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Despite tremendous progress and steep increase in R & D expenditure in the field of oncology research, cancer still remains a major worldwide health concern (Mou, Kesari, Wen, & Huang, 2011). Today the success of novel cancer therapies depends on identification of potential targets responsible for tumour initiation and survival (King et al., 2006). Therefore, there seems to be a paradigm shift in the development process of novel therapeutic agents for this dreadful disease. Accordingly, more attention is now being accorded to treatments that focus on specific molecular targets generated in cancer cells instead of non-specific cytotoxic chemotherapies that affect all dividing cells in the body (Harrison, Holen, & Liu, 2009). Uncontrolled proliferation of cells or abnormality in early stages of the cell cycle is one of the major causes in prognosis of human tumor/cancer (Jordan, & Wilson, 2004). Mitosis is a critical stage in the cell cycle which assures the consistent inheritance of the genetic material by the cellular family at the same time prohibiting chromosomal instability (CIN) and aneuploidy (Hanahan, & Weinberg, 2011; Gordon, Resio, & Pellman, 2012). The ubiquitous involvement of mitotic kinases in essentially all the signal transmitting pathways provides a clear cut indication for pursuing research towards developing targeted kinase inhibitors as anti-cancer agents (Miduturu et al., 2011). Tyrosine threonine kinase (TTK), also called monopolar spindle1 (MPS1) is amongst the top 25 genes abnormally unregulated in tumors of different origins (Malumbres, & Barbacid, 2007; Carter, Eklund, Kohane, Harris, & Szallasi, 2006; Carcer De, Perez de Castro, & Malumbres, 2007) and invariable with its expression in cell cycle evolution (Doua et al., 2004). Over expression of TTK may promote tumor initiation and survival of genomically unstable and aneuploid cancer cells (Kilpinen, Ojala, & Kallioniemi, 2010). Basically, TTK is a serine/threonine and tyrosine kinase that regulates chromosome alignment during mitosis (Malumbres, 2011). This family of dual specificity kinase is widely but not ubiquitously distributed in eukaryotes and constitutes an important element of spindle assembly checkpoint (SAC) (Jemaa et al., 2013). SAC pathway monitors transit via the cell cycle at various phases, i.e., mitotic spindle attachment at kinetochores during prometaphase, restrict anaphase initiation until all of the chromosomes made stable bipolar connection to centrosomes and correctly aligned at the metaphase plate (Musacchio, & Salmon, 2007; Teixeira et al., 2014). Deregulation of MPS1 kinase activity results in abnormal chromosome number or CIN and consequently, in aneuploidy (Hanahan, & Weinberg, 2011) which is an incessant feature of cancer cells and generally regarded as possible cause of carcinogenesis (Thompson, & Compton, 2008).