DESIGNED ANTICANCER CHEMICAL HYPERPHARMACOPHORE MOLECULES WITH QUANTUM-MOLECULAR BINDING AFFINITY TO SIGNAL TRANSDUCTION TARGETS AND MOTIF REGIONS THEREOF RELATING TO GLIOMA IN HUMANS

摘要

71 20190100013 Aim of the invention is the determination of a drug target, the determination of a target structure, the determination of the target site/binding site, and the selection of the drug design method for proposed lead components (drug lead evaluation) and of an optimized drug lead against signal transduction peptide and protein target molecules and motif regions thereof by modelling, molecular recognition and molecular dynamics techniques for the treatment of glioma in human. The present invention claims a new optional-evaluation function with factorial combination of terms from two or more different evaluation functions, as a new computational tool for compacting active pharmacophores in order to generate a hyperpharmacophore with optimized quantum docking properties for the computational design of new chemical drug structures of high total binding energy on the active sites of the mutation motif peptides responsible for glioma in humans. It should be mentioned that the present invention claims more complex non-linear techniques for the computation of the free binding energy from the evaluation vector, which better depict the real binding energy even when any of these attempts to capture a total of the binding at the maximum possible of the binding information present in the binding affinity evaluation-prediction vector of the ligand GLYBATOMAOTM. Aim of the invention is to claim the Components and Quantum-mechanical Standardisation methods via a motif chemogenomic computer-assisted quantum-molecular approximation (CAMSPCPL) for the chemoinformative design of a polypharmacophore MEFLWAPLLGLCCSLAAA peptidomimetic molecule targeting against the signal-transduction peptide molecules and motif regions thereof for the of the peptide molecule derived signal transduction against the motif regions thereof, in order to eventually suppress the overexpression of the mutant form of the genes and proteins thereof EGFR, EGFRvlll, MGMT, MSH6, PI3K, Src-STAT, p16INK4A, VEGF, Akt, mTOR, HER2 mRNA and MET in the same tumors for the treatment of glioma in humans.