Aveta Biomics has developed multiple assets with worldwide rights. We expect these assets to treat other cancers with common underlying disease biology.
Head and Neck Cancer
The worldwide incidence of Head and Neck Cancer is about 900,000 with a five-year mortality rate of about 50% which has remained unchanged for decades. Highly molecularly heterogeneous tumor poses serious challenges for targeted approaches. The recurrence rates exceed 30%. APG-157, through a multi-targeted mechanism, kills active tumor through selective apoptosis and simultaneously stimulates the immune system. It further aims to prevent recurrence through the arrest of cancer stem cells. It is the first drug of its kind that is administered orally and thus has topical application as well as systemic absorption through the oral cavity.
High-Grade Glioma
High-grade gliomas include glioblastoma, gliosarcoma, H3K27M mutant glioma, anaplastic astrocytoma, and anaplastic oligodendroglioma. About 80% of the patients get Bevacizumab monotherapy with poor outcomes. APG-157, working through a novel mechanism, is expected to overcome the resistance mechanisms for Bevacizumab and also potentially complement tumor killing by additional mechanisms including microglia reprogramming from M2 to tumoricidal M1 state. This study opens up expansion opportunities to combine APG-157 with Bevacizumab for other cancers.
Diffuse Intrinsic Pontine Glioma (DIPG)
Diffuse Intrinsic Pontine Glioma (DIPG) is a highly aggressive and difficult-to-treat brain tumor that arises from the glial tissue of the brainstem, specifically the pons. It primarily affects children, typically between the ages of 5 and 10 years old. DIPG accounts for approximately 10-15% of all pediatric brain tumors. In the United States, around 150-300 children are diagnosed with DIPG each year, with similar incidence rates observed worldwide. The prognosis for DIPG is extremely poor, with a median survival time of less than one year from diagnosis and a nearly 100% mortality rate, as current treatments are largely ineffective at extending survival. AMAX126 invokes a novel mechanism to treat this cancer with promising early, pre-clinical results.