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's the prolonged neuroinflammation that kills neurons.

Therefore, our approach is to deplete the number of microglia available at the source (Aβ) 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-β 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 carried out by Charles River Discovery Research Services Finland. Ltd. Trials using Tg2576 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 memory improvement and blocking activity of inflammation by our drug candidate S26.

Phase 1 Trial Results

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 in "Memory for Cue" tests approaching that of normal, wild type mouse controls. These results will guide us in optimizing doses for future trials.

Treated mice that demonstrated improved memory shown in "Memory for Cue" were then euthanised and their brains examined for inflammation, by sectioning and staining for microglia and astrocytes. The objective of this study was to evaluate the efficacy of S26 to decrease neuroinflammation concomitant with their memory improvement. Examination of stained sections of the hippocampus showed no decrease in the percentage of microglial IBA-1-positive cells but the GFAP-positive astrocytes population was clearly decreased after exposure to S26. These data suggest that S26 may act to block astrocyte-mediated activation of microglia.

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.