Meptyldinocap

Meptyldinocap (2,4-DNOPC) is a fungicide and cytotoxic agent that acts against powdery mildew. Meptyldinocap upregulates the phosphorylation levels of ERK1/2, JNK and p38. Meptyldinocap induces apoptosis and endoplasmic reticulum stress, disrupts calcium homeostasis, inhibits cell proliferation and migration, downregulates the expression of proliferation- and pregnancy-related genes, and triggers mitochondrial dysfunction. Meptyldinocap can be used in studies related to powdery mildew and implantation failure^[1][2]. In Vitro:Meptyldinocap (10-500 nM; 48 h) reduces the viability of pTr and pLE cells in a concentration-dependent manner^[2].
Meptyldinocap (150 nM; 48 h) reduces the expression levels of proliferation-related genes PCNA and CDK1 in pTr and pLE cells^[2].
Meptyldinocap (150 nM; 24 h) reduces the protein expression levels of proliferation markers PCNA and Ki67 in pTr and pLE cells^[2].
Meptyldinocap (50-150 nM; 48 h) increases the proportions of early and late apoptosis in pTr cells; after 48 h of treatment, the 150 nM concentration increases the proportion of early apoptosis in pLE cells, while the 100 and 150 nM concentrations increase the proportion of late apoptosis in pLE cells^[2].
Meptyldinocap (50-150 nM; 48 h) induces concentration-dependent cell cycle arrest in pTr cells^[2].
Meptyldinocap (150 nM; 24 h) significantly reduces the maximal mitochondrial respiration level of pTr cells; after 24 h of treatment, it shows a non-significant trend of decreased mitochondrial respiration parameters in pLE cells^[2].
Treatment with Meptyldinocap (150 nM; 48 h) significantly reduces the mitochondrial membrane potential (MMP) of pTr cells and pLE cells to 207.5% and 271.1%, respectively^[2].
Meptyldinocap (50-150 nM; 48 h) upregulates the expression of endoplasmic reticulum stress-related proteins GRP78 and p-eIF2α in pTr cells^[2].
Meptyldinocap (50-150 nM; 48 h) reduces the cytoplasmic calcium concentration in pTr cells and pLE cells, thereby disrupting calcium homeostasis^[2].
Meptyldinocap (50-150 nM; 30 min) upregulates the phosphorylation levels of ERK1/2, JNK and p38 in pTr cells, thereby altering the MAPK signaling cascade^[2].