A desirable property of mitostatic drugs, like paclitaxel or nocodazole, is their ability to induce mitotic arrest, followed by apoptosis, rather than exerting cytotoxic effects that lead to acute cell death. The former scenario reduces the risk of inflammation and damage to surrounding tissues in the context of the organism, making mitostatics less toxic compared to drugs that cause cell death through necrosis or other less regulated mechanisms. We noticed, that similar to nocodazole but in contrast to 2a and 3a, compound 3c exerted the mitostatic effect without displaying acute cytotoxicity, which was evidenced by the lack of decrease of the plateau in Fig. , compared to nocodazole (red dotted line). It is conceivable that the presence of meta-hydroxy group in the exocyclic phenyl substituent in compound 3c, may be important to reduce potential off-target interactions with other cellular receptors, enabling a higher specificity of this compound for tubulin.