The alpha (α)-amylase is a calcium metalloenzyme that aids digestion by breaking down polysaccharide molecules into smaller ones such as glucose and maltose. In addition, the enzyme causes postprandial hyperglycaemia and blood glucose levels to rise. α-Amylase is a well-known therapeutic target for the treatment and maintenance of postprandial blood glucose elevations. Various enzymatic inhibitors, such as acarbose, miglitol and voglibose, have been found to be effective in targeting this enzyme, prompting researchers to express an interest in developing potent alpha-amylase inhibitor molecules. The review mainly focused on designing different derivatives of drug molecules such as benzofuran hydrazone, indole hydrazone, spiroindolone, benzotriazoles, 1,3-diaryl-3-(arylamino) propan-1-one, oxadiazole and flavonoids along with their target-receptor interactions, IC 50 values and other biological activities.
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Glycogen Synthase Kinase 3 (GSK3) is one of the Serine/Threonine protein kinases that has gained a lot of
attention for its role in a variety of pathways. It has two isoforms, GSK3α and GSK3β. However, GSK3β is
highly expressed in different areas of the brain and has been implicated in Alzheimer’s disease as it is involved
in tau phosphorylation. Due to its high specificity concerning substrate recognition, GSK3 has been considered
as an important target. In the last decade, several GSK3 inhibitors have been reported and two molecules are in
clinical trials. This review collates the information published in the last decade about the role of GSK3 in
Alzheimer’s disease and progress in the development of its inhibitors. Using this collated information, medicinal
chemists can strategize and design novel GSK3 inhibitors that could be useful in the treatment of Alzheimer’s
disease.
Astrocytes, the star shaped glial cells, are known to possess supportive and homeostatic role for the neurons. Recently, reactive gliosis, which involves alterations in functioning and phenotype of different glial cells, has been implicated in Alzheimer's Disease (AD). Studies have revealed that astrocyte response to gross tissue damaging injury leads to anisomorphic astrogliosis reinforcing a cascade of events, eventually increasing the pathogenesis of AD and many other neurodegenerative disorders. This review presents the involvement of reactive astrocytes in reduced Aβ clearance and in neuro-neglect hypothesis. Understanding of reactivity and fundamental biology of astrocytes may open new avenues of alternative treatments and therapeutic strategies targeting astrocytes and related events for the treatment of AD.
Human Immunodeficiency Virus Type 1 Integrase or HIV-1 integrase (IN) is a 288 amino acid protein that incorporates the retrotranscribed viral DNA into the host chromosomal DNA. Over the past 30 years, large number of derivatives have been evaluated for their inhibitory potential against IN. There is vast literature available which need to be collated to help scientists plan the future drug design. This review discusses the reports of past 25 years on analogs of quinoline, coumarin and other related heterocycles, which exhibit low micromolar inhibitory potency against IN.
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