Tailoring precursor reactivity in colloidal nanocrystals (NCs) is a powerful strategy to achieve the uniformity. The gold precursor reactivity was engineered in multistep cation exchange reactions of Ag-Au-S quantum dots (QDs) through ligand coordination, metal-metal bonding, and steric effects, resulting in a series of discrete exchange pathways. With the conventional precursor HAuCl₄, Ag₂S QDs undergo complete conversion to Au₂S QDs via Ag₃AuS₂ and AgAuS alloy QD intermediates; however, this process yields compositionally inhomogeneous QDs or QD mixtures of multiple phases, producing broad or bimodal photoluminescence (PL). In contrast, the mononuclear phosphine-coordinated precursor AuPPh₃Cl selectively halts exchange at AgAuS QDs even in large excess, affording phase-pure Ag₃AuS₂ and AgAuS QDs with brighter and narrower PL. Further suppression of reactivity was achieved with multinuclear AgAu<i>_m</i>(PPh₃)_<i>n</i>Cl_<i>m</i>+1 complexes, which stalled exchange precisely at Ag₃AuS₂ QDs as phase-pure. Mechanistic analyses using ³¹P NMR and mass spectrometry revealed that AuPPh₃Cl undergoes in situ transformation into multinuclear Ag-Au-phosphine complexes that attenuate exchange through Ag-Au interactions and steric hindrance. This reactivity-controlled exchange enables precise phase targeting across a QD size series while preserving the size and morphology, yielding narrow and tunable emission spanning 1.04-1.87 eV (663-1192 nm) in the red-to-near-infrared spectral region. These findings establish precursor reactivity engineering as a powerful design principle for achieving phase-pure alloyed NCs and broaden opportunities for optoelectronic devices, infrared bioimaging, and other applications requiring spectrally precise nanomaterials.

Dopamine (DA) is an essential neuromodulator that underlies critical aspects of cognitive processes, motor function, and reward systems. Disruptions in DA signaling contribute to various neurodegenerative diseases, including Parkinson's disease (PD). Despite its important role in neuronal function, the impact of DA release/uptake on neurochemical imbalances during neuronal development remains unclear. We propose a novel application of near-infrared catecholamine nanosensor (NIRCat) for real-time visualization of DA neurotransmission among neurodegenerative disease cells. The near-infrared fluorescence (900-1400 nm) of NIRCat allows the semi-quantitative measurement of DA release in living neurons and offers insights into cellular dynamics and neuropathological development. In this study, we applied NIRCat to elucidate DA release in human induced pluripotent stem cells (hiPSCs)-derived dopaminergic neurons from both healthy control and PD patient carrying GBA1 mutations. We accurately quantified electrically stimulated DA release events, identifying distinct 'hotspots' of activity across DA neuronal cells. Our findings present a significantly enhanced spatial and temporal resolution of DA signaling, providing a deeper understanding of the role and balance of DA release in the progression of neurodegenerative disease.