Three novel gold(III) complexes (1–3) of general composition [Au(Bipydc)(S₂CNR₂)]Cl₂ (Bipydc = 2,2′-bipyridine-3,3′-dicarboxylic acid and R = methyl for dimethyldithiocarbamate (DMDTC), ethyl for diethyldithiocarbamate (DEDTC), and benzyl for dibenzyldithiocarbamate (DBDTC)) have been synthesized and characterized by elemental analysis, FTIR and NMR spectroscopic techniques. The spectral results confirmed the presence of both the Bipydc and dithiocarbamate ligands in the complexes. The in vitro cytotoxic studies demonstrated that compounds 1–3 were highly cytotoxic to A549, HeLa, MDA-231, and MCF-7 cancer cells with activities much higher (about 25-fold) than cisplatin. In order to know the possible mode of cell death complex 2, [Au(Bipydc)(DEDTC)]Cl₂ was further tested for induction of apoptosis towards the MCF-7 cells. The results indicated that complex 2 induces cell death through apoptosis.

Four novel phosphanegold(I) complexes of the type [Au(PR₃)(DMT)].PF₆ (1–4) were synthesized from 3-Thiosemicarbano-butan-2-one oxime ligand (TBO) and precursors [Au(PR₃)Cl], (where R = methyl (1), ethyl (2), tert-butyl (3), and phenyl (4)). The resulting complexes were characterized by elemental analyses and melting point as well as various spectroscopic techniques, including FTIR and (¹H, ¹³C, and ³¹P) NMR spectroscopy. The spectroscopic data confirmed the coordination of TBO ligands to phosphanegold(I) moiety. The solution chemistry of complexes 1–4 indicated their stability in both dimethyl sulfoxide (DMSO) and a mixture of EtOH:H₂O (1:1). In vitro cytotoxicity of the complexes was evaluated relative to cisplatin using an MTT assay against three different cancer cell lines: HCT116 (human colon cancer), MDA-MB-231 (human breast cancer), and B16 (murine skin cancer). Complexes 2, 3, and 4 exhibited significant cytotoxic effects against all tested cancer cell lines and showed significantly higher activity than cisplatin. To elucidate the mechanism underlying the cytotoxic effects of the phosphanegold(I) TBO complexes, various assays were employed, including mitochondrial membrane potential, ROS production, and gene expression analyses. The data obtained suggest that complex 2 exerts potent anticancer activity against breast cancer cells (MDA-MB-231) through the induction of oxidative stress, mitochondrial dysfunction, and apoptosis. Gene expression analyses showed an increase in the activity of the proapoptotic gene caspase-3 and a reduction in the activity of the antiapoptotic gene BCL-xL, which supported the findings that apoptosis had occurred.

The complex was found to display cytotoxic effect via oxidative stress-mediated intrinsic apoptotic pathway in MDA-MB-231 cancer cells, as indicated by Annexin V-FITC/Propidium iodide double staining, ROS production, mitochondrial membrane potential and migration assays.

Four novel dinuclear phosphanegold(I) complexes containing bis(diphenylphosphano)alkanes and (biphenyl-2-yl)di-tert-butylphosphane (Bdbp), [Au₂(Bdbp)₂(Dppe)](PF₆)₂ (1), [Au₂(Bdbp)₂(Dppp)](PF₆)₂ (2), [Au₂(Bdbp)₂(Dppb)](PF₆)₂ (3) and [Au₂(Bdbp)₂(Dpma)](PF₆)₂ (4) (where Dppe = 1,2-bis(diphenylphosphano)ethane, Dppp = 1,3-bis(diphenylphosphano)propane, Dppb = 1,4-bis(diphenylphosphano)butane and Dpma = bis[2-(diphenylphosphano)methyl]amine), were synthesized and characterized by elemental analysis, FTIR and NMR spectroscopies. The structures of three of the complexes (1, 2 and 4) were determined by X-ray crystallography, which reveals that the complexes exist as dinuclear species, in which the gold(I) atom is linearly coordinated to the phosphorus (P2) and (P1) atoms. The in vitro cytotoxicity of the complexes was investigated against two established human cancer cell models, colorectal (HCT-116) and breast (MCF7) cancer cells. All four complexes showed excellent cytotoxicity against both cell models with significantly lower IC₅₀ values than that of cisplatin. The mitochondrial membrane potential (ΔΨ_m) was also assessed to get a better understanding of the underlying molecular mechanism of toxicity. The exposure of the complexes for 24 hours resulted in mitochondrial depolarization (reduced mitochondrial health) thereby potentially triggering the release of cytochrome c and apoptotic cell death. Together, the findings of our studies demonstrate that the novel gold(I) complexes have superior anticancer activity compared to conventional cisplatin, which is potentially mediated through the disruption of ΔΨ_m and induction of apoptosis.

Purpose: This study sought to extract and characterize fucoidan from brown seaweed Padina tetrastromatica for the synthesis of fucoidan–gold nanoparticles (F-AuNPs) and to assess their physicochemical properties, as well as their antioxidant, anti-inflammatory, and anticancer activities, alongside potential molecular interactions with specific cancer-related targets. Methods: The extracted fucoidan-rich fraction was characterized for its sulfate content. Citrate-stabilized plain gold nanoparticles (plain AuNPs) were prepared and characterized as non-fucoidan nanoparticle controls. Comprehensive physicochemical characterization, including UV–Vis spectroscopy, Fourier-transform infrared spectroscopy (FTIR), transmission electron microscopy (TEM), X-ray diffraction (XRD), dynamic light scattering (DLS), zeta-potential analysis, and thermogravimetric analysis (TGA), was performed on the resultant fucoidan-functionalized AuNPs (F-AuNPs). Biological activities were assessed using different techniques: antioxidant potential (Ferric Reducing Antioxidant Power (FRAP) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) assays), anti-inflammatory effects (NO inhibition in macrophages), and anticancer efficacy against HepG2 cells (MTT and flow cytometry). Potential molecular targets relevant to these activities were further explored in silico using molecular docking against key cancer-related proteins, providing hypotheses for future experimental validation. Results: The fucoidan-rich fraction showed a sulfate content of 10.08%. Strong antioxidant activity was observed, especially in FRAP (11.20 ± 0.29 mg TE g⁻¹ DW). F-AuNPs exhibited enhanced cytotoxicity against HepG2 cells (IC₅₀ 138.1 µg mL⁻¹) compared to plain AuNPs (IC₅₀ 271.2 µg mL⁻¹) and the fucoidan-rich fraction (IC₅₀ 390.2 µg mL⁻¹), inducing G1 phase arrest. In addition, F-AuNPs reduced nitric oxide production in LPS-stimulated RAW 264.7 macrophages, reaching 21.42 ± 1.29% inhibition at 100 µg mL⁻¹. As an exploratory, hypothesis-generating step, an in silico target-prioritization screen identified HPSE and MMP-2 as the highest-scoring candidate proteins, proposed solely as targets for future experimental validation. Conclusions: F-AuNPs represent a promising multifunctional nanoplatform with antioxidant, anti-inflammatory, and antiproliferative activities. The integration of in vitro biological evaluation with in silico target prediction supports the potential biomedical relevance of F-AuNPs and generates testable hypotheses regarding their molecular targets, which require experimental validation.