Aspartyl(Asparaginyl)-Beta-Hydroxylase (ASPH) is a 2-oxoglutarate (2OG). ASPH catalyzes post-translational hydroxylation of critically positioned aspartic acids and asparagines in specific calcium-binding Epidermal Growth Factor (cbEGF) domains. Mutations in ASPH are linked with Traboulsi syndrome in humans, and a mouse knock-out demonstrates similar features. Hepatocellular carcinoma and pancreatic cancer are known to significantly over-express ASPH on the cell surface, conferring an aggressive, invasive phenotype. ASPH has been demonstrated to aberrantly activate the NOTCH signaling pathway, and cleaved ASPH is capable of suppressing NK cell activity. ASPH inhibitors have been rationally designed and synthesized, and demonstrate predicted activities in vitro, including suppression of migration, invasion, and NOTCH pathway related proteins. Experiments demonstrate significant suppression of tumor growth at 1mg/kg. These compounds have demonstrated context dependent Notch pathway inhibition in vivo.

Chair:

- Mathew Cherian, VP of Operations and R&D, ReVive Biotechnology, USA

Co-moderator:

- Qurrotul Aini Shodiquna, Head of Regulatory Affairs, PT Ibu Bumi Sejahtera, Indonesia

Panellist:

- Mark Olsen PhD, Associate Professor, Pharmaceutical Sciences, Mid-Western University, Glendale, Arizona, USA