HIGH POINT — VTV Therapeutics Inc. saw its stock price fall by more than 65 percent in after-market trading Monday after it disclosed disappointing results from the clinical trial of an experimental Alzheimer’s medication.
The High Point-based company announced that the Phase 3 clinical trial assessing the effects of the drug Azeliragon in patients with mild Alzheimer’s disease failed to achieve either co-primary endpoint.
Shares of VTV Therapeutics plunged 65 percent to $1.14, down $2.12 per share, in after-hours trading as of 6:15 p.m.
VTv Therapeutics announced the company will terminate all current clinical trials of azeliragon, which included two separate Phase 3 trials each with about 400 participants per trial.
More information about vTv Therapeutics can be found online.
Posts tagged as “Alzheimer’s”
Little yellow and blue flowers peeped out of melting snow, you snapped your fingers, trying to remember their name.
Alzheimer’s disease (AD) accounts for the majority of dementia cases.
But memory problems start 16 years earlier.
The kind of memory loss associated with AD is insidious, progressive.
Grocery list, to-do list, bucket list.
In other words, is dominantly inherited AD the same or different from sporadic AD?
The findings to date indicate that despite having different causes, familial and sporadic AD on the whole share the same pathophysiology and progression.
Autosomal-dominant and sporadic AD have different triggers, but converge on the same pathophysiologic process.
People with a familial AD mutation (red lines) experience more aggressive amyloidosis than do people with sporadic AD (blue lines).
ADNI participants had more years of education than DIAN participants on average, and they were all from North America whereas DIAN is worldwide.
9932394 entitled, “Single Chain Intrabodies that Alter Huntingtin Mutant Degradation”.
Issued claims cover composition of matter as well as both the Huntingtin and Tau protein targets with the potential for treatment of both Huntington’s and Alzheimer’s diseases.
Our current focus is on Huntington’s disease where we are planning IND enabling studies,” said Lee Henderson, Vybion CEO.
Vybion scientists have previously published findings demonstrating that INT41 accelerates degradation of the toxic gain of function fragment of the mutant huntingtin protein thereby decreasing gene dysregulation and perinuclear aggregation caused by this huntingtin protein degradation fragment (http://dx.doi.org/10.1155/2016/7120753).
About Vybion, Inc. Vybion is a development stage Company with proprietary technologies for Intrabody development currently pursuing strategies to treat neurodegenerative diseases such as Huntington's, SBMA and SCA1, 3, 7 and Alzheimer’s.
It is well known that memory problems are the hallmarks of Alzheimer's disease.
"The mice develop Alzheimer's disease in a very close manner to the human patients with early-onset form of the disease.
The results indicate that caffeine alters the behaviour of healthy mice and worsens the neuropsychiatric symptoms of mice with Alzheimer's disease.
In mice with Alzheimer's disease, the increase in neophobia and anxiety-related behaviours exacerbates their BPSD-like profile.
"Our observations of adverse caffeine effects in an Alzheimer´s disease model together with previous clinical observations suggest that an exacerbation of BPSD-like symptoms may partly interfere with the beneficial cognitive effects of caffeine.
In Alzheimer’s, scientists have hypothesized that dying brain cells break apart and release proteins, including tau, which then form the tangles that are a hallmark of the disease.
New research from Washington University in St. Louis shows, however, that tau secretion is actually an active process, not a byproduct of cell death—findings that could refine tau-targeting treatments for Alzheimer’s.
A variety of approaches are in the works to address the dearth of new Alzheimer’s treatments.
Other methods include targeting genetic variants in neurological cells to boost the immune system’s ability to fight Alzheimer’s.
"Our results showing that tau production is increased suggest that we might want to target tau production therapeutically."
(WHAM photo)Pittsford, N.Y. (WHAM) - A mother of two who was diagnosed with early on-set Alzheimer's disease at the age of 43 has died.
Amy Norton and her family were gracious enough to allow reporters with 13WHAM News to follow her journey over the last four years, beginning in 2014.
2015 - Early On-Set Alzheimer's: One Year Later2016 - Putting a face on early onset Alzheimer's to raise awareness2017 - A family's continued journey with early-onset Alzheimer's diseaseThrough the fight, the Nortons have become Alzheimer's advocates.
Early on-set Alzheimer's affects about 200,000 people under the age of 65 each year.
Box 278996Rochester NY 14627The Alzheimer's Association435 E Henrietta Rd.
Immune cells in the brain have a trigger, and when it is pulled, it prompts immune cells to degrade toxic β-amyloid (Aβ) proteins.
This new finding, from Sanford Burnham Prebys Medical Research Institute (SBP), helps explain why a faulty trigger appears to raise the risk of Alzheimer’s disease.
Increasing the genetic expression of the trigger—a way of pulling the trigger more often—could prevent or reduce the severity of Alzheimer’s disease and other neurodegenerative disorders.
The second study (“Elevated TREM2 Gene Dosage Increase Reprograms Microglia Responsivity and Ameliorates Pathological Phenotypes in Alzheimer's Disease Models”) added TREM2 to a mouse model with aggressive Alzheimer's disease.
"We could use brain immune cells to solve what's becoming a public health crisis."