Annovis Bio
Chief Executive Officer
Maria L. Maccecchini PhD Maria Maccecchini founded Annovis Bio, Inc. to develop treatments for Alzheimer’s (AD), Parkinson’s (PD) and other neurodegenerative diseases by normalizing axonal transport and restoring homeostasis in the brain. The company is developing three classes of drugs for the treatment of neurodegeneration. One targets chronic conditions like AD and PD and may stop the progression of the diseases. The second one targets acute conditions, like Traumatic Brain Injury and Stroke. Whereas the third one targets late stage AD and may stabilize the decline. ANVS-401, the lead compound, successfully completed three phase I and two phase 2 studies demonstrating that improves cognition in AD measured by ADAScog and WAIS and motor function in PD measured by UPDRS and WAIS. As expected it is safe; enters the brain; restores axonal transport by normalizing brain levels of neurotoxic proteins back to the levels seen in healthy normal volunteers; reduces inflammation and protects nerve cells from dying. Dr. Maccecchini did one postdoc at Caltech and one at the Roche Institute of Immunology, her PhD in biochemistry is from the Biocenter of Basel with a 2-year visiting fellowship at The Rockefeller University.

Presenter of 1 Presentation

POSITIVE CLINICAL OUTCOMES OF POSIPHEN IN TWO PHASE 2A STUDIES -- ALZHEIMER'S DISEASE AND PARKINSON'S DISEASE

Session Type
SYMPOSIUM
Date
Sun, 20.03.2022
Session Time
09:05 AM - 11:05 AM
Room
ONSITE: 113
Lecture Time
09:35 AM - 09:50 AM

Abstract

Aims

Posiphen has been shown in animal models to reduce multiple neurotoxic proteins, restore axonal transport, lower inflammation and protect nerve cells from dying. To show that Posiphen reverses the toxic cascade and potentially shows efficacy in humans, we started two double-blind, placebo- controlled clinical phase 2a studies in AD and PD patients.

Methods

In the first part, we enrolled 14 AD and 14 PD patients (4 placebo and 10 treated with 80 mg posiphen QD for 25 +/- 2 days). We measured markers of neurotoxic proteins, axonal transport, inflammation and neurodegeneration. The second part enrolled an additional 40 PD patients with the same study design to test biomarkers and efficacy at different concentrations of posiphen.

Results

From the first part of the study, we report statistically significant improvements in ADAS-Cog 11 and WAIS coding in treated AD patients comparing to baseline. Posiphen reduced sAPPα, sAPPβ, Tau, p-Tau and improved the Ab42/40 ratio. In PD patients, we see statistically significant improvements in the WAIS coding test comparing to control and strong trends in all 4 UPDRS parts. Posiphen significantly reduced inflammation in treated patients.

We expect to finish analyzing all the remaining biomarkers of part 1 and report on the part 2 data mid October.

Conclusions

In conclusion, our data from the first 28 patients shows that Posiphen improves cognition in AD and motor function in PD as well as reverses the toxic cascade. The expected additional markers and the new part 2 data will solidify and confirm that Posiphen works in AD and PD patients.

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