Nocodazole

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Background

Nocodazole, an anti-mitotic drug, is a rapidly-reversible inhibitor of microtubule polymerization which inhibits Abl, Abl(E255K) and Abl(T315I)with theIC50 value of 0.21 μM, 0.53 μM and 0.64 μM in cell-free assays, respectively[1].
In vitro: 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 [1]. At high concentrations, Nocodazole rapidly depolymerized microtubules in cells, while low concentrations of Nocodazole inhibited microtubule dynamic instability [2].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 [3]. 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[4].
In vivo: In athymic mice bearing COLO 205 tumor xenografts,after 6 wk of treatment with Ketoconazole (50 mg/kg/three times per week)plus Nocodazole (5 mg/kg/three times per week), the antitumor effects of ND were significantly potentiated by KT. The tumor volume and tumor weight of the mice are significantly reduced as compared with those treated with Ketoconazole or Nocodazole alone. Nocodazole treatment in combination with Ketoconazole strongly enhanced apoptosis of COLO 205 tumor xenografts treated with Ketoconazole or Nocodazole alone [5].

[1]. Park H, Hong S, Hong S. Nocodazole is a High‐Affinity Ligand for the Cancer‐Related Kinases ABL, c‐KIT, BRAF, and MEK[J]. ChemMedChem, 2012, 7(1): 53-56.
[2]. Xu K, Schwarz P M, Ludue a R F. Interaction of nocodazole with tubulin isotypes[J]. Drug development research, 2002, 55(2): 91-96.
[3]. Nara A, Aki T, Funakoshi T, et al. Hyperstimulation of macropinocytosis leads to lysosomal dysfunction during exposure to methamphetamine in SH-SY5Y cells[J]. Brain research, 2012, 1466: 1-14.
[4]. Liao G, Nagasaki T, Gundersen G G. Low concentrations of nocodazole interfere with fibroblast locomotion without significantly affecting microtubule level: implications for the role of dynamic microtubules in cell locomotion[J]. Journal of Cell Science, 1995, 108(11): 3473-3483.
[5]. Wang Y J, Jeng J H, Chen R J, et al. Ketoconazole potentiates the antitumor effects of nocodazole: In vivo therapy for human tumor xenografts in nude mice[J]. Molecular carcinogenesis, 2002, 34(4): 199-210.