Colcemid

Colcemid is a colchicine derivative that inhibits tubulin polymerization as potently as colchicine (IC50 = 2.1 and 2.4 μM, respectively) but is less toxic.[1],[2],[3] At very low (nanomolar) concentrations, colcemid suppresses microtubule dynamicity and inhibits cell migration, while at micromolar levels it blocks microtubule assembly, arresting cells in metaphase.[3],[4],[5] Mitotic block by colcemid is used to synchronize cells and for karyotyping in cytogenetic studies.[4],6 Prolonged exposure to colcemid can activate p53, leading to apoptosis.[7]

Reference:
[1]. Muzaffar, A., Brossi, A., Lin, C.M., et al. Antitubulin effects of derivatives of 3-demethylthiocolchicine, methylthio ethers of natural colchicinoids, and thioketones derived from thiocolchicine. Comparison with colchicinoids. J. Med. Chem. 33(2), 567-571 (1990).
[2]. Rieder, C.L., and Palazzo, R.E. Colcemid and the mitotic cycle. Journal of Cell Science 102(3), 387-392 (1992).
[3]. Jordan, M.A., and Wilson, L. Microtubules as a target for anticancer drugs. Nature Reviews.Cancer 4(4), 253-265 (2004).
[4]. Curlej, J., Bulla, J., and Chrenek, P. Occurrence of chromosomal aneuploidy in rabbit oocytes and embryos at different developmental stages. Zygote 18(3), 203-207 (2010).
[5]. Yang, H., Ganguly, A., and Cabral, F. Inhibition of cell migration and cell division correlates with distinct effects of microtubule inhibiting drugs. The Journal of Biological Chemisty 285(42), 32242-32250 (2010).
[6]. Bayani, J., and Squire, J.A. Preparation of cytogenetic specimens from tissue samples. Current Protocols in Cell Biology 22(22.2), 1-15 (2004).
[7]. Sablina, A.A., Chumakov, P.M., Levine, A.J., et al. p53 activation in response to microtubule disruption is mediated by integrin-Erk signaling. Oncogene 20(8), 899-909 (2001).