Cassava Sciences Announces Phase 2a Study of PTI-125 Published in The Journal of Prevention of Alzheimer’s Disease (JPAD)

AUSTIN, Texas, Feb. 11, 2020 (GLOBE NEWSWIRE) -- Cassava Sciences, Inc. (Nasdaq: SAVA), a clinical-stage biotechnology company focused on Alzheimer’s disease, today announced that The Journal of Prevention of Alzheimer’s Disease (JPAD), a peer-reviewed journal for the research community, published results from the Company’s Phase 2a study demonstrating that its lead drug candidate, PTI-125, reduced biomarkers of disease in Alzheimer’s patients.

Nadav Friedmann, MD, PhD, Chief Medical Officer at Cassava Sciences commented, “We are pleased to share these study results in JPAD. This publication provides clinical insights into how our lead drug candidate, PTI-125, could make an important difference for patients living with Alzheimer’s disease. In this study, PTI-125 reduced multiple biomarkers of Alzheimer’s disease, including neurodegeneration and neuroinflammation. To our knowledge, no other drug has shown such effects in Alzheimer’s patients.”

Published results from this study demonstrate that biomarkers of Alzheimer’s disease pathology (P-tau, total tau and Aβ₄₂), neurodegeneration (NfL and neurogranin) and neuroinflammation (YKL-40, IL-6, IL-1β and TNFα) improved significantly after 28 days of treatment with PTI-125. Biomarker reductions were at least p< 0.001 by paired t-test. Biomarkers effects were seen in all patients in both cerebrospinal fluid (CSF) and plasma. PTI-125 was safe and well tolerated, with no observable drug-related adverse events.

Lindsay H. Burns, PhD, VP Neuroscience at Cassava Sciences, added, “This publication supports PTI-125 as a new and potentially disease-modifying drug treatment for Alzheimer’s disease. Significant improvements observed across multiple biomarkers imply a slower rate of neurodegeneration or a suppression of disease processes. These treatment effects are consistent with the drug’s mechanism of action and over ten years of basic research and preclinical data.”

Key results published from the Phase 2a study include:

• Total tau (T-tau) decreased 20% (p<0.001)
• Phosphorylated tau (P-tau) decreased 34% (p<0.0001)
• Neurofilament light chain (NfL), a marker for neurodegeneration, decreased 22% (p<0.0001)
• Neurogranin, a marker for cognitive decline, decreased 32% (p<0.0001)
• Neuroinflammatory marker YKL-40, an indicator of microglial activation, decreased 9% (p<0.0001)
• Proinflammatory Interleukin 6 (IL-6) decreased 14% (p<0.0001)
• Proinflammatory Interleukin 1 beta (IL-1β) decreased 11% (p<0.0001)
• Proinflammatory Tumor Necrosis Factor alpha (TNFα) decreased 5% (p<0.001)
• The ratio of CSF P-tau to Aβ₄₂, a widely accepted biochemical value of Alzheimer’s disease, improved in all patients (p<0.001)

Although cognition and function were not assessed in this small Phase 2a study, independent research has shown that high levels of CSF biomarkers of P-tau and total tau/Aβ₄₂ ratio correlate with worse performance on a wide range of memory and attention tests. Conversely, lowering biomarkers of disease may benefit patients.