buntanetap

[Parkinsonjisung]

Is it designed to clear asyn clumps or stop asyn from clumping? Couldn't find a clear answer on that.

[park_bear]

It reduces production of asyn.

[Parkinsonjisung in reply to park_bear]

So the theory is that if there's less asyn, there'll be less clumping?

[park_bear in reply to Parkinsonjisung]

That is my understanding.

[Parkinsonjisung]

Is there any evidence that people with parkinsons have higher levels of asyn?

[Skydome in reply to Parkinsonjisung]

The answer to your question is ‘YES’ with a great deal of certainty. Yet 3 weeks ago the PD world at large did not know this:

.michaeljfox.org/news/breaki...

[SanMateoPD in reply to Skydome]

I think we knew it was in people's brains from autopsies, and people with PD had more lewy/as. But we didn't know it also appeared in spinal fluid. Somewhat surprisingly, there are a small number of people with clinically diagnosed idiopathic PD who do NOT have AS in their spinal fluid. Perhaps there is another type of PD (evidence: the high amount of variation in symptom presentation and progression of PD patients), or possibly they don't have it yet (evidence: we will know more when they do more longitudinal studies of patients, including autopsy, who have been have repeatedly had this assay), or maybe there is a problem with the test (no evidence of this)

[WinnieThePoo in reply to Skydome]

Hardly. 3 years ago I was on a biogen clinical trial for a monoclonal a-syn antibody.

[Boscoejean]

"Many other experimental drugs against neurodegenerative diseases attack, as a rule, plaques, tangles, and other aggregates of neurotoxic proteins (and Lewy bodies in Parkinson’s) as the final stage of pathology. Buntanetap acts differently, as it prevents such neurotoxic cascades. No, buntanetap does not eliminate amyloid beta, alpha-synuclein, and tau — it reduces their levels, doing so in a clinically meaningful way, that is, before their concentrations acquire a toxic threshold.

When the brain is damaged, levels of neurotoxic proteins rise to fight the damage. When the damage is mild, these proteins eventually disappear, but when the damage is severe, their levels remain elevated, worsening the condition. Buntanetap tries to reverse the neurotoxic cascade. Since neurotoxic proteins are conserved (as they evolved and diverged, they retained one commonality), the action of buntanetap is very specific and does not affect normal proteins."

biopharma.media/buntanetap-...

[gaga1958 in reply to Boscoejean]

do you know how they determine in the study if this drug has indeed helped anybody’s neurotroxic cascade levels? Is it only based on symptoms being reduced?

[Boscoejean in reply to gaga1958]

Honestly I do not know because I found this information by trying to find the answer to whether it would just prevent alpha synuclein or would deal with alpha synuclein that is already there but I can look around and see if this information is available.

"In those with PD, who comprised a larger cohort of 54 participants, statistically significant improvements on the Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) and the SDCT both occurred."

"Maria Maccecchini, PhD founder and chief executive of Annovis said, "We are pleased with the safety seen in our phase 1 and 2 clinical trials and grateful to all the participants in those trials. It is exciting to see strong signals of treatment effects across multiple neurodegenerative diseases, which speaks to the power of targeting translation of multiple neurotoxic misfolded proteins, potentially providing a multimodal approach with a single daily oral treatment. "

"Buntanetap, previously known as posiphen, is a novel drug with a unique mechanism of action targeting multiple proteins implicated in neurodegenerative diseases, including amyloid β, tau, α-synuclein, and TDP43. When misfolded, all of these proteins aggregate and impair axon transport, resulting in neuronal cell death. Buntanetap binds a conserved loop region of mRNA in these neurotoxic proteins to prevent translation (production) of misfolded proteins. "

practicalneurology.com/news...

[Boscoejean in reply to gaga1958]

This is from the previous clinical trial that was finished recently.

"After completion of Part 1 of the study, the plasma and CSF samples will be analyzed for the biomarkers to determine if changes are needed to the biomarkers to be measured in Part 2. Since the conduct of the study in Part 2 will be identical to the conduct of the study in Part 1, recruitment will continue uninterrupted. The only potential change between Part 1 and Part 2 are the biomarkers to be measured."

clinicaltrials.gov/ct2/show...

"A CSF analysis is a group of tests that use a sample of your cerebrospinal fluid to help diagnose diseases of the brain and spinal cord and other conditions that affect the central nervous system."

medlineplus.gov/lab-tests/c....

[gaga1958 in reply to Boscoejean]

thank you, appreciate it

[Parkinsonjisung in reply to Boscoejean]

Thanks. This is exactly what I was looking for

[1953bullard]

so it should t reverse symptoms but hopefully will stop progression?

[Peter-Jan]

link.springer.com/article/1...

"Participants

14 early AD patients and 54 early PD patients.

Conclusions

Buntanetap is well tolerated and safe at doses up to 80mg QD in both AD and PD patients. Cmax and AUC increase with dose without evidence for a plateau up to 80mg QD. The drug shows promising evidence in exploratory biomarker and efficacy measures. Further evaluation of buntanetap in larger, longer-term clinical trials for the treatment of AD and PD are warranted.”