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.