Vernodalin

Vernodalin (5-40 μM; 24 h) inhibits the proliferation and induces apoptosis of SGC-7901 and AGS cells in a concentration-dependent manner, increases the levels of nuclear pyknosis and fragmentation, and induces a significant decrease in mitochondrial membrane potential^[1].
Vernodalin (20 μM; 24 h pre-incubation, 60 and 100 min adhesion period) reduces the adhesion of SGC-7901 and AGS cells to extracellular matrix components at the 60 and 100 min time points^[1].
Vernodalin (20 μM; 24 h) downregulates the protein expression of uPA, MMP-2 and MMP-9, while upregulates the protein expression of TIMP-1 and TIMP-2 in SGC-7901 and AGS cells. It inhibits the FAK/PI3K/AKT/mTOR signaling pathway by reducing the protein expression of FAK, p-PI3K, p-AKT, p-mTOR and RhoA in cells, and inhibits the MAPKs signaling pathway by reducing the protein expression of phosphorylated JNK, JUN, p38MAPK and ERK in cells^[1].
Vernodalin (3.12-150 µM; 24 h) reduces the viability of HT-29 and HCT116 cells in a dose-dependent manner, with IC₅₀ values of 7.17 µg/mL and 3.17 µg/mL, respectively^[3].
Vernodalin (1-20 μM; 24-72 h) inhibits the proliferation of A549 lung cancer cells in a time-dependent manner, with IC₅₀ values of 65.80 μM (24 h), 39.90 μM (48 h), and 25.85 μM (72 h), respectively^[4].
Vernodalin (0.016-50 μg/mL; 48 h) potently inhibits the viability of a variety of human cancer cell lines (A549, HeLa, HuCCA-1, HepG2, H69AR, T47-D, MDA-MB-231, S102, HL-60, MOLT-3), with IC₅₀ values ranging from 2.28 μM to 21.47 μM, and exhibits selective cytotoxicity toward cancer cells compared to normal MRC-5 fibroblasts^[6].
Vernodalin (3-12 h) induces time-dependent oxidative stress in HT-29 and HCT116 cells by increasing ROS production, which is associated with cell necrosis and apoptosis^[3].
Vernodalin (5-15 µg/mL for HT-29, 2.5-10 µg/mL for HCT116; 24 h) induces apoptosis in HT-29 and HCT116 cells in a dose-dependent manner, upregulates the expression of Bax and caspase 3, downregulates the expression of Bcl-2, and thereby increases the Bax/Bcl-2 ratio^[3].
Vernodalin (10 μM; 48 h) [missing action in source text], accompanied by observable morphological changes in cells^[6].
Vernodalin (5-20 µg/mL; 1.5-24 h) activates the JNK, ERK and p38 MAPK pathways in HT-29 and HCT116 cells in a time- and dose-dependent manner^[3].
Vernodalin (26 μM; 72 h) induces excessive ROS production in A549 lung cancer cells^[4].
Vernodalin (26 μM; 72 h) enhances oxidative stress in A549 lung cancer cells by increasing MDA levels and reducing the antioxidant defense capacities of SOD, CAT, GPX and GSH. It also impairs the endogenous antioxidant defense system by decreasing the mRNA expression levels of Nrf2 and HO-1, as well as the enzymatic activity of HO-1^[4].
Vernodalin (26 μM; 72 h) activates the pro-apoptotic signaling pathway in A549 lung cancer cells by upregulating the mRNA expression of p38 MAPK, caspase-3, caspase-9 and Bax, downregulating the mRNA expression of Bcl-2, and increasing the activities of caspase-3 and caspase-9^[4].
Vernodalin potently inhibits the growth of bloodstream-form trypomastigotes of *Trypanosoma brucei rhodesiense* (strain STIB 900), with an IC₅₀ value of 0.16 µM^[5].
Vernodalin (10 μM; 48 h) induces apoptosis in 10.9% of HepG2 cells, triggers G₂/M phase cell cycle arrest, and reduces the proportions of cells in the G₀/G₁ and S phases^[6].

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