Our Mission

A Transformational Approach to Treating Alzheimer’s Disease … and more.

T3D Therapeutics’ mission is to develop its lead drug product candidate, T3D-959, as a potential ‘First-in-Class’ and ‘Best-in-Class’ disease-modifying, breakthrough medicine for the treatment of Alzheimer’s disease with the potential to slow, stop or reverse the course of the disease. The Company is also seeking to maximize the therapeutic utility of T3D-959 and has initiated pre-clinical studies in Huntington’s Disease models.

T3D-959 is designed as an orally-delivered, once-a-day medicine being evaluated for the treatment of Alzheimer’s disease patients with mild to moderate disease severity, and potentially also for patients with mild cognitive impairment (MCI). The mechanism of action of T3D-959 may provide therapeutic benefit in other central nervous system (CNS) or neurodegenerative disorders via improving dysfunctional brain glucose energy and lipid metabolism which in turn, can address cerebral structural and stress events aberrations.

Innovative Ideas

Treating Alzheimer’s disease as a neuro-metabolic disease: Our lead product candidate, T3D-959, is designed to treat both the ‘starvation’ of the brain (insufficient energy metabolism in the brain) and the resulting ‘strangulation’ of the brain (via amyloid plaques, tau tangles and inflammation).

Unique Mechanism of Action

T3D-959 is a PPAR delta / gamma nuclear receptor agonist. To our knowledge, no other drug in development for the treatment of Alzheimer’s disease possesses this unique mechanism of action.

T3D-959 is a PPAR delta agonist with lesser PPAR gamma activity. It is 15 times more potent for PPAR delta than for its secondary target, PPAR gamma. This particular combination confers unique biological activity and safety profiles with the potential to address the multiple medical impairments found in Alzheimer’s disease patients.

It's Time for a New Paradigm

The Company’s therapeutic approach to slow, stop or reverse the progression of Alzheimer’s disease is based on two fundamental concepts:

Target ‘upstream’ defects found in Alzheimer’s disease, as opposed to later-occurring, ‘downstream’ manifestations of the disease by addressing DCGM (Decreased Cerebral Glucose Metabolism), which precedes and is predictive of cognitive decline.
Target multiple defects manifested by the disease, not one, with a single drug therapy.

Clear Results to Date

Disease reversal has been demonstrated pre-clinically in an Alzheimer’s animal model. Early quantitative and qualitative results in Alzheimer’s patients in our two-week, non-placebo-controlled 36-subject Phase 2a feasibility study preliminarily indicate:

Potential improvement in cognition
Potential to improve motor function / coordination
Effective drug penetration into the human brain
High safety potential
A probable low dose range for effectiveness

Broad Application (Huntington’s Disease)

The mechanism of action of T3D-959 provides a potential to improve dysfunctional glucose and lipid metabolism that is inherent in other neurodegenerative diseases, including certain orphan diseases. Extensive research on Huntington’s disease has demonstrated a central role for interference with the function of the nuclear receptor transcription regulator PPAR delta (the primary target of T3D-959) in contributing to HD pathogenesis.