Hydrogen-bonding compounds from mutant p53 co-crystal structures stabilize Y220C-like variants, recover DNA binding, and trigger apoptosis.
OmniTAC compounds link a target protein to a modifier protein to drive specific intracellular modification and reactivate disease-associated proteins.
One-pot acryloyl polymerization stabilizes alpha-helix peptides, resolving synthesis complexity and yield issues while enabling multi-target interactions.
p53 gene therapy suppresses infections and reduces tissue fibrosis by activating broad-spectrum immune responses.
Cross-linked peptidomimetic macrocycles stabilize the p53 alpha-helix to prevent MDM2-mediated degradation and restore tumor suppressor function.
Peptides block Agr2 binding to POLR2A to activate p53, enhancing chemotherapy efficacy specifically in wild-type TP53 tumors.
Crosslinked peptidomimetic macrocycles prevent rapid p53 degradation by HDM2, extending half-life and enhancing apoptosis in cancer cells.