NMT-IN-9

NMT-IN-9 (compound 8b) potently inhibits fungal NMT by directly binding to conserved active site residues, with an IC₅₀ of 93.20 nM^[1].
NMT-IN-9 binds directly to fungal NMT with a K_d value of 5.57 × 10^-9 M, indicating strong target affinity^[1].
NMT-IN-9 (0.125-64 μg/mL; up to 48 h) exhibits MIC values of 2, 4, 2, 8, and 16 μg/mL against C. albicans SC5314, C. glabrata ATCC 36852, C. tropicalis ATCC 14028, C. neoformans ZKCC 2209, and A. fumigatus KM8001, respectively^[1].
NMT-IN-9 (0.125-64 μg/mL; up to 48 h) exhibits MIC values of 8, 8, 16, 16, and 16 μg/mL against fluconazole-resistant Candida strains CaR, 17#, 632, 901, and 904, respectively^[1].
NMT-IN-9 increases the proportion of apoptotic cells in C. albicans SC5314, expands the necrotic cell population, and reduces the viability of fungal cells^[1].
NMT-IN-9 elongates and diffuses the DNA tail in the comet assay of C. albicans SC5314, inducing significant DNA damage and fragmentation^[1].
NMT-IN-9 (48-96 h) induces morphological and ultrastructural damage in C. albicans SC5314; irregular morphology, surface shrinkage and uneven membrane thickness appear at 48 h, while outer membrane thinning or disruption, indentation or leakage, accompanied by intracellular structural disorder, occur at 96 h^[1].
NMT-IN-9 (32-128 μg/mL; 48 h) shows no obvious cytotoxicity against HeLa and L02 cells^[1].
NMT-IN-9 (1 μM; 48 h) reduces the cell density of C. albicans SC5314, significantly enhances intracellular ROS fluorescence, and induces oxidative stress^[1].
NMT-IN-9 (1 μM; 24 h) reduces the proportion of C. albicans SC5314 cells with normal mitochondrial membrane potential to 29.2% and increases the proportion of cells with mitochondrial membrane depolarization to 64.2%, resulting in significant mitochondrial dysfunction^[1].

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