Lotusine

Lotusine is an orally active signaling pathway modulator and enzyme inhibitor, with an IC₅₀ of 30.60 μg/mL against α-amylase and an IC₅₀ of 36.15 μg/mL against α-glucosidase. Lotusine inhibits the EGFR-Akt-ERK signaling pathway by reducing the levels of phosphorylated EGFR, Akt and ERK. Lotusine induces apoptosis, triggers G₀/G₁ cell cycle arrest and inhibits cancer cell proliferation. Lotusine reduces lipid peroxidation and increases the activities of SOD, CAT and GPx. Lotusine is applicable to researches related to non-small cell lung cancer, type 2 diabetes and autism spectrum disorder^[1][2][3][4]. In Vitro:Lotusine (2, 4, 10 μM; 24, 48, 72 h) potently inhibits proliferation of EGFR-mutant HCC827 NSCLC cells and EGFR-wildtype A549 NSCLC cells in time- and concentration-dependent manners, with stronger activity against HCC827 cells (73% inhibition at 10 μM for 72 h)^[1].
Lotusine (2.5, 5, 10 μM; 24 h) induces concentration-dependent apoptosis in EGFR-mutant HCC827 NSCLC cells, with 80% of cells undergoing apoptosis at 10 μM for 24 h^[1].
Lotusine (2.5, 5, 10 μM; 24 h) disrupts mitochondrial membrane potential in EGFR-mutant HCC827 NSCLC cells in a concentration-dependent manner, as evidenced by reduced JC-1 fluorescence ratios at 2.5, 5, and 10 μM for 24 h^[1].
Lotusine (2.5, 5, 10 μM; 72 h) induces concentration-dependent G0/G1 phase cell cycle arrest in EGFR-mutant HCC827 NSCLC cells, halting progression into the DNA synthesis phase^[1].
Lotusine (2.5, 5, 10 μM; 24 h) inhibits the EGFR-Akt-ERK signaling pathway in EGFR-mutant HCC827 NSCLC cells in vitro in a concentration-dependent manner, reducing p-EGFR, p-Akt, and p-ERK levels most significantly at 10 μM for 24 h^[1].
Lotusine (25-50 μM; 48-72 h) does not significantly reduce the viability of HepG2 cells when administered alone or in combination with 25 mM D-glucose, maintaining 85-90% cell viability^[2].
Lotusine (25-50 μM; 48-72 h, co-treated with 25 mM D-glucose) reverses hyperglycemia-induced reductions in SOD, CAT, and GPx antioxidant enzyme activities and lowers elevated MDA levels in HepG2 cells^[2].
Lotusine (1.56-200 μg/mL; 10 min) inhibits alpha-amylase activity with an IC₅₀ of 30.60 μg/mL, and achieves 80.36% inhibition at a concentration of 200 μg/mL in a cell-free biochemical assay^[2].
Lotusine (1.56-200 μg/mL; 20 min) inhibits alpha-glucosidase activity with an IC₅₀ of 36.15 μg/mL, and achieves 82.6% inhibition at a concentration of 200 μg/mL in a cell-free biochemical assay^[2].
Lotusine (10-1000 μM; 24 h) exhibits low cytotoxicity in H9c2 cells, with an IC₅₀ of 701 μM, and concentrations of 10, 50, and 100 μM maintain cell viability near control levels^[3].
Lotusine (10-100 μM) enhances endogenous antioxidant (SOD, CAT, GSH) levels in H9c2 cells exposed to doxorubicin, supporting protection against oxidative stress^[3].
Lotusine (10-100 μM) significantly reduces doxorubicin-induced lipid peroxidation in H9c2 cells, with 50 μM showing the greatest reduction^[3].
Lotusine (10-50 μM; 24 h pretreatment) prevents doxorubicin-induced morphological and nuclear abnormalities in H9c2 cells^[3].
Lotusine (10-50 μM) completely inhibits doxorubicin-induced ROS generation in H9c2 cells^[3].
Lotusine (10-50 μM) modulates apoptotic gene expression in H9c2 cells exposed to doxorubicin, upregulating Bcl-2 and downregulating Bax and Cas-3 to inhibit apoptosis^[3].
Lotusine (10-50 μM; 24 h pretreatment) reduces doxorubicin-induced caspase-3/7 activity in H9c2 cells, with 50 μM showing activity comparable to control cells^[3].
Lotusine (50 μM; 3 h) directly interacts with and stabilizes DRD1 protein in PC12 cells^[4].
Lotusine (3.12-25 μM; 48 h following 1 h 38 mM PPA pretreatment) protects PC12 cells against PPA-induced cytotoxicity^[4]. In Vivo:Lotusine (50 mg/kg bw; diet supplementation; daily; 4 weeks) restores antioxidant vitamin levels and liver protein content, improves growth performance, and normalizes relative organ weight in streptozotocin-induced diabetic rats^[2].
Lotusine (5-20 mg/kg; p.o.; daily; 5 days) ameliorates propionic acid-induced ASD-like social deficits and cognitive impairments in mice, with 10 and 20 mg/kg doses also restoring mPFC neuronal activity and AMPA receptor function via upregulation of c-fos and phosphorylated GluA1 levels^[4].