NOCODAZOLE CAS 31430-18-9
Introduction：Basic information about NOCODAZOLE CAS 31430-18-9, including its chemical name, molecular formula, synonyms, physicochemical properties, and safety information, etc.
NOCODAZOLE Basic informationBackground
| Product Name: | NOCODAZOLE |
| Synonyms: | [5-(2-THIENYLCARBONYL)-1H-BENZIMIDAZOL-2-YL]CARBONIC ACID, METHYL ESTER;METHYL[5-(2-THIENYLCARBONYL)-1H-BENZIMADAZOL-2-YL]CARBAMATE;METHYL-(5-[2-THIENYLCARBONYL]-1H-BENZIMIDAZOL-2-YL)CARBAMATE;METHYL [5-(2-THIENYLCARBONYL)-1H-BENZ-IMIDAZOLE-2-YL]-CARBAMATE;METHYL-(5-[2-THIENYLCARBONYL]-1H-BENZIMODAZOL-2YL)-CARBAMATE;METHYL N-(5-THENOYL-2-BENZIMIDAZOLYL)CARBAMATE;Methyl N-(5-thenoyl-2-benzimidazolyl)carbamate, Oncodazole, R 17934, [5-(2-Thienylcarbonyl)-1H-benzimidazol-2-yl]-carbamic acid methyl ester, Methyl [5-(2-thienylcarbonyl)-1H-benzimidazol-2-yl]carbamate;N-[6-(2-Thienylcarbonyl)-1H-benzimidazol-2-yl]carbamic Acid Methyl Ester |
| CAS: | 31430-18-9 |
| MF: | C14H11N3O3S |
| MW: | 301.32 |
| EINECS: | 250-626-5 |
| Product Categories: | Inhibitors;Aromatics Compounds;Aromatics;Heterocycles;Intermediates & Fine Chemicals;Pharmaceuticals;Caspases/Apoptosis |
| Mol File: | 31430-18-9.mol |
NOCODAZOLE Chemical Properties
| Melting point | 300 °C (dec.) |
| density | 1.490 |
| refractive index | 1.6740 (estimate) |
| storage temp. | -20°C |
| solubility | DMSO: 10 mg/mL, soluble |
| pka | 10.67±0.10(Predicted) |
| form | powder |
| color | white |
| biological source | synthetic |
| BRN | 1085978 |
| Stability: | Stable for 2 years as supplied. Solutions in DMSO may be stored at -20° for up to 2 months. |
| InChI | InChI=1S/C14H11N3O3S/c1-20-14(19)17-13-15-9-5-4-8(7-10(9)16-13)12(18)11-3-2-6-21-11/h2-7H,1H3,(H2,15,16,17,19) |
| InChIKey | KYRVNWMVYQXFEU-UHFFFAOYSA-N |
| SMILES | C(OC)(=O)NC1NC2=CC(C(C3SC=CC=3)=O)=CC=C2N=1 |
| CAS DataBase Reference | 31430-18-9(CAS DataBase Reference) |
| EPA Substance Registry System | Nocodazole (31430-18-9) |
Safety Information
| Hazard Codes | T,C,F,Xn |
| Risk Statements | 61-40-36/37/38-34-11-68-63 |
| Safety Statements | 53-45-36/37/39-26-16-36/37 |
| RIDADR | 2811 |
| WGK Germany | 3 |
| RTECS | DD6521000 |
| HazardClass | 6.1(b) |
| PackingGroup | III |
| HS Code | 29349990 |
| Storage Class | 11 - Combustible Solids |
| Hazard Classifications | Muta. 2 Repr. 2 |
| Toxicity | sln-smc 1 ppm/16H MUREAV 141,15,84 |
| Description | Nocodazole reversibly binds tubulin and alters tubulin- |
| Chemical Properties | Amber Powder |
| Uses | Antineoplastic;Microtubule poison |
| Uses | A potent Tubulin production inhibitor and anti-neoplastic agent |
| Uses | Nocodazole has been shown to enhance CRISPR genome editing efficiency. To see other small molecule CRISPR enhancers, visit sigma.com/CRISPR-enhancers. |
| Uses | A synthetic chemotherapeutic agent with antineoplastic, antifungal and anthelmintic activities. Microtubule inhibitor; inhibits mitosis |
| Definition | 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. |
| General Description | White powder. |
| Air & Water Reactions | Insoluble in water. |
| Reactivity Profile | NOCODAZOLE may be sensitive to heat. . |
| Health Hazard | ACUTE/CHRONIC HAZARDS: When heated to decomposition NOCODAZOLE emits toxic fumes of sulfur oxides and nitrogen oxides. |
| Fire Hazard | Flash point data for NOCODAZOLE are not available; however, NOCODAZOLE is probably combustible. |
| Biological Activity | Microtubule inhibitor; inhibits mitosis. |
| Biochem/physiol Actions | 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. |
| Safety Profile | 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 |
| 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]. |
| storage | +4°C |
| Background | Nocodazole is an anti-neoplastic agent that reversibly interferes with the polymerization of microtubules. Widely-used as a cell cycle synchronizing agent in cell biology labs to induce mitotic arrest, investigators have demonstrated that high concentrations of nocodazole induce microtubule depolymerization, whereas low concentrations alter spindle microtubule dynamics, but microtubules do not depolymerize. Recent research studies have demonstrated nocodazole to be a common inhibitor of various cancer-related kinases, including: ABL, c-KIT, BRAF, MEK1, MEK2, and MET. |
| References | [1] M A JORDAN L W D Thrower. Effects of vinblastine, podophyllotoxin and nocodazole on mitotic spindles. Implications for the role of microtubule dynamics in mitosis.[J]. Journal of cell science, 1992, 102 ( Pt 3): 401-416. DOI:10.1242/jcs.102.3.401 [2] BRIAN STORRIE Wei Y. Dynamics of the interphase mammalian Golgi complex as revealed through drugs producing reversible Golgi disassembly[J]. Biochimica et biophysica acta. Molecular cell research, 1998, 1404 1: Pages 127-137. DOI:10.1016/s0167-4889(98)00053-6 [3] MARISAN R. MEJILLANO Richard H H B D Shivanna. Studies on the Nocodazole-Induced GTPase Activity of Tubulin[J]. Archives of biochemistry and biophysics, 1996, 336 1: Pages 130-138. DOI:10.1006/abbi.1996.0540 [4] T H WANG. Microtubule-interfering agents activate c-Jun N-terminal kinase/stress-activated protein kinase through both Ras and apoptosis signal-regulating kinase pathways.[J]. The Journal of Biological Chemistry, 1998, 273 9: 4928-4936. DOI:10.1074/jbc.273.9.4928 |
NOCODAZOLE Preparation Products And Raw materials
| Raw materials | Sodium hydroxide-->Hydrochloric acid-->Methanol-->Dichloromethane-->Acetic acid-->Nitric acid-->Sodium sulfate-->Acetic anhydride-->Ammonia-->Sodium bicarbonate-->Palladium-->Aluminum chloride-->Isopropyl alcohol-->Hydrogen-->Dimethyl sulfoxide-->Sodium acetate-->Diisopropyl ether-->2-Methyl-2-thiopseudourea sulfate-->Methyl chloroacetate-->Thiophene-->4-Methoxybenzoyl chloride |
