microtubule in human tumor cells

Cevipabulin (TTI-237) 是一种微管活性的、口服有效的抗肿瘤化合物，可抑制 [3H] 长春碱与微管蛋白的结合，对人癌细胞的 IC50 值为 18-40 nM。

Cevipabulin (TTI-237) fumarate is a microtubule-active antitumor compound and inhibits the binding of [3H] vinblastine to tubulin (IC50: 18-40 nM in the human tumor cell line).

ER-076349 作为一种微管蛋白聚合抑制剂，不仅可以诱导 G2-M 细胞周期的停滞，还能破坏有丝分裂纺锤体。该化合物有效抑制癌细胞和多种人类肿瘤异种移植小鼠模型中肿瘤的生长。此外，ER-076349 是 Halichondrin B 的类似物。

Microtubule destabilizing agent-2 (Compound 21) 是一种选择性靶向微管蛋白的口服抗肿瘤化合物。它通过破坏微管蛋白稳定性和抑制微管聚合，导致人肿瘤细胞在G0 G1期停滞，并通过激活Caspase级联途径诱导细胞凋亡 (Apoptosis)。此外，Microtubule destabilizing agent-2 还具有抗炎特性，能够在体外抑制TNF-α和IL-6的产生，并可抑制小鼠异种移植瘤的生长。

CAY10701 is a 7-deazahypoxanthine analog that prevents microtubule formation, blocking the proliferation of HeLa and MCF-7 cells (GI50s = 22 and 38 nM, respectively). It also inhibits the growth of several different colorectal cancer cell lines (GI50 values range from 9 to 17 nM), while being at least 1,500-fold less effective against normal human fibroblast WI38 cells. CAY10701 is effective in vivo, reducing tumor volume in colorectal cell xenografts in mice without significantly altering body weight.

IG-105 is a potent microtubule inhibitor with potential anticancer activity. IG-105 inhibits microtubule assembly by binding at colchicine pocket. IG-105 shows a potent anticancer activity in vitro and in vivo and has good safety in mice. IG-105 showed a potent activity against human leukemia and solid tumors in breast, liver, prostate, lung, skin, colon, and pancreas with IC(50) values between 0.012 and 0.298 mumol L. It was also active in drug-resistant tumor cells and not a P-glycoprotein substrate. It inhibited microtubule assembly followed by M-phase arrest, Bcl-2 inactivation, and then apoptosis through caspase pathways.

MPT0B098 is a potent microtubule inhibitor through binding to the colchicine-binding site of tubulin. MPT0B098 is active against the growth of various human cancer cells, including chemoresistant cells with IC50 values ranging from 70 to 150 nmol L. MPT0B098 arrests cells in the G2–M phase and subsequently induces cell apoptosis. In addition, MPT0B098 effectively suppresses VEGF-induced cell migration and capillary-like tube formation of HUVECs. Distinguished from other microtubule inhibitors, MPT0B098 not only inhibited the expression levels of HIF-1α protein but also destabilized HIF-1α mRNA. The mechanism of causing unstable of HIF-1α mRNA by MPT0B098 is through decreasing RNA-binding protein, HuR, translocation from the nucleus to the cytoplasm. Notably, MPT0B098 effectively suppresses tumor growth and microvessel density of tumor specimens in vivo. Taken together, our results provide a novel mechanism of inhibiting HIF-1α of a microtubule inhibitor MPT0B098. MPT0B098 is......

MPT0B214 is a novel and potent microtubule inhibitor with potential anticancer activity. MPT0B214 inhibited tubulin polymerization through strongly binding to the tubulin's colchicine-binding site and had cytotoxic activity in a variety of human tumor cell lines. After treatment with MPT0B214, KB cells were arrested in the G2-M phase before cell death occurred, which were associated with upregulation of cyclin B1, dephosphorylation of Cdc2, phosphorylation of Cdc25C and elevated expression of the mitotic marker MPM-2. Furthermore, the compound induced apoptotic cell death through mitochondria caspase 9-dependent pathway. Notably, several KB-derived multidrug-resistant cancer cell lines were also sensitive to MPT0B214 treatment. ( PLoS One. 2013;8(3):e58953).