In our study we’ve investigated the molecular mechanisms leading to SU6656 induced polyploidy, cell death and senescence with emphasis on the probable cross reactivity with Aurora kinases in several cell lines, i. Elizabeth. ES cells, MEFs, and NMuMG Fucci cells. Upon SU6656 exposure all screened cell lines show the same reaction, morphologically the cells become very enlarged and flattened, and the increase in size for the initial few days subsequently accompanied by multinucleated pattern clusters. Within a few minutes of exposure the cells fail to undergo mitosis. Indeed, even cells that morphologically seem to be Ivacaftor price in late stage mitosis from the beginning of exposure fail daughter cell separation and cytokinesis. Interestingly, while SU6656 comes exclusively as a particular SFK chemical from the number of popular providers, Bain et al. confirmed in 2007 that SU6656 show clear crossreactivity at very low concentrations together with the Aurora family of serine/threonine protein kinases. This group of kinases is famous to play critical roles all through mitosis, and the inhibition of said kinases has in the literature been shown to induce a similar result as described above for SU6656, raising the problem whether our results were due to SFK inhibition or unspecific cross reactivity with Aurora kinases. wild type MEFs and to help expand throw doubt on results being due to inhibition of SFK, Src, Yes, Fyn tripleknockout MEF cell line showed the same reaction to SU6656 while the ES cells. To compare consequences, Aurora kinases were damaged by the second era uniqueness verified chemical SNS 314 and not so remarkably various different Skin infection cell types were equally affected by the Aurora kinases and SU6656. We also received similar responses with the Aurora kinase inhibitor VX680, nevertheless, this inhibitor has consequently been proven to cross react with SFKs and cannot be looked at to be specific enough to further strengthen our theory. Moreover, we established that SU6656 quickly prevent phosphorylation of histone H3 at 10, a genome wide hallmark of mitosis compound library on 96 well plate catalyzed by Aurora B kinase that plays an essential function in chromosome condensation and segregation. These results, together with our data showing that the effects induced by another Src family chemical PP2 clearly diverge from those of SU6656, signify that the extended impairment of cell division seen with SU6656 in the present study are usually not attributed to its inhibition of SFKs but instead the Aurora kinases. Usually cells die both by apoptosis or necrosis shortly after dysregulated/failed mitosis, often preceded by mitotic devastation, a cell death style easily distinguishable because of its micro and/ or multinucleation.