Septa Therapeutics Inc. is a biotechnology company devoted exclusively to the development of an effective treatment for Alzheimer’s Disease (AD).

Our new technology is designed to stop the disease before it begins

It has been known for some time that Amyloid beta (Abeta) accumulates in the brains of AD patients, and it was thought to somehow serve as the “trigger” that initiates the disease. Earlier approaches in drug development were therefore focused on the removal of the Abeta, from the CNS with very limited results.

However recent studies have implicated inflammation, with huge increases in the microglial cell population , as the trigger that initiates and amplifies the progression of AD.

Septa Therapeutics proposes a new approach based on platform technology developed earlier by CEO Diane Van Alstyne, Ph.D.

hMCP-1 chemokine activity as been identified resident in the Abeta molecule itself. This activity transforms rat brain stem cells into microglia. Therefore, as the concentration of Abeta increases in the brain, a corresponding increase in the microglial population will occur over time, leading to neuron death.

Our new approach will block the chemokine activity while allowing the inactive Abeta to accumulate.

These data are contained in: US Patent Application 16/959,990 and PCT/CA2019/05004. Septapeptides associated with neurodegeneracy. D. Van Alstyne. Date 01/04/2018

We have also presented this data at 2 international conferences:

Keystone Symposia: Advances in Neurodegenerative Disease Research and Therapy. June 20, 2018. Peptides representing common epitopic sites for AD-associated agents have hMCP-1 activity. #3035. Session Z3. D. Van Alstyne.

23rd International Conference of Alzheimer's Disease International, July 26-29, 2018, Chicago, USA. An Amyloid beta-Derived Peptide Transforms rat glial progenitor cells into microglia. Published in:Alzheimers' and Dementia 14(7):P1529 and doi.1016/j.jalz2018.07.049

Our presentation at the Keystone Symposia attracted the attention of Morgan Sheng, VP Neuroscience, Genentech. We were preparing to initiate "Proof of Concept", preclinical trials in mice. However, the collaboration was cancelled when Morgan left the pharmaceutical industry to return to an academic position at the Broad Institute, Boston.