1. Protein Tyrosine Kinase/RTK
  2. ALK

Alectinib (Synonyms: CH5424802; AF802)

Cat. No.: HY-13011 Purity: 99.34%
Handling Instructions

Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM.

For research use only. We do not sell to patients.

Alectinib Chemical Structure

Alectinib Chemical Structure

CAS No. : 1256580-46-7

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Free Sample (0.5-1 mg)   Apply now  
10 mM * 1 mL in DMSO USD 79 In-stock
Estimated Time of Arrival: December 31
5 mg USD 72 In-stock
Estimated Time of Arrival: December 31
10 mg USD 90 In-stock
Estimated Time of Arrival: December 31
50 mg USD 120 In-stock
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100 mg USD 192 In-stock
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200 mg USD 312 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Other Forms of Alectinib:

    Alectinib purchased from MCE. Usage Cited in: Cancer Lett. 2017 Aug 1;400:61-68.

    Alectinib inhibits PI3K/Akt/mTOR signaling and induces apoptosis in NB cells. NB-19, Kelly, IMR-32, SH-SY5Y, SK-N-AS and LA-N-6 cells are treated with 10 mM alectinib for various time points as indicated. The anti-b-Actin antibody is used as a loading control for whole cell extracts.

    Alectinib purchased from MCE. Usage Cited in: Cancer Lett. 2017 Aug 1;400:61-68.

    In contrast to tumors treated with DMSO, tumors treated with Alectinib exhibits significantly decreased levels of p-Akt and p-S6. Furthermore, increased PARP and Caspase 3 cleavages are observed in tumors treated with Alectinib compared to controls.

    Alectinib purchased from MCE. Usage Cited in: Cell Death Discov. 2018 May 10;4:56.

    NB39-nu cells are treated with either 1000 nM Crizotinib (CR) or Alectinib (AL) for the indicated times and subjected to immunoblot analysis. CLTC is the loading control.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References


    Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with an IC50 of 1.9 nM.

    IC50 & Target

    IC50: 1.9 nM(ALK), 1 nM (ALKF1174L), 3.5 nM (ALKR1275Q)[1]
    Kd: 2.4 nM (ALK)[1]

    In Vitro

    Alectinib (CH5424802) prevents autophosphorylation of ALK in NCI-H2228 NSCLC cells expressing EML4-ALK, and Alectinib also results in substantial suppression of phosphorylation of STAT3 and AKT, but not of ERK1/2[1]. Alectinib (CH5424802) shows high kinase selectivity and strong anti-proliferative activity against KARPAS-299 with an IC50 value of 3 nM[2].

    In Vivo

    In the NCI-H2228 model, once-daily oral administration of Alectinib (CH5424802) results in dose-dependent tumor growth inhibition (ED50=0.46 mg/kg) and tumor regression. Treatment of 20 mg/kg Alectinib shows rapid tumor regression (168% tumor growth inhibition; p<0.001), the tumor volume in any mouse is <30 mm3 after 11 days of treatment (at day 28), a potent antitumor effect is maintained, and tumor re-growth dpes not occur throughout the 4-week drug-free period[1]. Oral administration of Alectinib (CH5424802) at 20 mg/kg displays significant tumor regression without body weight loss in an established ALK fusion gene-positive NSCLC xenograft model in mice[2]. Alectinib (Alectinib) at 60 mg/kg causes tumor regression against EML4-ALK-positive NCI-H2228 xenograft model and decreases the levels of phosphorylated ALK in this model. In addition, in mice at dose levels up to 60 mg/kg of CH5424802, there is no body weight loss, no significant change in peripheral blood cell count, no elevations of aspartate aminotransferase or alanine aminotransferase, and no substantial change in electrolytes. Oral administration of CH5424802 at 60 mg/kg for 4 days results in significant tumor regression seen in the luminescence signal[3].

    Clinical Trial
    Solvent & Solubility
    In Vitro: 

    DMSO : 6.2 mg/mL (12.85 mM; Need warming)

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.0720 mL 10.3601 mL 20.7202 mL
    5 mM 0.4144 mL 2.0720 mL 4.1440 mL
    10 mM 0.2072 mL 1.0360 mL 2.0720 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Alectinib is dissolved in 15% polyethyleneglycol-400 (PEG-400), 15% 2-hydroxypropyl-β-cyclodextrin (HPCD), 10% Cremophor EL, 10% DMSO, and 0.02 N HCl[4].

    Kinase Assay

    The inhibitory ability against each kinase except for MEK1 and Raf-1 is evaluated by examining their ability to phosphorylate various substrate peptides in the presence of Alectinib using time-resolved fluorescence resonance energy transfer (TR-FRET) assay or fluorescence polarization (FP) assay. The inhibitory activity against MEK1 is evaluated by quantitative analysis of the phosphorylation of a substrate peptide by a recombinant ERK2 protein in the presence of Alectinib. The inhibitory activity against Raf-1 is evaluated by examining the ability of the kinases to phosphorylate MEK1 in the presence of Alectinib[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay

    Cells are cultured in 96-well plates overnight and incubated with various concentrations of Alectinib for the indicated time. For spheroid cell growth inhibition assay, cells are seeded on spheroid plates, incubated overnight, and then treated with Alectinib for the indicated times. The viable cells are measured by the CellTiter-Glo Luminescent Cell Viability Assay. Caspase-3/7 assay is evaluated using the Caspase-Glo 3/7 Assay Kit[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    Cell lines are grown as s.c. tumors in SCID or nude mice. Therapeutic experiments are started (day 0) when the tumor reaches ~250 or ~350 mm3. Mice are randomized to treatment groups to receive vehicle or Alectinib (oral, qd) for the indicated duration. Final concentration of vehicle is 0.02 N HCl, 10% DMSO, 10% Cremophor EL, 15% PEG400, and 15% HPCD (2-hydroxypropyl-β-cyclodextrin). The length (L) and width (W) of the tumor mass are measured, and the tumor volume (TV) is calculated as: TV=(L×W2)/2. Tumor growth inhibition is calculated using the following formula: tumor growth inhibition=[1−(T−T0)/(C−C0)]×100. The ED50 is calculated from the values of tumor growth inhibition on the final experimental day.
    Plasma and brain (cerebrum and cerebellum) samples are prepared at various time points between 4 and 168 h after a single oral administration of 14C-labeled Alectinib (Alectinib) at 1 mg/kg to a rat. The radioactivity concentrations in plasma are determined by a liquid scintillation counter, and the radioactivity concentrations in brain are quantified using quantitative whole-body autography.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight




    CAS No.




    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month

    Room temperature in continental US; may vary elsewhere

    Purity: 99.34%

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    Cat. No.: HY-13011