From the reaction of 1-methylimidazole (1a), 4,5-dichloro-1H-imidazole (1b(I)) and 1-methylbenzimidazole (1c) with p-cyanobenzyl bromide (2a), non-symmetrically substituted N-heterocyclic carbene (NHC) [(3a-c)] precursors, 5,6-dimethyl-1H-benzimidazole (1d) and 4,5-diphenyl-1H-imidazole (1e) with p-cyanobenzyl bromide (2a) and benzyl bromide (2b), symmetrically substituted N-heterocyclic carbene (NHC) [(3d-f)] precursors were synthesised. These NHC-precursors were then reacted with silver(i) acetate to yield the NHC-silver complexes (1-methyl-3-(4-cyanobenzyl)imidazole-2-ylidene)silver(i)acetate (4a), (4,5-dichloro-1-(4-cyanobenzyl)-3-methyl)imidazole-2-ylidene)silver(i)acetate (4b), (1-methyl-3-(4-cyanobenzyl)benzimidazole-2-ylidene)silver(i)acetate (4c), (1,3-bis(4-cyanobenzyl)5,6-dimethylbenzimidazole-2-ylidene) silver(i) acetate (4d), (1,3-dibenzyl-5,6-dimethylbenzimidazole-2-ylidene) silver(i) acetate (4e) and (1,3-dibenzyl-4,5-diphenylimidazol-2-ylidene) silver(i) acetate (4f) respectively. Three NHC-precursors 3c-e and four NHC-silver complexes 4b and 4d-f were characterised by single crystal X-ray diffraction. Preliminary in vitro antibacterial activity of the NHC-precursors and NHC-silver complexes was investigated against Gram-positive bacteria Staphylococcus aureus, and Gram-negative bacteria Escherichia coli using the qualitative Kirby-Bauer disk-diffusion method. NHC-silver complexes have shown very high antibacterial activity compared to the NHC-precursors. All six NHC-silver complexes were tested for their cytotoxicity through MTT based in vitro tests on the human renal-cancer cell line Caki-1 in order to determine their IC₅₀ values. NHC-silver complexes 4a-f were found to have IC₅₀ values of 6.2 (±1.0), 7.7 (±1.6), 1.2 (±0.6), 10.8 (±1.9), 24.2 (±1.8) and 13.6 (±1.0) μM, respectively. These values represent improved cytotoxicity against Caki-1, most notably for 4c, which is a three times more cytotoxic than cisplatin (IC₅₀ value = 3.3 μM) itself.

p‐Methoxybenzyl‐substituted and benzyl‐substituted N‐heterocyclic carbene (NHC) [(3a–c) and (6a–c)] precursors were synthesised from the reaction of 1H‐imidazole (1a), 4,5‐dichloro‐1H‐imidazole (1b), and 1H‐benzimidazole (1c) with p‐methoxybenzyl bromide (2) and benzyl bromide (5). These NHC precursors were then treated with silver(I) acetate to yield the NHC–silver complexes [1,3‐bis(4‐methoxybenzyl)imidazol‐2‐ylidene]silver(I) acetate (4a), [4,5‐dichloro‐1,3‐bis(4‐methoxybenzyl)imidazol‐2‐ylidene]silver(I) acetate (4b), [1,3‐bis(4‐methoxybenzyl)benzimidazol‐2‐ylidene]silver(I) acetate (4c), (1,3‐dibenzylimidazol‐2‐ylidene)silver(I) acetate (7a), (1,3‐dibenzyl‐4,5‐dichloroimidazol‐2‐ylidene)silver(I) acetate (7b), and (1,3‐dibenzylbenzimidazol‐2‐ylidene)silver(I) acetate (7c), respectively. The NHC precursor 3c, four NHC–silver complexes 4c and 7a–c were characterised by single‐crystal X‐ray diffraction method. The preliminary antibacterial activity of all the compounds was studied against Gram‐negative bacteria Escherichia coli, and Gram‐positive bacteria Staphylococcus aureus using the Kirby–Bauer disk‐diffusion method. Almost all the NHC–silver complexes have shown high antibacterial activity compared to the NHC precursors. In addition, the NHC–silver complexes had their cytotoxicity investigated through MTT‐based preliminary in vitro testing on the Caki‐1 cell lines in order to determine their IC50 values. NHC–silver complexes 4a–c and 7a–c were found to have IC50 values of 7.3 (+/–6), 12.7(+/–3), 25.2 (+/–5), 2.5 (+/–3), 10.8 (+/–4) and 12.5 (+/–4) μM respectively on the Caki‐1 cell line.

Titanium(IV) complexes with a salan or cyclopentadienyl ligand showed different biological behaviour concerning binding to biomolecules, cellular accumulation and intracellular distribution. Binding efficacy as well as trafficking on the cellular level are crucial parameters for their biological effects.

N-Heterocyclic carbene (NHC) complexes bromo(1,3-dibenzyl-1,3-dihydro-2H-imidazol-2-ylidene)silver(I) (2a), bromo[1-(4-cyanobenzyl)-3-methyl-1,3-dihydro-2H-imidazol-2-ylidene]silver(I) (2b), and bromo[1-(4-cyanobenzyl)-3-methyl-1,3-dihydro-2H-benzimidazol-2-ylidene]silver(I) (2c) were prepared by the reaction of 1,3-dibenzyl-1H-imidazol-3-ium bromide (1a), 3-(4-cyanobenzyl)-1-methyl-1H-imidazol-3-ium bromide (1b), and 3-(4-cyanobenzyl)-1-methyl-1H-benzimidazol-3-ium bromide (1c), respectively, with silver(I) oxide. NHC Complexes chloro(1,3-dibenzyl-1,3-dihydro-2H-imidazol-2-ylidene)gold(I) (3a), chloro[1-(4-cyanobenzyl)-3-methyl-1,3-dihydro-2H-imidazol-2-ylidene]gold(I) (3b), and chloro[1-(4-cyanobenzyl)-3-methyl-1,3-dihydro-2H-benzimidazol-2-ylidene]gold(I) (3c) were prepared via transmetallation of corresponding (bromo)(NHC)silver(I) complexes with chloro(dimethylsulfido)gold(I). The complex 3a was characterized in two polymorphic forms by single-crystal X-ray diffraction showing two rotamers in the solid state. The cytotoxicities of all three bromo(NHC)silver(I) complexes and three (chloro)(NHC)gold(I) complexes were investigated through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bormide (MTT)-based preliminary in vitro testing on the Caki-1 cell line in order to determine their IC 50 values. (Bromo)(NHC)silver(I) complexes 2a -2c and (chloro)(NHC)gold(I) complexes 3a -3c were found to have IC 50 values of 27 AE 2, 28 AE 2, 34 AE 6, 10 AE 1, 12 AE 5, and 12 AE 3 mm, respectively, on the Caki-1 cell line.

From the reaction of 1H‐imidazole (1a), 4,5‐dichloro‐1H‐imidazole (1b), 1H‐benzimidazole (1c), 1‐methylimidazole (1d), 4,5‐dichloro‐1‐methylimidazole (1e) and 1‐methylbenzimidazole (1f) with p‐nitrobenzyl bromide (2), symmetrically and non‐symmetrically p‐nitrobenzyl‐substituted N‐heterocyclic carbene (NHC) [(3a–f)] precursors were synthesised. These NHC‐precursors were then reacted with silver(I) acetate to yield the NHC‐silver acetate complexes [1,3‐bis(4‐nitrobenzyl)imidazol‐2‐ylidene]silver(I) acetate (4a), [4,5‐dichloro‐1,3‐bis(4‐nitrobenzyl)imidazol‐2‐ylidene]silver(I) acetate (4b), [1,3‐bis(4‐nitrobenzyl)benzimidazol‐2‐ylidene]silver(I) acetate (4c), [1‐methyl‐3‐(4‐nitrobenzyl)imidazole‐2‐ylidene] silver(I) acetate (4d), [4,5‐dichloro‐1‐methyl‐3‐(4‐nitrobenzyl)imidazole‐2‐ylidene] silver(I) acetate (4e) and [1‐methyl‐3‐(4‐nitrobenzyl)benzimidazole‐2‐ylidene] silver(I) acetate (4f), respectively. The two NHC–silver(I) acetate complexes 4a and 4e were characterised by single‐crystal X‐ray diffraction. All compounds studied in this work were preliminary screened for their antimicrobial activities in vitro against Gram‐positive bacteria Staphylococcus aureus, and Gram‐negative bacteria Escherichia coli using the qualitative Kirby–Bauer disk‐diffusion method. All NHC–silver(I) acetate complexes exhibited medium to high antibacterial activity with areas of clearance ranging from 3 to 7 mm at the highest amount used, whereas the NHC‐precursors showed significantly lower activity. In addition, NHC–silver(I) acetate complexes 4a–f had their preliminary cytotoxicity tests on the human renal‐cancer cell line Caki‐1 and showed medium to high cytotoxicity with IC50 values ranging from 15 (+/–1) to 27 (+/–2) μM.