Nocodazole reversibly binds tubulin and alters tubulin-associated GTP hydrolysis as well as microtubule dynamics. While nocodazole is used to study many aspects on microtubule function, it is most commonly used to synchronize cell cycling in culture. Typically, nanomolar concentrations of nocodazole reduce both microtubule elongation and shortening velocities, resulting in arrest of cycling in a G2/M phase. Nocodazole is also used to induce the formation of Golgi ministacks in eukaryotic cells.
Nocodazole has been shown to enhance CRISPR genome editing efficiency. To see other small molecule CRISPR enhancers, visit
sigma.com/CRISPR-enhancers.
A potent Tubulin production inhibitor and anti-neoplastic agent
Antineoplastic;Microtubule poison
A synthetic chemotherapeutic agent with antineoplastic, antifungal and anthelmintic activities. Microtubule inhibitor; inhibits mitosis
ChEBI: A member of the class of benzimidazoles that is benzimidalole which is substituted at position 2 by a (methoxycarbonyl)amino group and at position 5 by a 2-thienoyl group. It is an antineoplastic agent that exerts its effect by depolymerising microtubules.
NOCODAZOLE may be sensitive to heat. .
ACUTE/CHRONIC HAZARDS: When heated to decomposition NOCODAZOLE emits toxic fumes of sulfur oxides and nitrogen oxides.
Flash point data for NOCODAZOLE are not available; however, NOCODAZOLE is probably combustible.
Microtubule inhibitor; inhibits mitosis.
Nocodazole is an anticancer drug that has been shown to interfere with the structure and function of microtubules in interphase and mitotic cells. Malignant cells may be more susceptible to the antimicrotubular effect of nocodazole than nonmalignant cells. Mammalian cells cultured in vitro can be treated with 0.04-10 μg/mL doses for cell synchronization experiments. Prolonged arrest of cells in mitosis due to nocodazole treatment typically results in cell death by apoptosis. Higher concentrations could not be used because of insolubility. High specificity of action may explain low toxicity to bone marrow cells and lack of neurotoxicity. Nocodazole is thought to bind directly to tubulin causing conformational changes resulting in increased exposure of some sulfhydryl and possibly tyrosine residues. Nocodazole′s apparent synergism with cytosine arabinofuranoside has been demonstrated on L1210 leukemic cells.
Poison by intraperitoneal route.An experimental teratogen. Other experimentalreproductive effects. Human mutation data reported.When heated to decomposition it emits toxic fumes ofSOx and NOx. See also CARBAMATES
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 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) Jordan et al. (1992), Effects of vinblastine, podophyllotoxin and nocodazole on mitotic spindles. Implications for the role of microtubule dynamics in mitosis; J. Cell Science, 102 401
2) Storrie et al. (1998), Dynamics of the interphase mammalian Golgi complex as revealed through drugs producing reversible Golgi disassembly; Biochim. Biophys. Acta, 1404 127
3) Mejillano et al. (1996), Studies on the nocodazole-induced GTPase activity of tubulin; Arch. Biochem. Biophys., 336 130
4) Wang et al. (1998), Microtubule-interfering agents activate c-Jun N-terminal kinase/stress-activated protein kinase through both Ras and apoptosis signal-regulating kinase pathways; J. Biol. Chem., 273 4928
