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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.

Sinónimos:

Colchicine, Colchicum autumnale

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About This Item

Fórmula empírica (notación de Hill):
C22H25NO6
Número de CAS:
Peso molecular:
399.44
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

assay

≥94% (HPLC)

form

powder

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

yellow to off-white

solubility

ethanol: 10 mg/mL
water: soluble

shipped in

ambient

storage temp.

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

InChI key

IAKHMKGGTNLKSZ-INIZCTEOSA-N

General description

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.

Biochem/physiol Actions

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

Warning

Toxicity: Highly Toxic & Carcinogenic / Teratogenic (I)

Other Notes

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.
Due to the nature of the Hazardous Materials in this shipment, additional shipping charges may be applied to your order. Certain sizes may be exempt from the additional hazardous materials shipping charges. Please contact your local sales office for more information regarding these charges.

Legal Information

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

pictograms

Skull and crossbonesHealth hazard

signalword

Danger

hcodes

Hazard Classifications

Acute Tox. 2 Oral - Muta. 1B

Storage Class

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

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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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
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 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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