T3D Therapeutics Announces Presentation of Phase 2a Preliminary Results of T3D-959 in Alzheimer’s Subjects at the 2016 Alzheimer’s Association International Conference

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An investigational new drug, T3D-959, elicited rapid improvement in ADAS-cog11 cognitive tests in 53% of subjects with mild to moderate Alzheimer’s disease in an exploratory, open label Phase 2a study, with average group improvements sustained at follow-up, 7 days post-dosing. A subset of patients (31%) in the study, 50% of whom had moderate disease severity, had an average improvement in ADAS-cog11 of 6.03 points at follow-up.

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"“These promising preliminary data from our Phase 2a study provide further confidence in T3D-959 as a potential disease-modifying therapy, and support the design of a future Phase 2b trial in mild and moderate Alzheimer’s subjects."

T3D Therapeutics, Inc., a clinical stage drug development company engaged in the development of a new orally administered treatment for Alzheimer’s disease (AD), today announced that preliminary Phase 2a data with T3D-959 in mild to moderate Alzheimer’s disease subjects were reviewed in a poster presentation at the 2016 Alzheimer’s Association International Conference (AAIC). In this open label exploratory study 36 subjects with mild to moderate disease (MMSE 14-26) were randomized to receive 1 of 4 doses of T3D-959 dosed orally once-a-day for 14 days. Thirty four subjects completed the study. Preliminary results show that in 53% of the subjects, T3D-959 elicited rapid cognitive test improvements in ADAS-cog11 (Alzheimer's Disease Assessment Scale - Cognitive Subscale) and 56% of subjects improved on a second cognitive test, DSST (Digit Symbol Substitution Test). There was a high concordance of DSST improvement with improvement in ADAS-cog11. Average improvements in both cognitive tests observed across all cohorts after 14 days of dosing were sustained 7 days after dosing cessation (at follow-up). No relationship between cognitive score improvements and disease severity was observed, both mild and moderate AD subjects showed improvements in cognitive testing. In this study the drug was well-tolerated, produced no significant safety findings and had no negative effects on cognitive function in the study subjects.

“T3D-959 is the only Alzheimer’s treatment in clinical development of which we are aware that works by dually activating two nuclear receptors PPAR delta and gamma to control lipid and energy homeostasis regulating fatty acid oxidation, energy dissipation, and mitochondrial respiration,” commented John Didsbury, Ph.D., Chief Executive Officer of T3D Therapeutics. “These promising preliminary data from our Phase 2a study provide further confidence in T3D-959 as a potential disease-modifying therapy, and support the design of a future Phase 2b trial in mild and moderate Alzheimer’s subjects. Furthermore, the results are in support of a growing recognition in the field that targeting neuro-metabolic dysfunction in AD is a viable and attractive new avenue to developing effective AD therapeutics.”


At end of treatment 53% of subjects had a one point or more improvement in ADAS-cog11 with an average improvement of 4.14 points from baseline, 44% of subjects had a two point or more improvement with an average improvement of 4.78 points from baseline and 31% of subjects had a three point or more improvement with an average improvement of 5.76 points from baseline. The group of subjects with a three point or more average improvement at end of treatment had continued improvement 7 days post-dosing with an average ADAS-cog11 improvement for the group of 6.03 points from baseline at follow-up. This same group of subjects had a 3 point average improvement in DSST at end of treatment and a 9 point average improvement 7 days post-dosing. Half of these subjects had moderate disease severity (MMSE = 14-19). As a group, subjects in the high dose cohort (90mg) improved on DSST (average improvement at end of treatment = 1.72 points from baseline and at follow-up = 6.63 points from baseline) but did not have an average improvement in ADAS-cog 11.

About T3D-959

T3D-959, the Company’s lead product candidate, is a small molecule, orally-delivered, brain-penetrating PPAR delta/gamma dual nuclear receptor agonist. T3D-959 is designed to improve neuro-metabolic dysfunction present in Alzheimer’s disease. In published preclinical studies T3D-959 has been observed to regulate Abeta, tau, oxidative stress and inflammation providing significant improvement in memory and motor function in an animal model of sporadic Alzheimer’s disease.

About the Phase 2a Trial

The trial entitled “Phase 2a Feasibility Study of T3D-959 in Subjects with Mild to Moderate Alzheimer's Disease” (ClinicalTrials.gov Identifier NCT02560753) is a randomized, parallel, 4-dose design in subjects with mild-to-moderate Alzheimer’s disease. Subjects are randomized to one of 4 doses of T3D-959 (3, 10, 30, 90mg). T3D-959 is administered orally once daily for 14 days. Subjects are evaluated for safety and tolerability and changes from baseline in cerebral metabolic rate of glucose (FDG-PET imaging), functional connectivity of the hippocampus (BOLD-fMRI), and cognitive function (DSST and ADAS-cog11). The Digit Symbol Substitution Test (DSST) evaluates attention, speed in completing tasks, visual tracking, decision making and transformation of information stored in active memory. The second test, the Alzheimer's Disease Assessment Scale - Cognitive Subscale (ADAS-cog11), evaluates memory, attention, reasoning, language and orientation. The Company currently anticipates reporting final results from this study in the first quarter of 2017.

About T3D Therapeutics, Inc.

T3D Therapeutics, Inc. is a privately-held, Research Triangle Park, NC-based company incorporated in 2013. The Company has an exclusive license to T3D-959, its lead product candidate, and a platform of structurally-related molecules. T3D Therapeutics’ mission is to develop and commercialize T3D-959 for the treatment of Alzheimer’s disease and Mild Cognitive Impairment. The Company believes that due to its mechanism of action, T3D-959 may also have therapeutic benefit in other central nervous system and other neurodegenerative diseases.

For more information, please visit http://www.t3dtherapeutics.com/.

Forward-Looking Statements

Statements contained in this release that are not statements of historical fact are forward-looking statements, including those statements relating to the Company's expectations regarding clinical studies and developments, and the future potential of its product candidates, including T3D-959, and other statements that are predictive in nature or that depend upon or refer to future events or conditions. Without limiting the generality of the foregoing, words such as “may,” “will,” “expect,” “believe,” “anticipate,” “intend,” “could,” “estimate” or “continue” are intended to identify forward-looking statements. Readers are cautioned that certain important risks and uncertainties, and assumptions, which if they do not materialize or prove incorrect, may affect the Company’s actual results and could cause such results to differ materially from any forward-looking statements which may be made in this release or which are otherwise made by or on behalf of the Company. Factors which may affect the Company’s results include, but are not limited to, uncertainties and/or unexpected results related to research and development and clinical testing, the timing, costs and uncertainty of obtaining any required regulatory approvals, changes in the regulatory landscape, uncertainties related to obtaining additional capital as needed to meet the Company’s needs on acceptable terms, or at all, the absence of any guarantee of product demand, market acceptance or competitive advantage for any of the Company’s product candidates, if approved, and certain trade, legal, social and economic risks. Any forward-looking statement in this release speaks only as of the date on which it is made, and the Company assumes no obligation to update or revise any such forward-looking statement.

Investor & Media Contact:

John Didsbury, Ph.D., CEO
T3D Therapeutics, Inc.
Email: info (at) t3dtherapeutics (dot) com

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