AUSTIN, Texas, Dec. 14, 2017 — Pain Therapeutics, Inc. (Nasdaq:PTIE), a biopharmaceutical company, today announced a new publication for PTI-125, a clinical-stage drug candidate with a novel mechanism of action for the treatment of Alzheimer’s disease.
The new publication in Neuroimmunology and Neuroinflammation describes an altered form of a protein called filamin A (FLNA) that is critical to the formation of neuropathologies associated with Alzheimer’s disease. PTI-125, a small molecule drug, reverses these neuropathologies by selectively binding the altered form of FLNA and restoring its normal shape. These data, while still subject to clinical translation, support a promising new therapeutic approach to slow the course of Alzheimer’s disease.The new publication can be freely accessed online: http://nnjournal.net/article/view/2313“This is very exciting data that we believe supports a sound scientific rationale to continue with the clinical evaluation of PTI-125 in Alzheimer’s disease,” said Remi Barbier, President & CEO.Pain Therapeutics recently announced the completion of a successful Phase I study with PTI-125 under an Investigational New Drug (IND) application filed with the U.S. Food and Drug Administration (FDA). Full results of the Phase I study were presented by Company scientists at the 10th Annual International Conference on Clinical Trials on Alzheimer’s Disease, in Boston, MA.The underlying technology around PTI-125 also supports the development of a diagnostic/biomarker to detect Alzheimer’s disease with a simple blood test. Following a competitive evaluation of the Pain Therapeutics’ technology for scientific and technical merit, the NIH's National Institute on Aging, awarded the Company a $1.8 million research grant in September 2017 to develop a blood-based diagnostic for Alzheimer’s disease.About Alzheimer's Disease and PTI-125
Alzheimer’s Disease (AD) is a progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. There is no approved drug therapy to slow, or even halt, the course of AD. PTI-125 is an oral, small molecule drug candidate that was designed in-house and characterized by outside collaborators. PTI-125 has been shown to significantly improve AD neuropathologies in mouse models of the disease and in post-mortem brain tissue from AD patients, including receptor dysfunctions, neuroinflammation, tau hyperphosphorylation, insulin resistance and plaques and tangles that are hallmarks of AD.
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