NR12S

NR12S (0.5-1 µM) binds strongly to lipid vesicles with phase-dependent emission spectra and quantum yields, exhibiting blue-shifted emission in cholesterol-rich liquid ordered phases compared to liquid disordered phases^[1].
NR12S selectively stains the outer leaflet of U87MG human glioblastoma cell plasma membranes, with emission spectra that correlate with membrane cholesterol content, enabling quantitative monitoring of cholesterol depletion and enrichment dynamics^[1].
NR12S orientation is strongly conditioned by lipid environment (two orientations in disordered bilayers, one vertical orientation in ordered bilayers) and interacts transiently with cholesterol, which likely influences its fluorescence response^[6].
NR12S stains both liquid ordered (Lo) and liquid disordered (Ld) phases of model GUV membranes, with a preference for the Ld phase^[7].
NR12S (40 nM) binds to the plasma membrane of living HeLa cells, reports on lipid order via green/red fluorescence ratio, and is not significantly quenched by bQ10S due to its partitioning into both ordered and disordered membrane environments^[7].
NR12S (40 nM) reports on heterogeneous lipid order environments (resembling model Lo and Ld phases) in the plasma membranes of living HeLa, CHO, and 293T cells, with bQ10S selectively quenching its fluorescence in disordered (Ld-like) domains to reveal ordered (Lo-like) domain signal^[7].
NR12S (1 mol%; 12 h) exhibits REES in both liquid-disordered POPC LUVs (9 nm) and liquid-ordered POPC/40 mol% cholesterol LUVs (19 nm), with a larger magnitude in liquid-ordered phase membranes^[2].
NR12S (0.5-1 mol%; 12 h) exhibits phase-dependent intensity-averaged mean fluorescence lifetimes in POPC (3.86 ns), DPPC (3.48 ns), and POPC/40 mol% cholesterol (4.25 ns) LUVs, with the longest lifetime in liquid-ordered phase membranes^[2].
NR12S (10-20 nM; room temperature) shows HeLa cell plasma membranes saturate with it more rapidly than lipid vesicles, and the probe exhibits no detectable phototoxicity when used at 10-20 nM, making this the optimal concentration range for cellular studies^[4].
NR12S (0.01 μM; 7 min) detects decreases in outer plasma membrane lipid order in HeLa cells induced by cholesterol extraction, cholesterol oxidation, sphingomyelin hydrolysis, and apoptosis; intact HeLa and U87MG cells exhibit outer membrane lipid order similar to liquid ordered phase lipid vesicles^[4].
NR12S (0.05 μM; 7 min) enables two-photon ratiometric microscopy to visualize decreased outer plasma membrane lipid order in HeLa cells induced by cholesterol extraction and apoptosis^[4].
NR12S (0.01 μM; 7 min) enables flow cytometry to accurately detect apoptotic/dead HeLa cells, with results correlating closely to the gold-standard FITC-annexin V assay, identifying 21-47% apoptotic/dead cells depending on the apoptosis-inducing agent^[4].
NR12S (0.01 μM; 7 min) detects reduced plasma membrane lipid order in HeLa cells treated with cholesterol-depleting, 7-ketocholesterol-enriching, sphingomyelin-hydrolyzing, or apoptosis-inducing agents (Camptothecin (HY-16560), IPA-3 (HY-15663)), with this response blocked by caspase-3 inhibition, and detects increased lipid order in cholesterol-enriched HeLa cells^[6].
NR12S (0.02 μM; 7 min) specifically stains the outer plasma membrane of HeLa cells and detects reduced lipid order in cholesterol-depleted or apoptosis-induced (Camptothecin, IPA-3) HeLa cells via a decreased green/red fluorescence intensity ratio^[6].
NR12S (0.01 μM; 7 min) detects apoptosis in HeLa cells via flow cytometry, showing a strong correlation with caspase-3 activation (FITC-DEVD-FMK) and phosphatidylserine exposure (GFP-Annexin V) over the 0-24 h time course of camptothecin-induced apoptosis, and detects plasma membrane lipid order changes from membrane-modifying agents via population-wide shifts in the green/red fluorescence intensity ratio^[6].
NR12S (40 nM) identifies Ld-like phase domains in the form of apoptotic blebs in IPA-353-treated apoptotic HeLa cells, with bQ10S selectively quenching NR12S fluorescence in these blebs to confirm their disordered lipid environment^[7].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.