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Colchicine, Colchicum autumnale

Colchicine, Colchicum autumnale, CAS 64-86-8, is an inhibitor of mitosis that disrupts microtubules and inhibits tubulin polymerization. Induces apoptosis in PC12 and cerebellar granule cells.

Sinonimo/i:

Colchicine, Colchicum autumnale

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About This Item

Formula empirica (notazione di Hill):
C22H25NO6
Numero CAS:
Peso molecolare:
399.44
Numero MDL:
Codice UNSPSC:
12352200
NACRES:
NA.77

Livello qualitativo

Saggio

≥94% (HPLC)

Forma fisica

powder

Produttore/marchio commerciale

Calbiochem®

Condizioni di stoccaggio

OK to freeze
protect from light

Colore

yellow to off-white

Solubilità

ethanol: 10 mg/mL
water: soluble

Condizioni di spedizione

ambient

Temperatura di conservazione

10-30°C

InChI

1S/C22H25NO6/c1-12(24)23-16-8-6-13-10-19(27-3)21(28-4)22(29-5)20(13)14-7-9-18(26-2)17(25)11-15(14)16/h7,9-11,16H,6,8H2,1-5H3,(H,23,24)/t16-/m0/s1
IAKHMKGGTNLKSZ-INIZCTEOSA-N

Descrizione generale

Inhibitor of mitosis that is useful in cell division studies. Disrupts microtubules and inhibits tubulin polymerization. Induces apoptosis in PC12 cells and in cerebellar granule cells.
Major alkaloid of Colchicum autumnale. Inhibitor of mitosis used in cell division studies. Disrupts microtubules and inhibits tubulin polymerization. Induces apoptosis in pheochromocytoma (PC12) cells and in cerebellar granule cells.

Azioni biochim/fisiol

Cell permeable: no
Primary Target
Inhibitor of mitosis
Product does not compete with ATP.
Reversible: no

Attenzione

Toxicity: Highly Toxic & Carcinogenic / Teratogenic (I)

Altre note

Bonfoco, E., et al. 1995. Exp. Cell Res.218, 189.
Lindenboim, L., et al. 1995. J. Neurochem.64, 1054.
Leung, M.F., and Sartorelli, A.C. 1992. Leuk. Res.16, 929.
Santell, L. 1992. Exp. Cell Res. 201, 358.
Salmon, E.D., et al. 1984. J. Cell Biol.99, 1066.
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Note legali

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Pittogrammi

Skull and crossbonesHealth hazard

Avvertenze

Danger

Indicazioni di pericolo

Classi di pericolo

Acute Tox. 2 Oral - Muta. 1B

Codice della classe di stoccaggio

6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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Demecolcine ≥98% (HPLC)

Sigma-Aldrich

D7385

Demecolcine

Colcemid solution, suitable for blocking, sterile; 0.2 μm filtered

Roche

10295892001

Colcemid

E Bonfoco et al.
Experimental cell research, 218(1), 189-200 (1995-05-01)
Exposure to 1 microM colchicine, a microtubule disrupting agent, triggered apoptosis in rat cerebellar granule cells (CGC). Apoptotic nuclei began to appear after 12 h followed by oligonucleosomal DNA laddering, whereas inhibition of the mitochondrial 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide metabolism became significant between
L Santell et al.
Experimental cell research, 201(2), 358-365 (1992-08-01)
The expression of certain proteolytic enzymes involved in cell migration (collagenase, urokinase) can be enhanced by the disruption of cellular cytoskeletal organization, suggesting an association between cell shape and gene expression. We have examined the effect of cytoskeleton-disrupting agents on
E D Salmon et al.
The Journal of cell biology, 99(3), 1066-1075 (1984-09-01)
At metaphase, the amount of tubulin assembled into spindle microtubules is relatively constant; the rate of tubulin association equals the rate of dissociation. To measure the intrinsic rate of dissociation, we microinjected high concentrations of colchicine, or its derivative colcemid
M F Leung et al.
Leukemia research, 16(9), 929-935 (1992-09-01)
We and others have previously shown that microtubules (MT) are stained more intensely and are organized differently in differentiating leukemia cells. To study the effects of the MT disrupting drugs, colchicine (Coln) and vincristine (VCR), on the maturation process, HL-60
L Lindenboim et al.
Journal of neurochemistry, 64(3), 1054-1063 (1995-03-01)
Pheochromocytoma (PC12) cells have been shown to undergo apoptosis (programmed cell death) when deprived of serum and to be rescued by nerve growth factor, fibroblast growth factor, dibutyryl cyclic AMP, aurintricarboxylic acid, or exogenous expression of bcl-2. We show here

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