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    Nocodazole (Oncodazole; R17934)
    Nocodazole (Oncodazole; R17934)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1608
    CAS #: 31430-18-9Purity ≥98%

    Description: Nocodazole (Oncodazole; R17934) is a potent and rapidly-reversible inhibitor of microtubule polymerization, also inhibits Abl, Abl(E255K) and Abl(T315I) with IC50 of 0.21 μM, 0.53 μM and 0.64 μM in cell-free assays, respectively. Nocodazole is used as an anti-cancer agent which exerts its effect in cells by interfering with the polymerization of microtubules. Nocodazole induces apoptosis in chronic lymphocytic leukemia cells. It inhibits insulin-stimulated glucose transport. Nocodazole decreases apoptosis in some human colon carcinoma cells.

    References: ChemMedChem. 2012 Jan 2;7(1):53-6; Mol Carcinog. 2002 Aug;34(4):199-210.

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    Molecular Weight (MW)301.32
    FormulaC14H11N3O3S
    CAS No.31430-18-9
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 7 mg/mL (23.2 mM)
    Water:<1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)1% DMSO+30% polyethylene glycol+1% Tween 80: 30 mg/mL 
    SynonymsOncodazole; R-17934; R 17934; R17934


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    In Vitro

    In vitro activity: Nocodazole is a high-affinity ligand for the cancer-related kinases including Abl phosphorylated, c-Kit, BRAF, and MEK with Kd of 0.091 μM, 1.6 μM, 1.8 μM and 1.6 μM, respectively. In addition, the Kd of Nocodazole for Abl(E255K) phosphorylated, Abl(T315I) phosphorylated, BRAF(V600E) and PI3Kγ is 0.12 μM, 0.17 μM, 1.1 μM and 1.5 μM, respectively. Nocodazole induces apoptosis in chronic lymphocytic leukemia cells. Nocodazole inhibits insulin-stimulated glucose transport. Nocodazole decreases apoptosis in some human colon carcinoma cells. Nocodazole impairs the morphology and directionality of migrating medial gan-glionic eminence cells. At high concentrations, Nocodazole rapidly depolymerizes microtubules in cells, while low concentrations of Nocodazole inhibit microtubule dynamic instability. Mitotic cells incubated with different concentrations of Paclitaxel are inhibited from progressing to G1 phase 6 hours after release from the Nocodazole block, with a median inhibitory concentration of 4 nM. Nocodazole-pretreated cells exposed to Paclitaxel in the absence of Nocodazole only form free-floating microtubules, whereas pretreated cells exposed to Paclitaxel in the presence of Nocodazole-assembled centrosome organize microtubules. Nocodazole disrupts microtubules by binding to β-tubulin. Nocodazole prevents the formation of one of the two interchain disulfide linkages. Nocodazole impairs the transport of vesicles. Nocodazole suppress METH-induced cell death and lysosomal dysfunction. METH-induced cell death is significantly decreased by Nocodazole pretreatment in comparison to METH alone.


    Kinase Assay: Nocodazole is a high-affinity ligand for the cancer-related kinases including Abl phosphorylated, c-Kit, BRAF, and MEK with Kd of 0.091 μM, 1.6 μM, 1.8 μM and 1.6 μM, respectively. In addition, the Kd of Nocodazole for Abl(E255K) phosphorylated, Abl(T315I) phosphorylated, BRAF(V600E) and PI3Kγ is 0.12 μM, 0.17 μM, 1.1 μM and 1.5 μM, respectively. 


    Cell Assay: Nocodazolewas a high-affinity ligand for the cancer-related kinases including Abl phosphorylated, c-Kit, BRAF, and MEK with the Kd values of 0.091 μM, 1.6 μM, 1.8 μM and 1.6 μM, respectively. In addition, the Kd for Abl(E255K) phosphorylated, Abl(T315I) phosphorylated, BRAF(V600E) and PI3Kγ was 0.12 μM, 0.17 μM, 1.1 μM and 1.5 μM, respectively. In chronic lymphocytic leukemia cells, Nocodazole induced apoptosis. In some human colon carcinoma cells, Nocodazole decrease D apoptosis. Also, Nocodazole inhibited insulin-stimulated glucose transport. Nocodazole impaired the morphology and directionality of migrating medial gan-glionic eminence cells. At high concentrations, Nocodazole rapidly depolymerized microtubules in cells, while low concentrations of Nocodazole inhibited microtubule dynamic instability.In SH-SY5Y cells, Nocodazole disrupted microtubules by binding to β-tubulin, prevented the formation of one of the two interchain disulfide linkages and impaired the transport of vesicles. Nocodazole significantly attenuated METH-induced cell death and lysosomal dysfunction. Nocodazole (≥ 50 nM) resulted in a rapid reduction in fibroblast locomotion to a new rate that was maintained for > 2 hours. Nocodazole(100 nM) decreased the rate of locomotion by more than 60%; and 300 nM nocodazole completely stopped cell locomotion.

    In VivoThe tumor volume and tumor weight of the mice treated with Ketoconazole  plus  Nocodazole are significantly reduced as compared with those treated with Ketoconazole or Nocodazole alone. Combined treatment with Ketoconazole  plus  Nocodazole strongly enhances apoptosis of COLO 205 tumor xenografts treated with Ketoconazole  or  Nocodazole alone.
    Animal modelNude mice with COLO-205 tumor xenografts
    Formulation & DosageDissolved in DMSO; 5 mg/kg; i.p. injection.
    ReferencesChemMedChem. 2012 Jan 2;7(1):53-6; Mol Carcinog. 2002 Aug;34(4):199-210.


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

    Nocodazole

    Western blot analysis of Dia 1 expression in whole cell lysates prepared from untreated (A) and Nocodazole-treated; (B) HeLa whole cell lysates.
     
    original image
    ChemMedChem. 2012 Jan 2;7(1):53-6.


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