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Merck

10295892001

Roche

Colcemid

solution, suitable for blocking, sterile; 0.2 μm filtered

Sinónimos:

Demecolcine, N-Deacetyl-N-methylcolchicine

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About This Item

Fórmula empírica (notación de Hill):
C21H25NO5
Número de CAS:
Peso molecular:
371.43
Beilstein/REAXYS Number:
2822892
MDL number:
UNSPSC Code:
12352207
PubChem Substance ID:

description

N-methyl-N-deacetyl-colchicine

Quality Level

sterility

sterile; 0.2 μm filtered

form

solution

packaging

pkg of 20 mL (10 μg/ml)

manufacturer/tradename

Roche

technique(s)

blocking: suitable

impurities

microbial, tested

solubility

water: miscible

storage temp.

2-8°C

SMILES string

CN[C@H]1CCc2cc(OC)c(OC)c(OC)c2C3=CC=C(OC)C(=O)C=C13

InChI

1S/C21H25NO5/c1-22-15-8-6-12-10-18(25-3)20(26-4)21(27-5)19(12)13-7-9-17(24-2)16(23)11-14(13)15/h7,9-11,15,22H,6,8H2,1-5H3/t15-/m0/s1

InChI key

NNJPGOLRFBJNIW-HNNXBMFYSA-N

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General description

Colcemid is also known as demecolcine. Its generic name is N-methyl-N-deacetyl-colchicine. Colcemid depolymerizes microtubules and blocks mitosis at metaphase.

Application

Colcemid inhibits the formation of mitotic spindles. It is used to increase the percentage of metaphase cells for chromosome analysis.

Biochem/physiol Actions

Often in karyotyping and cell cycle research it is desirable to increase the yield of mitotic cells in a particular phase of the cell cycle. This can be achieved in a variety of ways with the most popular being the use of a cell cycle synchronizing agent such as demecolcine. Demecolcine will arrest cells in metaphase with no remarkable effect on the biochemical events in mitotic cells or in synchronized G1 and S phase cells. White blood cells are often treated with demecolcine to arrest cells in metaphase.

Physical form

Solution (10 μg/ml), filtered through 0.2 μm pore size membrane.

Other Notes

For life science research only. Not for use in diagnostic procedures.

Storage Class

12 - Non Combustible Liquids

wgk_germany

nwg

flash_point_f

does not flash

flash_point_c

does not flash


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Johannes Bloehdorn et al.
Nature communications, 12(1), 5395-5395 (2021-09-15)
Knowledge of the genomic landscape of chronic lymphocytic leukemia (CLL) grows increasingly detailed, providing challenges in contextualizing the accumulated information. To define the underlying networks, we here perform a multi-platform molecular characterization. We identify major subgroups characterized by genomic instability
Naiara Zoccal Saraiva et al.
Cloning and stem cells, 11(1), 141-152 (2009-02-20)
This study aimed to evaluate the effect of demecolcine, a microtubule-depolymerizing agent, on microtubule kinetics; to determine the best concentration of demecolcine as a chemically assisted enucleation agent in metaphase I (MI) and metaphase II (MII) bovine oocytes, and to
Vasiliki Tasiou et al.
PloS one, 10(8), e0134672-e0134672 (2015-08-15)
The human RB1 gene is imprinted due to integration of the PPP1R26P1 pseudogene into intron 2. PPP1R26P1 harbors the gametic differentially methylated region of the RB1 gene, CpG85, which is methylated in the female germ line. The paternally unmethylated CpG85
Candice L Wike et al.
eLife, 5, e11402-e11402 (2016-02-18)
Phosphorylation of histone H3 threonine 118 (H3 T118ph) weakens histone DNA-contacts, disrupting the nucleosome structure. We show that Aurora-A mediated H3 T118ph occurs at pericentromeres and chromosome arms during prophase and is lost upon chromosome alignment. Expression of H3 T118E
Roshan L Shrestha et al.
The Journal of cell biology, 220(4) (2021-02-24)
Chromosomal instability (CIN) is a hallmark of many cancers. Restricting the localization of centromeric histone H3 variant CENP-A to centromeres prevents CIN. CENP-A overexpression (OE) and mislocalization have been observed in cancers and correlate with poor prognosis; however, the molecular

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