Anti-tau Alzheimer’s therapeutic pushes forward in phase III clinical trials
TauRx Therapeutics announced today that enough subjects have been enrolled in the second of two phase III clinical trials to continue validating a tau aggregation inhibitor called LMTX for the treatment of mild Alzheimer's disease.
This particular drug also engages TDP-43, recently recognized as an important biomarker for neurodegenerative pathology.
The latter trial, Protocol TRx-237-005, is a multi-center placebo-controlled trial geared toward the treatment of mild Alzheimer’s disease. A total of 700 participants with mild Alzheimer's disease have been enrolled to evaluate pharmacokinetics and safety of the drug.
The first of the two trials, Protocol TRx-237-015, reached an enrollment of 833 subjects in July to assess the drug for patients with mild to moderate Alzheimer’s disease. A third clinical trial, Protocol TRx-237-007, targets behavioral variant frontotemporal dementia and is scheduled to complete enrollment in the first quarter of 2015.
"Reaching our enrollment targets for both of our Phase III Alzheimer's disease clinical trials is a major milestone for our company and it is particularly apt that we can announce this on World Alzheimer's Day,” said Professor Claude Wischik, chairman and co-founder of TauRx, in a press release. “This achievement brings us another step closer to our objective to offer the first tau-targeted, disease-modifying treatment for Alzheimer's disease--an important treatment advance for patients."
World Alzheimer’s Day is Sept. 21 and was created to raise awareness of the disease. Both of the anti-tau Alzheimer’s studies are expected to be completed some time in 2016.
"Having a tau-targeted treatment that slows or halts the progression of Alzheimer's will be a breakthrough for people facing this disease worldwide,” added Serge Gauthier, MD, from the McGill Centre for Studies in Aging in Montreal, Canada. “With many failed attempts in alternative approaches, we could at last be on the right path towards altering the underlying pathology that leads to dementia."