Background

The most recent and hopeful new approach in drug development currently focuses on those cells that cause inflammation in the brain, specifically microglia (See Economist, June 7, 2025).

Septa's disease model shown in "Technology" suggests that while increasing microglial inflammation may be effective initially, prolonged or excessive activation would likely increase neuroinflammation and neuronal damage . The model says that it isn't chronic viral infection that causes the most damage in the brain – it's the prolonged neuroinflammation that kills neurons.

Therefore, our approach is to deplete the number of microglia available at the source (Abeta) and decrease neuroinflammation.

Septa Therapeutics' Pre-clinical trials

Septa Therapeutics has devoted 2024 and 2025 to the development of a series of inflammation blockers. We have employed cellulose-bound peptide arrays to construct blockers which will pass through nasal membranes, bind to Amyloid-beta in the brain and which meet all new US patent office requirements for patentability (USPTO eligibility statute 35 USC section 101). These latter requirements have been connected to recent political changes occurring since our earlier filing in 2018.

Pre-clinical trials have been initiated with Charles River Discovery Research Services Finland. Ltd. These trials test the efficacy of our drug candidate, S26, in the complete prevention of the appearance of symptoms, or the slowing of disease progression once symptoms have appeared.

Trials using Tg2476 mice, genetically engineered to present with the symptoms of Alzheimer's Disease, began in January, 2026. This small pilot study was designed to detect any blocking activity of inflammation by our drug candidate S26.

Phase 1 Trial Results - Preliminary

A small pilot study was undertaken to reveal efficacy at any level for our drug candidate S26. Two doses of S26 were tested. The lower dose had no activity in memory-related trials, while the higher dose showed improved memory in Tg2576 mice approaching that of normal, wild type mouse controls. These results will guide us in optimizing doses for future trials.

We are now in the process of identifying the location and number of microglia and astrocytes in sections of murine brains taken from the phase I trial.