Some fluoroquinazolinones (A–H) were designed, synthesized and biologically evaluated for their antitumor activity against the two cell lines, MCF-7 and MDA-MBA-231. New derivative G (IC₅₀ = 0.44 ± 0.01 µM) showed antitumor activity, better than that of the reference drug erlotinib (IC₅₀ = 1.14 ± 0.04 µM) against MCF-7. New derivative E (IC₅₀ = 0.43 ± 0.02 µM) showed higher activity than the reference drug erlotinib (IC₅₀ = 2.55 ± 0.19 µM) against MDA-MBA-231. Furthermore, the EGFR (epidermal growth factor receptor) and tubulin inhibition assays were carried out for the highest active derivatives to reveal the expected mechanism of action. They exhibited significant results compared to the reference drugs. Molecular docking simulations were performed on EGFR and tubulin binding sites to rationalize the experimental results and describe their binding modes. The results of the molecular modeling study were correlated with that of the antitumor screening.

A series of 3-(2H-1,2,4-triazol-5-yl)-1,3-thiazolidin-4-one derivatives (7c–l) was designed and synthesized. Their structures have been elucidated based on analytical and spectral data. They were evaluated for their antibacterial and antifungal activities. Compound 7h showed the highest activity against all tested strains, except P. vulgaris, with MIC 8 μg/mL and 4 μg/mL against S. aureus and C. albicans, respectively. Furthermore, Compounds 7c, 7h, and 7j demonstrated moderate anti-mycobacterium activity. The binding mode of the synthesized thiazolidinones to bacterial MurB enzyme was also studied. Good interactions between the docked compounds to the MurB active site were observed primarily with Asn83, Arg310, Arg188 and Ser82 amino acid residues.

A series of new fluoroquinazolinone 6–8 and 10a–g derivatives was designed, prepared and screened for their in vitro cytotoxic activity against human cancer cell lines MCF-7 and MDA-MBA-231. Compounds 6 (IC₅₀ = 0.35 ± 0.01 µM), 10f (IC₅₀ = 0.71 ± 0.01 µM), 10d (IC₅₀ = 0.89 ± 0.02 µM) and 10a (IC₅₀ = 0.95 ± 0.01 µM) displayed broad spectrum anticancer activity better than the reference drug gefitinib (IC₅₀ = 0.97 ± 0.02 µM) against MCF-7. Compounds 10e (IC₅₀ = 0.28 ± 0.02 µM), 10d (IC₅₀ = 0.38 ± 0.01 µM), 7 (IC₅₀ = 0.94 ± 0.07 µM) and 10c (IC₅₀ = 1.09 ± 0.01 µM) showed better activity than the reference gefitinib (IC₅₀ = 1.30 ± 0.04 µM) against MDA-MBA-231. Moreover, EGFR and tubulin inhibition assays were performed for the highest active derivatives and showed remarkable results comparing to the reference drugs. In order to assess and explain their binding affinities, molecular docking simulation was studied against EGFR and tubulin binding sites. The results obtained from molecular docking study and those obtained from cytotoxic screening were correlated.