John Didsbury (United States of America)
T3D Therapeutics, Inc.
Clinical Development
Dr. Didsbury is a seasoned Executive Manager with over 30 years of experience within the pharmaceutical and biotechnology industries in both small and large public and private companies. He routinely serves as a study section reviewer and committee chair for NIA/NIH Alzheimer’s disease clinical trial grants evaluations. Dr. Didsbury was formerly President/COO/CSO of DARA BioSciences, Inc. (now Midatech Pharma US (NASDAQ:CM – MTP). He played a key role in taking the company public in 2008 through a reverse merger. Prior to DARA, he was Head of Strategy and Operations at GlaxoSmithKline, Inc. where he was accountable for overall business planning and disease area strategies for one of six worldwide drug discovery centers. Previously, Dr. Didsbury served as Associate Director of Biology at Macronex, Inc., as Assistant Professor of Medicine at Duke University Medical Center and as a scientist at Genentech, Inc.

Presenter of 1 Presentation

 Conference Calendar

PIONEER, A PHASE 2 STUDY TO EVALUATE TREATMENT WITH T3D-959 IN PATIENTS WITH MILD TO MODERATE ALZHEIMER’S DISEASE: STUDY DESIGN AND UPDATE.

Session Name
1940 - ABETA AND OTHER TARGETING THERAPIES IN AD (ID 95)
Session Type
SYMPOSIUM
Date
Sun, 20.03.2022
Session Time
09:05 AM - 11:05 AM
Room
ONSITE: 113
Lecture Time
10:05 AM - 10:20 AM
Presenter

Abstract

Aims

T3D-959 is a novel (non-amyloid/non-tau-directed) new chemical entity aimed at improving dysfunctional brain glucose energy and lipid metabolism in Alzheimer’s disease (AD). To validate and expand upon observed efficacy signals in a Phase 2a trial, a larger and longer Phase 2 clinical trial is in progress, powered to measure significant differences versus placebo in outcome measures of cognition and function and assessments of multiple biomarkers of disease.

Methods

The ‘PIONEER’ Study is assessing three T3D-959 dose strengths vs. placebo. The trial is randomizing 256 AD patients dosed q.d., for 24-weeks. Eligible patients are 50-90y, have mild to moderate AD with a CDR-SB >3.0 and MMSE of 14-26. Co-primary outcome measures include ADAS-Cog11 and ADCS-CGIC. Secondary outcome measures include DSCT and change in plasma Aβ 42/40 ratio. Exploratory outcome measures include the effect of T3D-959 on absolute regional and whole brain CMRgl using FDG-PET, on plasma metabolomic, lipidomic and proteomic biomarkers, including NfL total tau, p-tau217, and p-tau181.

Results

Enrollment in PIONEER commenced in March 2021 and is ongoing [See ClinicalTrials.gov identifier NCT04251182].

Conclusions

The etiology of AD remains unknown. Brain metabolic dysfunction as causation is underserved in AD research. The PIONEER study fills this gap and supposes that aberrant glucose and lipid metabolism in AD causes protein misfolding which causes formation of plaques, tangles and promotes inflammation. The PIONEER Study will determine the clinical efficacy and safety profile of T3D-959 in individuals with mild to moderate AD. PIONEER is supported by NIA/NIH, under award R01AG061122 and by the Alzheimer’s Association’s Part the Cloud Gates Partnership Grant Program.

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