Journal of Physics Research and Applications

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Reformulation of relativistic quantum field theory on an advanced fragment-based multi-dimensional chemico-informatic region-like idealization approach for the in silico prediction of the microcrylaqtm compound; a novel t790m mutant regulator for avoiding egfr drug resistance in cancer nsclc treatme

Ioannis Grigoriadis

Biogenea Pharmaceuticals Ltd, Greece

: J Phys Res Appl


The existence of any elementary particle in universe requires the existence of some region of universe occupied by it. By taking the volume of this occupied region, the author will reformulate the relativistic quantum field theory using new 3-dimensional region-like idealization of elementary particles and hereinafter will call the total volume of all regions occupied by the elementary constituent particles of the quantum system the occupied volume. Also,we set of all regions of universe filled by elementary constituent particles of the quantum system the occupied path. Always any quantum system is existed at a head of its occupied path. This path is growing by mutual filling and leaving regions of universe by its elementary constituent particles. The conservation of this elementary constituent particle requires the conservation of its occupied volume during this process. Also in Hilbert’s representation of the quantum theory these wave functions are representing the components of the quantum state vector. The EGFR is one of the most popular targets for anticancer therapies and many drugs, such as erlotinib and gefitinib, have got enormous success in clinical treatments of cancer in past decade. However, the efficacy of these agents is often limited because of the quick emergence of drug resistance. Fundamental structure researches of EGFR in recent years have generally elucidated the mechanism of drug resistance. Here, for the first time we present the MicrocrylaqTM inhibitor which reformulated the transformation Quantum Theory of the regionlike quantum state of a hypothetical EGFR quantum system for the simulation of the docking effects against the T790M mutant regulator for avoiding EGFR drug resistance in cancer NSCLC treatments.


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