CMLD-2 is an inhibitor of HuR-ARE interaction (Ki: 350 nM) that competitively binds HuR protein and disrupts its interaction with adenine element-rich (ARE) mRNA targets.CMLD-2 induces apoptosis and exhibits antitumor effects through MAD2 downregulation. CMLD-2 (1-75 μM ; 24-72 h) had an inhibitory effect on the viability of thyroid cancer cells.CMLD-2 (20-30 μM ; 24-48 h) activated caspases and induced apoptosis in H1299 and A549 cells.CMLD-2 (30 μM ; 24-48 h) induced G1 cell cycle arrest in H1299 and A549 cells and mitochondrial perturbation. CMLD-2 (30 μM ; 24-48 h) reduced the expression of HuR and HuR-regulated mRNAs and proteins in H1299 cells.CMLD-2 (35 μM ; 72 h) decreased the directional migration ability of SW1736, 8505C, BCPAP and K1 cells.CMLD-2 induced the migration of SW1736, 8505C, BCPAP and K1 cells with a strong decrease in MAD2 mRNA levels.

HuR-ARE:350 nM(Ki)

CMLD-2 (35 μM ; 72 h) impairs directional migration ability and significantly diminishes MAD2 mRNA levels in SW1736, 8505C, BCPAP, and K1 cells.[2]
CMLD-2 (20-30 μM ; 24-48 h) triggers caspase activation and induces apoptosis in H1299 and A549 cells.[2]
CMLD-2 (30 μM ; 24-48 h) causes G1 cell cycle arrest and disrupts mitochondrial function in H1299 and A549 cells.[2]
CMLD-2 (30 μM ; 24-48 h) decreases the expression of HuR and HuR-regulated mRNAs and proteins in H1299 cells.[2]
CMLD-2 (1-75 μM ; 24-72 h) suppresses thyroid cancer cell viability.[3]
CMLD-2 (0.1-10 μM) reduced the activity of mouse and human sensory neurons.[5]

CMLD-2 (0.3 μg, 1 μg, 3 μg ; i.pl.) attenuated NGF (left), and IL-6 (right) induced mechanical hypersensitivity during the acute and priming phase in male mice.[5]