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Gold M.,Allon Therapeutics | Lorenzl S.,Ludwig Maximilians University of Munich | Stewart A.J.,Allon Therapeutics | Morimoto B.H.,Allon Therapeutics | And 3 more authors.
Neuropsychiatric Disease and Treatment | Year: 2012

Progressive supranuclear palsy (PSP) is a rare neurodegenerative disease characterized by the accumulation of tau protein aggregates in the basal ganglia, brainstem and cerebral cortex leading to rapid disease progression and death. The neurofibrillary tangles that define the neuropathology of PSP are comprised of aggregated 4R tau and show a well-defined distribution. Classically, PSP is diagnosed by symptoms that include progressive gait disturbance, early falls, vertical ophthalmoparesis, akinetic-rigid features, prominent bulbar dysfunction and fronto-subcortical dementia. There are currently no effective therapies for the treatment of this rapidly degenerating and debilitating disease. Davunetide is a novel neuroprotective peptide that is thought to impact neuronal integrity and cell survival through the stabilization of microtubules. Preclinical activity in models of tauopathy has been translated to clinical studies, demonstrating pharmacologic activity that has supported further development. Davunetide's efficacy and tolerability are being tested in a placebo-controlled study in PSP patients, making it the most advanced drug candidate in this indication. This review examines the disease characteristics of PSP, the rationale for treating PSP with davunetide and assesses some of the challenges of clinical trials in this patient population. © 2012 Gold et al.


Morimoto B.H.,Allon Therapeutics | Schmechel D.,Southeastern Neurology and Memory Clinic | Hirman J.,PNW Statistics Inc. | Blackwell A.,Cambridge Cognition | And 2 more authors.
Dementia and Geriatric Cognitive Disorders | Year: 2013

Background/Aims: AL-108-211 was a placebo-controlled, ascending-dose study that explored the safety, tolerability and efficacy of 12 weeks of treatment with AL-108 in subjects with amnestic mild cognitive impairment. Methods: A total of 144 subjects were randomized in a 2:1 drug:placebo ratio. Subjects were enrolled into the low-dose group or placebo and then to the high-dose group or placebo. Pooling of the placebo groups yielded 3 groups (approx. 48/group) whose baseline demographics and disease characteristics were well matched. Results: AL-108 was generally safe and well tolerated. Analyses of efficacy data failed to detect a statistically significant difference between the treatment groups on the composite cognitive memory score. Analyses of the individual cognitive tasks identified signals of potential efficacy in 2 tests of memory and attention. Conclusion: These data suggest that AL-108 was generally safe, well tolerated and merits additional investigation as a treatment for Alzheimer's disease. Copyright © 2013 S. Karger AG, Basel.


Karantzoulis S.,New York University | Novitski J.,Rosalind Franklin University of Medicine and Science | Gold M.,Allon Therapeutics | Randolph C.,Loyola University
Archives of Clinical Neuropsychology | Year: 2013

Current diagnostic criteria for mild cognitive impairment (MCI) due to Alzheimer's disease (AD) require standardized tests that are capable of measuring a range of neurocognitive abilities in healthy elderly individuals and sensitive to detect change over time. There currently is no clearly-established "gold standard" for this purpose. The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) is a widely used neuropsychological test battery for the clinical diagnosis/tracking of dementia also recently incorporated into clinical trials of new investigational medications for AD treatment. The RBANS has a number of design features that suggest possible utility in diagnosis/tracking of MCI. Eighty-one patients with MCI completed the RBANS and their scores were compared with 81 demographically matched healthy controls. RBANS Total Scale scores in both groups were normally distributed, demonstrating no floor/ceiling effects. The MCI group was most impaired on the Delayed Memory Index (DMI). Receiver operating characteristic analyses reflected good discrimination, with an area under the curve of 0.88 for the Total Scale score and 0.90 for the DMI score. The profile of performance for the MCI group was similar to that previously reported for mild AD patients. The RBANS may be a suitable neurocognitive battery for the detection and tracking of MCI presumed to be due to AD. © The Author 2013. Published by Oxford University Press. All rights reserved.


Gozes I.,Tel Aviv University | Gozes I.,Allon Therapeutics
Peptides | Year: 2011

NAP (davunetide) is an active fragment of activity-dependent neuroprotective protein (ADNP). ADNP and the homologous protein ADNP2 provide cell protection. ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. ADNP haploinsufficiecy inhibits social and cognitive functions, major hallmarks in schizophrenia. Imbalance in ADNP/ADNP2 expression in the schizophrenia brain may impact disease progression. NAP treatment partly ameliorates ADNP haploinsufficiecy. The microtubule, stable tubule-only polypeptide (STOP)-deficient mice were shown to provide a reliable model for schizophrenia. Daily intranasal NAP treatment significantly decreased hyperactivity in STOP-deficient mice and protected visual memory, supporting further clinical development. © 2010 Elsevier Inc.


Morimoto B.H.,Allon Therapeutics
Expert review of clinical pharmacology | Year: 2013

Davunetide is the first neuroprotective peptide in its class, and has preclinical evidence for neuroprotective, neurotrophic and cognitive protective properties. Davunetide has also been shown to prevent apoptosis or programmed-cell death in a range of in vitro and in vivo models by promoting microtubule stabilization. Potential clinical uses of davunetide include neurodegenerative disorders such as Alzheimer's disease (AD), progressive supranuclear palsy (PSP), frontotemporal dementia (FTD) or cognitive impairment in other diseases such as schizophrenia where microtubule structure and function is known to be impaired. The nonclinical and clinical safety of davunetide is reviewed here in detail. Pre-clinical toxicology studies in rats and dogs using the maximum feasible dose of davunetide provide strong evidence that davunetide is well-tolerated. Similarly, data from 10 separate clinical trials of davunetide, investigating safety and efficacy provide evidence that davunetide is generally safe and well-tolerated, and has shown some signs of clinical efficacy.


Patent
Allon Therapeutics and Tel Aviv University | Date: 2012-10-30

This invention relates to NAP-like and SAL-like peptide mimetics, polypeptides, or small molecules derived from them, and their use in the treatment of neuronal dysfunction, neurodegenerative disorders cognitive deficits, neuropsychiatric disorders, and autoimmune disease.


Patent
Allon Therapeutics and Tel Aviv University | Date: 2011-06-30

This invention relates to treatment of neurodegeneration, multiple sclerosis, or schizophrenia using an ADNF III polypeptide in combination with another therapeutic agent. Neurodegeneration, including neurodegeneration caused by dementia-related conditions, such as tauopathies, including Alzheimers disease, and aging-related dementia, is treated by a combination of an ADNF III polypeptide and an acetylcholinesterase inhibitor. Multiple sclerosis is treated by a combination of an ADNF III polypeptide and glatiramer acetate. Schizophrenia is treated with a combination of an ADNF III peptide and an antipsychotic drug, selected from Aripiprazole, Clozapine, Ziprasidone, Resperidone, Quetiapine, and Olanzapine.


Patent
Tel Aviv University and Allon Therapeutics | Date: 2010-02-18

This invention relates to NAP-like and SAL-like peptide mimetics, polypeptides, or small molecules derived from them, and their use in the treatment of neuronal dysfunction, neurodegenerative disorders cognitive deficits, neuropsychiatric disorders, and autoimmune disease.


News Article | February 18, 2008
Site: www.zdnet.com

We may finally be getting to the root of Alzheimer's Disease. Some 32 centers around the country are enrolling patients in 8 new trials of a drug that drags beta amyloid, the protein whose plaques cause brain cells to die, into the bloodstream for disposal. Elan-Wyeth, Merck, and Samaritan Pharmaceuticals of Las Vegas are all working on human trials of drugs based on dealing with beta amyloid. Most are based on a class of compound called spirostenols. (Picture from Samaritan Pharmaceuticals.) At the same time a Canadian company, Allon Therapeutics, is working with a compound focused on the neurofibrillary tangles which result from this and cause memory loss. The company made a presentation on its drug last week in New York, which is available online. It's estimated 1 in 15 of people who live a normal lifespan will develop Alzheimer's. If you reach age 90 the odds rise to 1 in 2. My grandfather died of Alzheimer's and I'm scared to death of it. Maybe soon I won't have to be.

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