New synthetic chitosan Schiff bases bearing pyranoquinolinone or benzonaphthyridine and their silver nanoparticles derivatives with potential activity as antioxidant and molecular docking study for EGFR inhibitors

RSC Adv. 2024 Sep 20;14(41):29919-29933. doi: 10.1039/d4ra05117c. eCollection 2024 Sep 18.

Abstract

In this study, two new carboxaldehydes 3, and 4 were synthesized by Vilsmeier-Haack formylation of 6-butyl-benzo[h][1,6]naphthyridine-2,5-dione 2 and 6-butyl-pyrano[3,2-c]quinolinone 1, respectively. Structures of newly synthesized compounds were achieved by IR, 1H NMR, 13C NMR, mass techniques, and elemental analyses. The two synthesized carboxaldehydes 3 and 4 were used as precursors for the synthesis of two new chitosan-based Schiff bases, CS1 and CS2. The new chitosan Schiff bases were grafted on silver nanoparticles, providing CS1/Ag and CS2/Ag structures. However, CS1 and CS2 and their silver nanoparticles were characterized by FT-IR, XRD, SEM-EDX, XRF, TEM, TGA, and DSC. The target compounds CS1, CS2, CS1/Ag, and CS2/Ag were assessed as radical scavengers against 1,1-diphenyl-2-picrylhydrazyl radicals (DPPH%). The results showed that CS1 and CS2 had a better ability to scavenge DPPH radical than its unmodified chitosan. CS1/Ag and CS2/Ag, combining the unique properties of silver and Schiff bases, displayed excellent antioxidant activity (IC50, 59.13, and 32.54 μg mL-1, respectively). In addition, the previous compounds were tested in vitro for inhibition of epidermal growth factor receptor (EGFR) tyrosine kinase using the EGFR kinase assay kit (Cat. #40321). In particular, compound CS1/Ag displayed potent inhibitory activity towards EGFR with IC50 20.45 μg mL-1 compared to reference drug sorafenib (IC50 = 0.76 μg mL-1). The bioactivity of new chitosan Schiff bases was studied by molecular docking to see how they bind with the EGFR receptor. The results implied that CS1 has a higher binding energy than CS2 and CS regarding EGFR kinase, which agreed with the results obtained from the experimental EGFR inhibition assay.