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 disease1-5 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 brain6.
The brain is the most metabolically active organ in the body and it relies on glucose, or sugar, for fuel7. 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 decline8-10. 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 death11-12. By improving these defects, a significant restoration of memory and motor function was observed in the T3D-959 preclinical studies.
Alzheimer’s disease is caused by the ‘starvation’ of the brain (due to poor energy metabolism in the brain) and the ‘strangulation’ of the brain (caused by inflammation, tau tangles and beta amyloid plaques in the brain).
In pre-clinical animal studies, T3D Therapeutics’ new drug candidate, T3D-959, has shown evidence of a reversal of the diseased state in the brain by histopathology (microscopic tissue analysis).
Mild Cognitive ImpairmentMild Cognitive Impairment (MCI) is a condition resulting from impairment in the brain’s glucose metabolism. MCI comes before cognitive decline in Alzheimer’s disease patients, and is evident early in the course of Alzheimer’s disease. Our lead drug candidate, T3D-959, is designed to improve neuro-metabolic dysfunction (the brain’s inability to efficiently create and metabolize, or utilize, energy), which we believe could dramatically affect molecular, biochemical and histopathological defects that cause cognitive impairment and motor dysfunction.
Diminished Cerebral Glucose Metabolism (DCGM) is also known as glucose hypometabolism. DCGM plays a pivotal role in the changes seen in Alzheimer’s disease patients (such as increasing oxidative stress and mitochondrial dysfunction, among other effects). This leaves neurons less able to utilize glucose as a fuel, and hences causes an energy shortage in the brain. DCGM occurs early in the course of Alzheimer’s disease and correlates with symptoms and disease progression (refs.13,14).
Other Neurodegenerative Diseases
Because T3D-959’s mechanism of action is designed to provide anti-inflammatory and anti-wasting effects, along with an ability to repair damaged nerve cells (remyelination), there is potential for T3D’s new drug candidate to address other neurodegenerative diseases, in addition to Alzheimer’s disease.
PPAR delta agonist compounds such as T3D-959 have recently been found to have strong neuroprotective effects that we believe make T3D-959 a candidate drug for development for potential treatment in a number of CNS diseases (e.g. Stroke, Multiple Sclerosis, Parkinson’s disease) (refs.15,16).
Beyond Alzheimer’s disease, these other diseases present added life cycle management opportunities for T3D-959 and other structurally-related compounds within the Company’s exclusive license.
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.