Samaritan Pharmaceuticals has announced animal study results that show its Alzheimer's drug SP-233 (caprospinol) not only stops amyloid plaque formation in the brain of an animal model, but also that treatment with caprospinol results in the disappearance of amyloid plaques in the brain.
This new study, conducted in a rat animal model of Alzheimer's disease and led by Samaritan collaborating researchers at Georgetown University, found that rats exhibiting an Alzheimer's disease-like phenotype treated with a placebo solution retained amyloid plaques formed in the hippocampus and cortex of the brain, whereas, rats treated with caprospinol found no detectable amyloid plaques.
Caprospinol demonstrates neuroprotective properties in preclinical studies. In vitro studies have demonstrated that caprospinol directly binds to beta-amyloid peptide, inhibits the formation of neurotoxic amyloid-derived diffusible ligands and protects the mitochondria function by a direct action of the peptide on the organelle, thus protecting neuronal cells from beta-amyloid-induced toxicity.