Molecular target<unk>  binds to microtubules reversibly with high affinity and has a maximum stoichiometry of 1 mole<unk>  per mole tubulin in microtubules. This binding stabilizes microtubules and prevents depolymerisation from calcium ions, decreased temperature and dilution, preferentially at the plus end of the microtubule.<unk>  has been found to accumulate to higher concentration in ovarian adenocarcinoma cells than kidney carcinoma cells, which may contribute to the more effective treatment of ovarian cancer by<unk> . It has also been found to lead to the phosphorylation of oncoprotein bcl-2, which is apoptosis-blocking in its oncoprotein form. Modes of action The cytotoxic activity of<unk>  is exerted by promoting and stabilising microtubule assembly, while preventing physiological microtubule depolymerisation/disassembly in the absence of GTP. This leads to a significant decrease in free tubulin, needed for microtubule formation and results in inhibition of mitotic cell division between metaphase and anaphase, preventing further cancer cell progeny. Because microtubules do not disassemble in the presence of<unk> , they accumulate inside the cell and cause initiation of apoptosis. Apoptosis is also encouraged by the blocking of apoptosis-blocking bcl-2 oncoprotein. Both in vitro and in vivo analysis show the anti-neoplastic activity of<unk>  to be effective against a wide range of known cancer cells, cooperate with other anti-neoplastic agents activity, and have greater cytotoxicity than paclitaxel, possibly due to its more rapid intracellular uptake. The main mode of therapeutic action of<unk>  is the suppression of microtubule dynamic assembly and disassembly, rather than microtubule bundling leading to apoptosis, or the blocking of bcl-2. Cellular responses<unk>  exhibits cytotoxic activity on breast, colorectal, lung, ovarian, gastric, renal and prostate cancer cells.<unk>  does not block disassembly of interphase microtubules and so does not prevent entry into the mitotic cycle, but does block mitosis by inhibiting mitotic spindle assembly. Resistance to paclitaxel or anthracycline doxorubicin does not necessarily indicate resistance to<unk> . Microtubules formed in the presence of<unk>  are of a larger size than those formed in the presence of paclitaxel, which may result in improved cytotoxic efficacy. Abundant formation of microtubules and the prevention of replication caused by<unk>  leads to apoptosis of tumour cells and is the basis of<unk>  use as a cancer treatment.<unk>  activity is significantly greater in ovarian and breast tumours than for lung tumours.
Docetaxel
Paclitaxel
Doxorubicin
Trastuzumab
Ifosfamide
Lipoplatin
Ribociclib
Cabazitaxel