Currently, there is neither a cure for Alzheimer’s disease (AD) nor a way to stop the progressive death of neuronal cells associated with this devastating aliment. To date, there are only medications that temporarily slow its progression, and do not interfere with its pathogenesis. One of the hallmarks of AD is the presence of amyloid-beta plaques derived from the metabolism of the amyloid precursor protein, via the cleavage by beta followed by gamma secretase. Homotaurine, a naturally occurring small molecule found in some seaweeds, and curcumin, a phenolic antioxidant found in Curcuma longa, have been extensively studied as potential compounds to prevent/reverse plaque formation. In this study, libraries of chalcones and extended chalcones based on curcumin, as well as aminopropylsulfonamides inspired by homotaurine, were synthesized. Using fluorescence spectroscopic analysis with Thioflavin T, the anti-aggregation effect on Aβ42 was determined. A select number of newly synthesized chalcones and extended chalcone analogs were revealed to be potential anti-amyloidogenic agents. These were further evaluated with regard to their neurotoxicity/neuroprotection. The extended chalcone analogs that displayed the most anti-aggregation effect on Aβ42 were further analyzed in an MTT assay. Although none of the compounds alone displayed any neurotoxicity, none were able to provide neuroprotection against Aβ42.
Biologics have seen an explosion in application for a myriad of diseases. Recently the term “biobetter” has entered the lexicon of the pharmaceutical industry. This marketing term refers to a drug that is supposedly a “better” version of a reference biologic. By this definition, these biologics must invariably have some improved pharmacologic and/or pharmacokinetic parameters, such as a better safety/efficacy profile. In actuality, this is not necessarily the case. Additionally, to-date there is neither a legal nor regulatory pathway in place for the development of said, biobetters. This lack of any classification has led to its inconsistent and often inaccurate use within scientific literature. To rectify this, a framework for the potential correct use of the term biobetter within scientific literature (not regulatory) has been provided. Additionally, an exhaustive reclassification of any drug that have been previously termed “biobetter” has been conducted. We believe this classification system, specifically: true-biobetter, potential-biobetter, or non-biobetter will prevent further misuse of the term in the scientific community without modifying the clinical application of such biological entities in practice and in research.
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