Roche AG’s disclosure in December that prasinezumab, partnered with Prothena plc, fell short of its primary phase IIb endpoint put the spotlight on microtubule binding region (MTBR)-targeting therapies in neurological disorders.
Voyager Therapeutics Inc.’s recent selection of a lead development candidate, VY-1706, for its tau silencing gene therapy program in Alzheimer’s disease brought renewed attention to the target, which continues to intrigue a substantial lineup of developers. Bellwether data rolled out this fall from UCB SA and Roche AG at the Clinical Trials in Alzheimer’s Disease meeting in Madrid.
Seoul, South Korea-based Adel Inc. raised ₩17 billion (US$12.39 million) in bridge financing to advance its pipeline of Alzheimer’s disease therapies, including its tau antibody-based ADEL-Y01 candidate, currently in a U.S.-based phase I study.
Sangamo Therapeutics Inc. put pen to paper on a would-be $1.9 billion-plus deal with Genentech, a unit of Roche AG, to develop intravenously administered genomic drugs for neurodegenerative conditions.
Seoul, South Korea-based Adel Inc. raised ₩17 billion (US$12.39 million) in bridge financing to advance its pipeline of Alzheimer’s disease therapies, including its tau antibody-based ADEL-Y01 candidate, currently in a U.S.-based phase I study.
An experimental drug that restored the normal function of ion channels in Alzheimer's disease (AD) prevented the loss of neurons and reduced the accumulation of amyloid-β (Aβ) plaques and hyperphosphorylated tau formed in this condition. A new class of small molecules, collectively called ReS19-T and developed by scientists at the Belgian biotechnology company Remynd NV, reorganized proteins that modulated calcium channels. Now in the clinical phase, this approach could benefit patients suffering from neurodegenerative disorders.
After decades of trying and dozens of failed trials, amyloid targeting has paid off with the first disease-modifying agents reaching the market. But success does not mean slam dunk. Aduhelm (aducanumab, Biogen Inc.) was dogged by controversy throughout its brief tenure, and Biogen pulled the plug on it in early 2024. Leqembi (lecanemab, Biogen Inc.) has received full approval. In this second installment of a three-part series on Alzheimer’s, BioWorld looks at the nuanced view of amyloid’s role in the disease.
After decades of trying and dozens of failed trials, amyloid targeting has paid off with the first disease-modifying agents reaching the market. But success does not mean slam dunk. Aduhelm (aducanumab, Biogen Inc.) was dogged by controversy throughout its brief tenure, and Biogen pulled the plug on it in early 2024. Leqembi (lecanemab, Biogen Inc.) has received full approval. In this second installment of a three-part series on Alzheimer’s, BioWorld looks at the nuanced view of amyloid’s role in the disease.
Alzheimer’s disease (AD) is recognized worldwide for its debilitating symptoms of declining cognitive function and gradual memory loss. What remains less clear is exactly what causes the neurodegenerative disease, and how to treat it. “Alzheimer’s disease is characterized by two key pathologies – beta-amyloid plaques and tau neurofibrillary tangles.” Seung-Yong Yoon, CEO of Adel Inc., told BioWorld. “Adel is looking to develop a tau-targeting drug, considering tau has been more correlated with AD symptom progression, and the industry’s need for tau pipelines.”
It is well known that protein tau forms aggregates in the brain in neurodegenerative diseases such as Alzheimer’s disease (AD) that are also known as tauopathies. Accumulation of protein tau in the brain leads to the cell toxicity and promotes the loss of synaptic plasticity, which in turn causes memory loss. As reported on Feb. 1, 2024, in The Journal of Clinical Investigation, assistant professor Tara Tracy and her research team from the Buck Institute for Research on Aging have discovered a protein in the brain that could restore this damage induced by protein tau.
