Cyclopiazonic acid is an endoplasmic reticulum calcium ATPase (ECAs) inhibitor and human respiratory syncytial virus ( RSV ) inhibitor ( EC 50 value of 4.13 μ M), which can reduce the antagonistic effect of 5-HT receptors in rat thoracic aorta, induce p53 dependent cell apoptosis and reproductive toxicity in mouse testes, and inhibit the biological activation of aflatoxin B [1][4][5] .
Products | Products > Disease Areas > Cancer | Products > Disease Areas > Infection | Products > Disease Areas > Neurological, Eye or Ear Disease | Products > Disease Areas > Inflammation or Immune System Disease | Products > Disease Areas > Blood or Cardio-cerebrovascular Disease | Products > Disease Areas > Metabolic or Endocrine Disease | Products > Disease Areas > Digestive System Disease | Products > Disease Areas > Neurodegenerative Disease | Products > Disease Areas > Cardiovascular Disease | Products > Disease Areas > Lipid Metabolism | Products > Disease Areas > Leukemia/Lymphoma/Myeloma | Products > Disease Areas > Blood Disease | Products > Disease Areas > Pancreatic Cancer | Products > Disease Areas > Digestive System Cancer | Products > Disease Areas > Viral Infection | Products > Disease Areas > Digestive System Inflammation | Products > Disease Areas > Alzheimer's Disease | Products > Disease Areas > Hypertension | Products > Disease Areas > Obesity | Products > Signaling Pathways > Membrane Transporter/Ion Channel | Products > Signaling Pathways > Neuronal Signaling | Products > Signaling Pathways > GPCR/G Protein | Products > Signaling Pathways > Apoptosis | Products > Signaling Pathways > Anti-infection | Products > Research Areas > Infection | Products > Signaling Pathways > Apoptosis | Products > Signaling Pathways > RSV | Products > Signaling Pathways > Calcium Channel | Products > Signaling Pathways > 5-HT Receptor | Products > Signaling Pathways > MDM-2/p53
Please leave a message for us or use the following ways to contact us, we will reply to you as soon as possible, and provide you with the most sincere service, thank you.