  2016 Jan 20;6:19423. 


    AZD3463 enhances the cytotoxic effect of Dox on NB cell lines.  2016 Jan 20;6:19423. 


    AZD3463 inhibits tumor growth in different orthotopic NB xenograft mouse models.  2016 Jan 20;6:19423. 


    AZD3463 inhibits the downstream signaling pathway of ALK, PI3K/AKT/mTOR, and induces apoptosis and autophagy in NB cells.IMR-32, NGP, SH-SY5Y and SK-N-AS cells were treated with 10 μM of AZD3463 for various time points (0–4 hrs), subjected to SDS-PAGE, and then immunoblotted with PARP, p-Akt, Akt, p-S6, S6, Caspase 3, LC3A/B, and β-Actin antibodies.  2016 Jan 20;6:19423. 


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