Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is one of the most frequently disrupted tumor suppressors in cancer. The lipid phosphatase activity of PTEN antagonizes the phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR pathway to repress tumor cell growth and survival. In the nucleus, PTEN promotes chromosome stability and DNA repair.
Consequently, loss of PTEN function increases genomic instability. PTEN deficiency is caused by inherited germline mutations, somatic mutations, epigenetic and transcriptional silencing, post-translational modifications, and protein-protein interactions.
- Development of small molecular anti-cancer agent by stabilizing PTEN (inhibiting binding between p34 protein and NEDD4-1 protein )
Development goals & strategy
- Development of targeted agent (first-in-class) to target PTEN
- Patient selection biomarker-based companion diagnostics
- New compounds for inhibiting binding between p34 protein and NEDD4-1 protein and use thereof (KR, PCT)