Nocodazole is a tubulin production inhibitor, also inhibits Abl, Abl(E255K) and Abl(T315I) with IC50 value of 0.21 μM, 0.53 μM and 0.64 μM, respectively  [1].
Nocodazole is an inhibitor of microtubule polymerization which inhibits insulin-stimulated glucose transport. It impairs the morphology and directionality of migrating medial gan-glionic eminence cells and disrupts microtubules by binding to β-tubulin. Nocodazole also prevents the formation of one of the two interchain disulfide linkages and impairs the transport of vesicles.
As a high-affinity ligand for the cancer-related kinases such as Abl phosphorylated, c-Kit, BRAF, and MEK, nocodazole inhibits BRAF, Abl phosphorylated, c-Kit and MEK with Kd value of 1.8 μM, 0.091 μM, 1.6 μM, and 1.6 μM, respectively. Additionally, nocodazole inhibits phosphorylated Abl(E255K), phosphorylated  Abl(T315I), BRAF(V600E) and PI3Kγ with the Kd value of 0.12 μM, 0.17 μM, 1.1 μM and 1.5 μM, respectively. Mitotic cells which incubated with different concentrations of paclitaxel, released from the nocodazole block, are inhibited from progressing to G1 phase in 6 hours with a median inhibitory concentration of 4 nM. In the absence of nocodazole, the cells which pretreated with nocodazole exposed to paclitaxel only form free-floating microtubules, while pretreated cells exposed to paclitaxel organized microtubules [1,2].
In vivo, the therapeutic efficacy of a treatment of combination of nocodazole (5 mg/kg/three times per week) and ketoconazole (50 mg/kg/three times per week) was tested by treating athymic mice bearing COLO 205 tumor xenografts. The antitumor effects of nocodazole were significantly potentiated by ketoconazole in mice after 6 wk of treatment. The tumor volume and tumor weight of the mice treated with a combination of ketoconazole and nocodazole are significantly reduced as compared with those treated with ketoconazole or nocodazole alone. Treatment with the combination of ketoconazole and nocodazole strongly enhances apoptosis of COLO 205 tumor xenografts treated with nocodazole or ketoconazole alone [3].
References:
[1]. Park H, Hong S, Hong S. Nocodazole is a High-Affinity Ligand for the Cancer-Related Kinases ABL, c-KIT, BRAF, and MEK. ChemMedChem, 2012, 7(1): 53-56.
[2]. Long bh，fairchild cr. Paclitaxel inhibits progression of mitotic cells to g(1) phase by interference with spindle formation without affecting other microtubule functions during anaphase and telephase. Cancer Research, 1994, 54(16): 4355-4361.
[3]. Wang YJ, Jeng JH, Chen RJ, et al. Ketoconazole potentiates the antitumor effects of nocodazole: In vivo therapy for human tumor xenografts in nude mice. Molecular Carcinogenesis, 2002, 34(4): 199-210.