Randomized, Placebo Controlled Trial of NPT088, A Phage-Derived, Amyloid-Targeted Treatment for Alzheimer’s Disease - 21/11/24
, J.M. Levenson 1, P. Aisen 3, K. Marek 4, M. Gray 1, F. Hefti 1
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Abstract |
The engineered fusion protein NPT088 targets amyloid in vitro and in animal models of Alzheimer’s disease. Previous studies showed that NPT088 treatment reduced β-amyloid plaque and tau aggregate loads in mouse disease models. Here, we present the results from an initial clinical study of NPT088 in patients with mild to moderate Alzheimer’s disease. Patients were treated with 4 dose levels of NPT088 for 6 months to evaluate its safety and tolerability. Exploratory measurements included measurement of change in β-amyloid plaque and tau burden utilizing Positron Emission Tomography imaging as well as measures of Alzheimer’s disease symptoms. At endpoint NPT088 was generally safe and well-tolerated with the most prominent finding being infusion reactions in a minority of patients. No effect of NPT088 on brain plaques, tau aggregates or Alzheimer’s disease symptoms was observed.
Le texte complet de cet article est disponible en PDF.Key words : Amyloid, Alzheimer’s disease, β-amyloid plaques t]tau tangles
Plan
| Disclosures: David Michelson, Richard Fisher, Franz Hefti, Michelle Gray, and Jonathan Levenson are all current or former employees of Proclara Biosciences. Michael Grundman and Paul Aisen were paid consultants to Proclara Biosciences. Kenneth Marek is a former employee of Invicro and has served as a paid consultant to Proclara Biosciences. |
Vol 6 - N° 4
P. 228-231 - octobre 2019 Retour au numéro
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