Metal‐Complex Extension of an Allylated Hydrazide/Thiosemicarbazide S4/S3 Ligand Pair: Donor‐Set Control of Spectral, Thermal, Antimicrobial, and MCF‐7 Screening Profiles

ABSTRACT Using a previously reported allylated hydrazide/thiosemicarbazide S4/S3 ligand platform, S4 (2‐(allyloxy)benzohydrazide) and S3 (2‐(2‐(allyloxy)benzoyl)‐ N ‐ethylhydrazine‐1‐carbothioamide) were prepared and extended to a first‐row metal‐complex series with Co (II), Ni (II), Cu (II), Mn (II), and Zn (II). The novelty lies in the metal‐complex extension and donor‐set‐dependent comparison of this known scaffold, not in rediscovery of the standalone ligands. The study compares the compact hydrazide O,N‐donor S4 platform with the sulfur‐containing thiosemicarbazide O,N,S‐donor S3 platform to examine complex formation, spectroscopic response, thermal behavior, disk‐diffusion antimicrobial screening, and MCF‐7 MTT activity. The ligands and isolated products were examined by elemental/metal analysis, FT‐IR, UV–Vis, ligand‐level 1 H NMR, magnetic susceptibility, TGA/DTG, antimicrobial disk diffusion, and MTT screening; selected 48‐h dose–response curves for S4‐Ni, S4‐Mn, and S4‐Co are provided in the Supporting Information as auxiliary IC 50 evidence. Convergent CHNS/metal elemental analysis, FT‐IR, UV–Vis, magnetic, and thermal observations support formation of metal–organic coordination solids, with O,N coordination proposed for S4‐derived complexes and O,N,S involvement proposed for S3‐derived complexes. Calculated/found CHNS/metal data support the selected empirical formulations, while the geometries are treated as proposed working coordination modes pending crystallographic confirmation. S4‐derived complexes showed the stronger antimicrobial profile, especially Co‐S4 against Staphylococcus aureus (16.85 ± 0.26 mm) and Ni‐S4 against Candida albicans (17.75 ± 1.10 mm). In the MCF‐7 single‐dose screen at 10 μg mL −1 , Zn‐S3 (87.79%), Ni‐S4 (80.16%), Co‐S3 (73.85%), and Ni‐S3 (73.50%) were the leading derivatives. Overall, sulfur incorporation did not act as a universal activity enhancer; instead, it redirected endpoint‐dependent metal behavior across the antimicrobial and MCF‐7 screens.