Medicenna

Medicenna Presents Preclinical Data on MDNA11 and Bizaxofusp at the 2024 Annual Meeting of the Society for Neuro-Oncology (SNO)

Medicenna Therapeutics Corp., a clinical-stage immunotherapy company focused on the development of Superkines, today announced the presentation of preclinical data on MDNA11, a long-acting "β-enhanced Not-α” IL-2 Superkine, and bizaxofusp (MDNA55), an IL-4 Empowered Superkine, at the 2024 Annual Meeting of the Society for Neuro-Oncology (SNO) held in Houston, Texas from November 21 - 24, 2024.

These data provide compelling evidence of their combined potential to simultaneously enhance immune activation with MDNA11 and weaken the tumor microenvironment (TME) with bizaxofusp, for the treatment of "cold tumors” such as glioblastoma (GBM).

Clinical results reported earlier this month have shown that MDNA11 can effectively attack aggressive cancers such as pancreatic and colon cancers, by boosting the quality and quantity of cancer fighting immune cells, such as CD8+ T cells and NK cells, in patients that have failed or do not benefit from blockbuster immunotherapies.

Bizaxofusp acts by targeted delivery of a potent toxin to several types of aggressive cancers that express the interleukin-4 receptor (IL-4R), such as GBM, without harming healthy cells. In addition, we have now shown that bizaxofusp weakens the TME, by selectively killing immunosuppressive cells, such as regulatory T cells (Tregs), which promote cancer cells to grow, metastasize, evade the immune system, and resist treatment.

The presentation, titled "Invigorating Effector Immune Cells With Highly Selective IL-2R Agonists and Potential Synergy With Tumor Targeting Therapeutics for Treatment of Glioblastomas", showcased the ability of MDNA11 and bizaxofusp to target GBM's immunosuppressive environment and synergize to elicit robust anti-tumor responses.

MDNA11 is a next-generation IL-2 superkine designed to selectively stimulate effector immune cells (CD8+ T cells and NK cells) by enhancing affinity for IL-2Rβ (CD122) while avoiding IL-2Rα (CD25), which reduces Treg activation and associated toxicities. Bizaxofusp is designed to target both the tumor and the TME, by selectively killing IL4R-expressing cancer cells, immune suppressive myeloid-derived suppressor cells (MDSCs) and Tregs.