Justin C. Holmes, Arinzechukwu C. Egwu, Sean Parkin, Sanjay Dutta, Sashen Ruhunage, Chad Risko, Samuel G. Awuah
Strategies for rationally designing gold‐based chemotherapeutics remain limited by an incomplete understanding of how ligand electronics shape structure and biological function. Here, we establish a direct link between σ‐donor strength, geometric distortion, and anticancer activity across a series of carbon‐stabilized Au(III) bisphosphine macrocycles derived from N , N′‐ (1,2‐phenylene)bis(2‐(diphenylphosphino)benzamide) (dppbH 2 ) and electronically tuned cyclometalated [C^N] templates. Systematic installation of substituents that modulate σ‐donation to Au(III) produces predictable shifts in Au—C and Au—P bond lengths, trans bite angles, and square planar deformation. σ‐donor character of complexes influences geometric distortion, aqueous stability, and up to an order‐of‐magnitude higher cytotoxicity in triple‐negative breast cancer and estrogen receptor–positive models compared to cisplatin. Mechanism of action studies supports acute mitochondrial uncoupling and mtROS production, leading to cell death by this class of compounds. This electronic–structural–biological correlation provides a rare, experimentally validated design principle for Au(III) scaffolds and positions electronically tuned macrocycles as a chemically tractable platform for targeting intracellular pathways.