evidence is emerging that the major two different spot mutations in PIK3CA represent functionally distinct oncogenic actions. The strains in PIK3CA primarily occur in two different parts of the gene. It’s not fully understood how these mutations contribute to the growth of tumours, nevertheless they do are capable of inducing tumours in vivo, are capable of inducing transformation of cultured cells and confer a small natural compound library increase in catalytic action. The full implications of PIK3CA gene amplification are not fully comprehended, but possibly act by increasing overall PI3K activity levels. The recognition of oncogenic mutations and amplifications in PIK3CA has spurred the development of the wide range of smallmolecule inhibitors targeting PI3K, with many of these currently in clinical trials. A lot of the compounds produced thus far target multiple PI3K isoforms and related kinases including mTOR. Compounds in this school show efficacy in inhibiting development of cells in culture and xenograft models. Plastid But, a question that remains to be answered is whether precisely targeting p110 might achieve similar results given that this seems to be the prevalent oncogenic form of class I PI3Ks. The possible importance of targeting p110 is shown by studies showing distinct genetic knockdown of PIK3CA does stop cell signalling and cell growth in a range of tumour lines. Currently having less suitable small molecule inhibitors has recommended that it’s not been possible to precisely evaluate whether pharmacological inhibition of p110 can achieve similar results. Only 1 number of small molecules has been described that has a high degree of selectivity for p110 compared with other PI3K isoforms. One person in this family, PIK 75, has been used to examine the role of p110, supplier Everolimus but was found to have significant off target activity, meaning it is difficult to know whether any actions of this drug are in fact because of its activity against PI3K. Despite these limitations, this drug is utilized in some studies to infer that blocking p110 is sufficient to prevent signalling to Akt/PKB in some cell types but not others. Furthermore, substances associated with PIK 75 have shown antitumour activity in vivo, hinting that p110 inhibitionmight become a of use therapeutic technique. However these studies can not be established until a suitably clear p110 selective chemical is available. In our paper, we report the properties of A66, a compound that was recently found to be a potent p110 inhibitor. We show this element features a high level of specificity and is highly selective for p110 over other PI3Ks as it doesn’t target other protein kinases tried. We make use of this to demonstrate that inhibition of p110 attenuates signalling in a subset of cell types that are characterized with kinase domain mutations in PIK3CA, high p110 levels and high total course 1a PI3K activity.