Welcome to T3D Therapeutics
T3D Therapeutics, Inc. was founded in 2013 with a daunting mission – to challenge the prevailing thinking over the last two decades in the development of solutions to effectively treat Alzheimer’s disease. Our mission is to develop a ground-breaking, disease-modifying, new drug for the treatment of Alzheimer’s disease.
Fundamental to our approach is the recognition that Alzheimer’s disease (refs.1-5) is a neuro-metabolic disease and, as such, we must first address poor energy metabolism in the brain – brain ‘starvation’ – which leads to neurodegeneration and brain ‘strangulation’, as evidenced by plaques, tangles and inflammation of the brain (ref. 6).
The brain is the most metabolically active organ in the body and it relies on glucose, or sugar, for fuel (ref. 7). If the brain loses its ability to efficiently process sugar into energy, the brain becomes starved. This ‘starvation’ causes a wasting process that then leads to cognitive and motor function deficits – this is Alzheimer’s disease.
The key principle to be exploited in Alzheimer’s drug development is that diminished cerebral sugar (glucose) metabolism in the brain (DCGM) is the earliest, most validated change in the brain of Alzheimer’s patients – fundamentally preceding and predictive of future cognitive decline (refs. 8-10). We believe that addressing this starvation of the brain provides a higher probability of slowing, stopping or reversing the course of the disease.
Our lead product candidate, T3D-959, is positioned to become a transformational therapy by targeting both the brain ‘starvation’ and ‘strangulation’ of Alzheimer’s disease and by treating multiple manifestations of the disease.
T3D-959 is being developed as a potential disease-modifying therapeutic for Alzheimer’s disease patients with mild-to-moderate disease severity. The drug is designed to be delivered orally once-a-day. Pre-clinical efficacy studies and Phase 1 trials in normal subjects have concluded. Dosing in a Phase 2a feasibility clinical trial in Alzheimer’s disease patients has been successfully completed, and a 26-week, open-label extension study for four of the subjects in the Phase 2a study is ongoing. Preparations for a Phase 2b clinical trial are in progress.
Results of preclinical proof-of-concept studies of T3D-959 in an Alzheimer’s animal model have demonstrated that, unlike drugs under development for the treatment of Alzheimer’s disease by other companies (of which we are aware), T3D-959 appears to improve the most important defects caused by Alzheimer’s disease: dysfunctional energy metabolism, inflammation, beta amyloid plaques, tau tangles, and neuronal death (refs. 11-12). By improving these defects, a significant restoration of memory and motor function was observed in the T3D-959 preclinical studies.
The brain accounts for only 2% of total body weight.
Oxygen is vital to metabolism. The adult brain uses 20% of the body's total oxygen consumption.