AC Immune Selected to Present Progress on its Tau Morphomer Program in the Late Breaking News Session at CTAD Conference in Barcelona
The presentation with the title "Identification and characterization of small molecule clinical candidates targeting intracellular tau pathology" was selected for the late breaking communication session to be held at
In
About Tau Morphomers
Several chemical series of small molecules (MorphomersTM) have been identified which selectively and potently reduce toxic intracellular misfolded and aggregated tau. Targeting intracellular misfolded and aggregated tau is widely recognized as an important and attractive approach for interfering with the spread of tau pathology throughout the brain. Pathological tau may act as a seed that induces native endogenous tau forms to misfold and aggregate into toxic species.
In proof-of-concept Tauopathy models, reduction of tau pathology was also accompanied by a reduction of associated neuroinflammatory markers - another key pathologic feature of Alzheimer's disease (AD).
The lead compound displays excellent absorption, distribution, metabolism and elimination or excretion (ADME) as well as pharmacokinetics properties suitable for targeting the central nervous system. The lead has completed preclinical assessment with the goal to initiate a clinical Phase 1 study by end 2018.
About the MorphomerTM technology platform
The rational chemical design enables
Three therapeutic (Morphomer tau, Morphomer Abeta and Morphomer a-syn) and three diagnostic development candidates (tau-PET imaging agent, a-syn-PET imaging agent, TDP-43-PET imaging agent) originate from the MorphomerTM technology platform.
About Tau in Alzheimer's disease and neurodegenerative diseases
It is becoming increasingly clear that Alzheimer's disease develops because of a complex series of events that take place in the brain over a long period of time. Two proteins - tau and amyloid-beta (Abeta) - are recognized as major hallmarks of AD. Pathological forms of tau aggregate inside neurons to form neurofibrillary tangles, and appear to propagate by cell-to-cell spread between neurons. By contrast, Abeta-containing plaques and oligomers form outside the brain cells of people with AD. Tau protein is mostly present in neurons and functions as a component of the cytoskeleton inside the cells. Misfolded tau protein aggregates in AD and other tau-related neurodegenerative diseases (e.g. progressive supranuclear palsy, frontotemporal dementia and others). In AD, accumulation of tau pathology is accelerated in the presence of Abeta pathology. The progression of tau pathology throughout the brain is closely associated with the onset and progression of cognitive decline, underscoring the importance of tau-targeted therapies.
About
Forward looking statements
This press release contains statements that constitute "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Forward-looking statements are statements other than historical fact and may include statements that address future operating, financial or business performance or
For further information, please contact:
| In Europe Beatrix Benz AC Immune Corporate Communications Phone: +41 21 345 91 34 E-mail: beatrix.benz@acimmune.com |
In the US Lisa Sher AC Immune Investor Relations Phone: +1 970 987 26 54 E-mail: lisa.sher@acimmune.com |
| Nick Miles/Toomas Kull Cabinet Privé de Conseils s.a. Phone: +41 22 552 46 46 E-mail: miles@cpc-pr.com kull@cpc-pr.com |
Ted Agne The Communications Strategy Group Inc. Phone: +1 781 631 3117 E-mail: edagne@comstratgroup.com |
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