Novel NO Pincer Type 2‐(5,6‐Dichlorobenzo[d]thiazol‐2‐yl)phenol and Its Complex of Pt (II): Synthesis, Spectral Characterization, DFT Calculations, Cell Cycle Arrest, Apoptosis Assay, Cytotoxicity, DNA Binding, and Biological Evaluation Study

ABSTRACT A new novel NO pincer type bezo[ d ]thiazole ligand, 2‐(5,6‐dichlorobenzo[d]thiazol‐2‐yl)phenol (HDCBTP) is synthesized through reacting 2‐amino‐4,5‐dichlorobenzenethiol and 2‐hydroxybenzoic acid in 1:1 ratio. Nano‐sized bivalent Pt (II) complex is created and subsequently characterized using various physical methods. The complex structural geometry is validated by employing the density functional theory (DFT) approach, utilizing DMOL 3 determinations. Based on the elemental analysis results, the complexes are inferred to follow the overall formula [Pt (DCBTP) 2 ]. Quantum chemical calculations, along with electronic spectra findings, indicate that Pt (II) complex exhibits a square planar configuration. The XRD, EDX, TEM, and AFM analyses of the studied complex unveil distinct and strong diffraction peaks, indicating its crystalline nature and providing evidence of its nano‐sized particle sizes. Viscosity measurements and absorption titration techniques were used to study the interaction between Pt (II) complex and CT‐DNA. The results showed that the complexes were bound to CT‐DNA via a typical intercalation binding mode. The in vitro antimicrobial efficacy of HDCBTP and its Pt (II) complex was inspected against various bacterial and fungal pathogens. The results highlight these compounds as a highly effective fungicides and bactericides. In vitro cytotoxic effects of the formulated complex were explored utilizing PC3 prostate cancer cell lines. According to IC 50 and selective index (SI) measurements, it was shown that the complex exhibited higher potency against HePG2 cell lines. Moreover, Pt (II) complex exhibited the capability for triggering DNA damage in HePG2 cells, resulting in dose‐dependent cell apoptosis. Subsequent investigations revealed that complex triggered cell cycle arrest during the S and G2 phases.