Rose bengal- Pioglitazone drug reaction novel products. Structures – biological activity and cytotoxicity relationship and evaluation with theoretical calculations.

Abstract

The PIOG-RBeng reaction novel products were characterized by thermal in comparison with spectroscopic data using FT-IR, 1H-NMR, and then confirmed by XRD measurements and Theoretical computational calculations. The software of Gaussian 09W package had been used for computations. The geometries of Rose bengal (RBeng), Pioglitazone (PIOG) drug and their reaction products were optimized using B3LYP method and (DFT)/GENECP level was obtained by using Def2TZVP basis set. The basis set 6-311++G (d, p) had been used for remainder atoms. The mixed basis set was used due to its flexibility. HOMO and LUMO energy values, chemical hardness and electronegativity had been calculated for compounds. NBO calculations were made for measurement qualitatively the intra-molecular delocalization in systems under investigation on the same level using (NBO 3.1) program implanted in Gaussian 09W.The theoretical calculations involved estimation of global reactivity descriptors, local descriptors and molecular electrostatic potential (MEP) maps. TD-DFT approximation was used to calculate the FT-IR and 1HNMR spectra of the studied compounds; which actually compared with practical data. Successful correlation between experimental and theoretical calculations had been made to confirm structures of studied compounds. The X-ray diffraction (XRD) was used to study the crystallographic structures of compounds under investigation. The practical results are also correlated to theoretical calculations of electronegativity (X), polarizability, HOMO and LUMO values of PIOG and PIOG-RBeng reaction products. The vibrational frequencies were evaluated in comparison with the corresponding normal modes at the optimized geometry. The investigated compounds are highly effective against Hepatocellular carcinoma, Breast carcinoma and Colon carcinoma cells. It is concluded that; cancer cells over expression promotes tumorigenic functions; can be suppressed by reaction products inhibitors.