Annovis Bio's Phase 3 trial of Buntanetap/Posiphen: Trial record has been updated (contacts and locations)

[jeffreyn]

There are now 18 locations mentioned in the updated trial record (September 12, 2022):

- one in Aventura, Florida (not yet recruiting);

- one in Boca Raton, Florida (not yet recruiting);

- two in DeLand, Florida (recruiting);

- one in Hallandale Beach, Florida (not yet recruiting);

- one in Homestead, Florida (not yet recruiting);

- four in Miami, Florida (not yet recruiting);

- one in Pembroke Pines, Florida (recruiting);

- one in Winter Park, Florida (not yet recruiting);

- one in Indianapolis, Indiana (recruiting);

- one in Kansas City, Kansas (not yet recruiting);

- one in Columbus, Ohio (not yet recruiting);

- one in Memphis, Tennessee (not yet recruiting);

- one in Round Rock, Texas (not yet recruiting);

- one in Spokane, Washington (recruiting).

The plan is to recruit 450 early-stage PwPs spread over 100 sites in the US and EU.

Estimated Study Completion Date: December 2023

Trial record:

clinicaltrials.gov/ct2/show...

Note:

This list of 18 sites is much smaller than the list of more than 40 sites contained in the spreadsheet provided to PDWarrior1900 by Annovis Bio (see link below). I'm not sure why this is so. The main difference between the two lists seems to be the inclusion of "recruitment status" information in the trial record (i.e. recruiting / not yet recruiting).

healthunlocked.com/cure-par...

[Farooqji]

I have very high expectations from this trial keeping in view the very positive results of Phase 2a. The company's CEO has wrote the following letter to the investors:

"Most importantly, this has been demonstrated in human clinical trials. In our

recent Phase 2 clinical trial in Alzheimer's disease and Parkinson's disease,

treatment with buntanetap resulted in reduction of aggregating proteins and

statistically significant improvement in motor function in Parkinson's disease

patients and cognition in Alzheimer's disease patients.

FUNCTION TEST SUBJECT

ANIMALS

Memory, learning Mazes AD mice, DS mice, stroke

mice, TBI rats

Movement Colonic motility, grip PD mice, tau mice

strength

Vision Sight Glaucoma rats

Infections Cell death P. Gingivalis mice, Covid

mice

HUMANS

Cognition, memory, ADAScog11 Early AD patients

learning

Attention, thinking speed WAIS coding Early AD patients

Movement, coordination MDS-UPDRS Early PD patients

Movement speed WAIS coding Early PD patients

Table 1: Summary of all animal and human study data.

We look forward to unlocking the full potential of buntanetap and addressing

unmet needs across a range of acute and chronic neurological conditions.

Maria L. Maccecchini, Ph.D.,

Founder, President, CEO and Executive Board Member"

bloomberg.com/press-release...

[Farooqji]

the drug could be launched as a disease-modifying Parkinson's disease therapeutic in 2026 in the U.S. and in 2027 in Europe.

[LauraYu in reply to Farooqji]

2026 or 2027? Do we have to wait for that long? I am highly confident of its therapeutic potential on PD. Wondering if the company is recruiting volunteers in Canada

[jeffreyn]

Mechanism of action (from Farooqji's link):

Buntenatap works by inhibiting specific neurotoxic proteins such as amyloid precursor protein (APP), Tau, alpha-synuclein (αSYN), TAR DNA binding protein 43 (TDP-43), huntingtin (HTT) and prion protein. These proteins have normal functions but in their neurotoxic aggregating form, they impair axonal transport, slow synaptic transmission, cause inflammation, and ultimately, kill nerve cells, resulting in the loss of affected function in various neurodegenerative conditions.

The overexpression and aggregation of these proteins is caused by elevated levels of iron in the nerve cell. The mRNAs of neurotoxic aggregating proteins contain an iron response element (IRE) which binds to an iron regulatory protein called IRP1. At normal iron levels, translation occurs at appropriate physiological levels. When iron flows into the cell, the mRNAs are released and translated at higher rates by the ribosome. When massive iron flows in, the mRNAs remain unbound for as long as the iron is high and the proteins for these neurotoxic aggregating proteins are overexpressed. In this high iron situation, buntanetap binds to the atypical IRE-IRP1 complex and prevents the mRNA from being released and, therefore, from being translated and overexpressed.

[jeffreyn in reply to jeffreyn]

It seems to me that Scripps Research are trying to do something similar, as described by Simon in this SoPD blog post:

scienceofparkinsons.com/202...