NAMI-A

NAMI-A (1-100 μM; 1 h) inhibits the autophosphorylation of FAK at the Tyr397 site in HCT-116 colorectal adenocarcinoma cells, with the strongest inhibitory effect observed at 1 μM and a moderate inhibitory effect at 10 μM^[1].
NAMI-A (1-100 μM; 1 h) potently inhibits the chemotactic invasion of HCT-116 colorectal adenocarcinoma cells through Matrigel at concentrations of 1 μM and 100 μM, reducing the invasive capacity by approximately 30% compared with untreated cells^[1].
NAMI-A (1-100 μM; 1 h) reduces the adhesion of HCT-116 colorectal adenocarcinoma cells to fibronectin, type I collagen, and laminin-111 in an inverse concentration-dependent manner, with the maximum inhibitory effect observed at 1 μM, and its action is mediated via the α5β1 integrin pathway^[1].
NAMI-A (1-100 μM; 1-72 h) exerts no significant effect on the proliferation or viability of TS/A adenocarcinoma cells even at concentrations up to 100 μM and with treatment durations as long as 72 h^[2].
NAMI-A (3-300 μM; 72 h) shows no cytotoxicity against HCT-116 colorectal adenocarcinoma cells at concentrations up to 100 μM after 72 h of incubation, and a decrease in cell viability is only observed at concentrations ≥300 μM^[1].

NAMI-A (1-20 μM; 24-72 h) potently inhibits proliferation and induces apoptosis in HL60, FLG 29.1, K562, 697 and REH leukemia cell lines, with LD₅₀ values ranging from 0.47 μM to 5.47 μM. However, it exhibits extremely low cytotoxicity against IGROV-1 ovarian cancer cells, with an LD₅₀ of 429.87 μM^[3].

NAMI-A (0-6 mM; 30 min at 4°C followed by 18 h at 37°C) inhibits the activities of MMP-2 and MMP-9 in the conditioned media of SK-N-BE neuroblastoma and HT-1080 fibrosarcoma cells in a concentration-dependent manner^[2].

NAMI-A (0.1 mM; 1 h) significantly alters the cell cycle distribution of KB epithelial cancer cells, shifting it toward the S and G₂-M phases; concurrent or subsequent administration of ascorbic acid, glutathione, or cysteine does not modify this effect^[6].

NAMI-A (20-80 μM; 24 h) inhibits chemotaxis of HUVEC and EA.hy926 cells in a dose-dependent manner. After 24 h of pretreatment, 40 μM NAMI-A reduces cell migration capacity by 50% without inducing cytotoxicity or proliferation inhibition^[5].

NAMI-A (0-100 μM) inhibits K⁺ currents in FLG 29.1 leukemia cells and selectively blocks KCa3.1 channels in HEK 293-KCa3.1 cells; the inhibition rate reaches approximately 30% at concentrations of 1-2 μM, and the inhibition shows a concentration-dependent pattern within the range of 0.2 μM to 100 μM^[3].