| Stereochemistry | ACHIRAL |
| Molecular Formula | C14H11N3O3S |
| Molecular Weight | 301.32 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
COC(=O)NC1=NC2=C(N1)C=CC(=C2)C(=O)C3=CC=CS3
InChI
InChIKey=KYRVNWMVYQXFEU-UHFFFAOYSA-N
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)
| Molecular Formula | C14H11N3O3S |
| Molecular Weight | 301.32 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Nocodazole is an anti-mitotic drug that has long been used as an experimental tool in cell biology. Nocodazole is known to bind with high affinity to tubulin and to inhibit microtubule assembly. The tubulin molecule is a α/β heterodimer; both α and β exist as various isotypes whose distribution and drug-binding properties are significantly different. Nocodazole has the highest affinity for αβIV and the lowest affinity for αβIII. In addition, nocodazole was investigated as an anticancer drug on xenografts model and it was revealed, that nocodazole possessed a high-affinity for the cancer-related kinases ABL, c-KIT, BRAF, and MEK, and inhibited Abl, Abl(E255K) and Abl(T315I).
Approval Year
PubMed
Patents
Sample Use Guides
Nocodazole potently induced LATS2 expression in HEK293T cells. Consistently, nocodazole significantly inhibited β-catenin-mediated transcription induced by LiCl or β-Cat overexpression. There also were found that nocodazole induced LATS2, but not LATS1, in a time-dependent manner in HCT116 cells and SW480 cells. While nocodazole significantly suppressed the expression of AXIN2 and MMP7 in HCT116 cells expressing scramble shRNA (HCT116/Scrsh), it could not affect the expression of AXIN2 and MMP7 in HCT116 cells expressing LATS2 shRNA (HCT116/LATS2sh). The restoration of LATS2 or LATS2N in HCT116/LATS2sh cells suppressed the expression of AXIN2 and MMP7, confirming the specificity of LATS2 shRNA. Moreover, ChIP assays found that nocodazole induced LATS2 binding to the promoter of AXIN2 or MMP7 in HCT116/Scrsh cells, but not in HCT116/LATS2sh cells. Consistently, was found that the occupancy of BCL9 on the promoter of AXIN2 or MMP7 was reduced in HCT116/Scrch cells, but not in HCT116/LATS2sh cells, upon nocodazole treatment. In contrast, nocodazole did not interfere with β-catenin presence on the promoter of AXIN2 or MMP7. The constitutive activation of Wnt/β-catenin plays a critical role in human colorectal tumor growth.
