Cortexyme’s Approach to Addressing a Key Underlying Cause of Alzheimer’s Detailed at Alzheimer’s Association International Conference 2019

Cortexyme, Inc. (Nasdaq: CRTX) today announced the presentation of clinical data that supports its ongoing work to pioneer a novel, disease-modifying therapeutic approach to treating a key underlying cause of Alzheimer’s and other degenerative diseases. In a poster presentation at the Alzheimer’s Association International Conference 2019 (AAIC), researchers highlighted the Phase 1b clinical development experience of COR388, the company’s lead investigational gingipain inhibitor, and provided an overview of the design for the GAIN trial, the company’s large, international Phase 2/3 trial in patients with mild to moderate Alzheimer’s disease (AD). AAIC is the largest international meeting dedicated to advancing dementia science and is being held this week in Los Angeles.

“In Phase 1a/b testing, COR388 was well tolerated and associated with encouraging signs of early clinical activity, providing a solid rationale for the GAIN trial, our ongoing Phase 2/3 study that seeks to enroll approximately 570 patients with mild to moderate Alzheimer’s disease,” said Michael Detke, M.D., Ph.D., Cortexyme’s chief medical officer. “The response from the Alzheimer’s investigator and patient communities has been strong, and we look forward to enrolling the study and fully evaluating COR388’s utility as a potential treatment for Alzheimer’s.”

GAIN Trial’s Scientific Foundation and Clinical Trial Design Detailed

In a Developing Topics poster (P4-663), researchers detailed the rationale for and design of the GAIN trial, which began enrolling subjects in the United States in April 2019. The trial represents the first large, randomized late-stage clinical study evaluating the gingipain hypothesis, which is based upon growing evidence that the bacterium most commonly associated with chronic periodontal disease, Porphyromonas gingivalis, plays a key role in the development of AD, given its identification in the brains of AD patients and ability to cause neurodegeneration, inflammation, and other pathology associated with Alzheimer’s in animal models. In these models, the pathological effects were blocked by COR388, which targets the gingipains, or toxic proteases, released by P. gingivalis as it colonizes tissue.