234115
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.
別名:
Colchicine, Colchicum autumnale
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About This Item
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品質水準
アッセイ
≥94% (HPLC)
形状
powder
メーカー／製品名
Calbiochem®
保管条件
OK to freeze
protect from light
色
yellow to off-white
溶解性
ethanol: 10 mg/mL
water: soluble
輸送温度
ambient
保管温度
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
詳細
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.
生物化学的／生理学的作用
Cell permeable: no
Primary Target
Inhibitor of mitosis
Inhibitor of mitosis
Product does not compete with ATP.
Reversible: no
警告
Toxicity: Highly Toxic & Carcinogenic / Teratogenic (I)
その他情報
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.
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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法的情報
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
シグナルワード
Danger
危険有害性情報
危険有害性の分類
Acute Tox. 2 Oral - Muta. 1B
保管分類コード
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
WGK
WGK 3
引火点(°F)
Not applicable
引火点(℃)
Not applicable
適用法令
試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。
Jan Code
234115-GM:
US2234115-1GM:
234115-1GM:
US2234115-5GM:
234115-5GM:
234115-1.1ML:
試験成績書（COA）
製品のロット番号・バッチ番号を入力して、試験成績書（COA） を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。
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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 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
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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