Novel API Coated Catheter Removes Amyloid-β from Plasma of Patients with Alzheimer's Disease.

Alzheimer's disease (AD) is the most common cause of dementia, characterized by the deposition of Amyloid-beta (Aβ) plaques in the brain. We have previously developed Amytrap peptide (the active pharmacological ingredient, API) and linked it to a sepharose bead matrix by click chemistry to form Amytrapper matrix, which was able to bind and remove Aβ from human sera and plasma spiked with biotinylated Aβ42 (bio-Aβ42) . To extend the logic of the previous studies, the current study investigates whether the Amytrap peptide coated inside a medically viable polycarbonate catheter (Amytrapper catheter) could bind and retain Aβ from the human sera.

Effect of AmyTrap, an amyloid-β binding drug, on Aβ induced mitochondrial dysfunction and tau phosphorylation in cultured neuroblastoma cells.

Alzheimer's Disease (AD) is the most common cause of dementia, affecting 25 million people worldwide. Accumulation of Amyloid-β (Aβ) in the mitochondria has been shown to adversely affect key enzymes including pyruvate dehydrogenase (PDH), succinate dehydrogenase (SDH), oxoglutarate dehydrogenase (OGDH). Accumulation of Aβ is also believed to increase Tau expression and pathology.

Pre-Clinical Safety and Efficacy Evaluation of Amytrap, a Novel Therapeutic to Treat Alzheimer's Disease.

Alzheimer's disease (AD) is the most common cause of dementia. Amyloid-β (Aβ) is implicated in AD pathogenesis. We have designed a non-immune based proprietary therapeutic, called Amytrap, a conjugate containing a retro-inverso peptide, polyethylene glycol, and human serum albumin.

'Amytrapper', a Novel Immobilized Sepharose API Matrix, Removes Amyloid-β from Circulation .

Alzheimer's disease (AD) is the most common cause of dementia among elderly patients afflicted by neurodegenerative diseases, caused by the accumulation of amyloid-β (Aβ). Therapeutic interventions in targeting and restricting Aβ production resulted in little or no success. However, recent studies have shown signs of success in validating Aβ as a target.

Protein Stains and Applications.

Staining of proteins separated on gels provides the basis for determination of the critical properties of these biopolymers, such as their molecular weight and/or charge. Detection of proteins on gels and blots require stains. These stains vary in sensitivity, ease of use, color, stability, versatility, and specificity.

Patents on potential drugs to treat Alzheimer's disease: special emphasis on small peptides.

The primary objective of this article is to review patents and the related scientific work on naturally occurring compounds, heterocyclic compounds and small peptides that are being explored for their utility for the treatment of Alzheimer's disease (AD). In this review, a special emphasis is given to the patents, including our patent issued in 2013, on peptides that bind to A. Utility of the peptides that prevent aggregation or those that help in clearance of Aβ is discussed as the latter can be considered as an important arm in combination therapy for AD.

Novel Detox Gel Depot sequesters β-Amyloid Peptides in a mouse model of Alzheimer's Disease.

Alzheimer's Disease (AD), a debilitating neurodegenerative disease is caused by aggregation and accumulation of a 39-43 amino acid peptide (amyloid β or Aβ) in brain parenchyma and cerebrovasculature. The rational approach would be to use drugs that interfere with Aβ-Aβ interaction and disrupt polymerization. Peptide ligands capable of binding to the KLVFF (amino acids 16-20) region in the Aβ molecule have been investigated as possible drug candidates.

Protein stains and applications.

Staining of proteins separated on gels provides the basis for determination of the critical properties of these biopolymers, such as their molecular weight and/or charge. Detection of proteins on gels and blots require stains. These stains vary in sensitivity, ease of use, color, stability, versatility, and specificity.

Detoxification depot for beta-amyloid peptides.

Alzheimer's Disease (AD) is caused by the deposition of insoluble and toxic amyloid peptides (Abeta) in the brain leading to memory loss and other associated neurodegenerative symptoms. To date there is limited treatment options and strategies for treating AD. Studies have shown that clearance of the amyloid plaques from the brain and thus from the blood could be effective in stopping and or delaying the progression of the disease.