PLAGL2-IN-1

Overview

PLAGL2-IN-1 is a inhibitor of pleiomorphic adenoma-like protein 2 ( PLAGL2 ) with a K d of 2.23 µM. PLAGL2-IN-1 suppresses PLAGL2 transcriptional activity, induces G0/G1 cell cycle arrest, and apoptosis , thereby inhibiting hepatocellular carcinoma (HCC) cell proliferation. PLAGL2-IN-1 disrupts extracellular matrix organization and suppresses the PI3K-AKT pathway by reducing AKT phosphorylation. PLAGL2-IN-1 inhibits tumor growth in an HCCLM3 xenograft mouse model. PLAGL2-IN-1 can be used for the research of HCC.

Application

Products | Products > Disease Areas > Blood or Cardio-cerebrovascular Disease | Products > Disease Areas > Digestive System Disease | Products > Disease Areas > Urogenital Disease | Products > Disease Areas > Lung Cancer | Products > Disease Areas > Breast Cancer | Products > Disease Areas > Colorectal Cancer | Products > Disease Areas > Digestive System Cancer | Products > Disease Areas > Prostate Cancer | Products > Disease Areas > Urogenital Cancer | Products > Disease Areas > Gastric Cancer | Products > Disease Areas > Liver Cancer | Products > Disease Areas > Leukemia/Lymphoma/Myeloma | Products > Disease Areas > Blood Disease | Products > Disease Areas > Ovarian Cancer | Products > Disease Areas > Cancer | Products > Signaling Pathways > Cell Cycle/DNA Damage | Products > Signaling Pathways > Apoptosis | Products > Signaling Pathways > PI3K/Akt/mTOR | Products > Research Areas > Cancer | Products > Research Areas > Cancer > Cancer Targeted Therapy | Products > Research Areas > Cancer > Cancer Metabolism and Metastasis | Products > Signaling Pathways > Zinc Finger Protein | Products > Signaling Pathways > Apoptosis | Products > Signaling Pathways > PI3K | Products > Signaling Pathways > Akt

Product Information

• Catalog No.: HY-180281
• CAS No.: 3099026-16-8
• Molecular Formula: C30H35Cl2N5O4S
• Molecular Weight: 632.60
• Purity: 99.98%
• Storage: Please store the product under the recommended conditions in the Certificate of Analysis.

Source

Original product source