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  As a metabolic and lifestyle disorder, diabetes mellitus poses a prodigious health risk. Out of the many key targets, DPP-IV is one of the very imperative therapeutic targets for the treatment of diabetic patients.
 
  In our current study, we have done the in silico simulations of ADME-T properties for naturally originated potent DPP-IV inhibitors like quinovic acid, stigmasterol, quinovic acid-3-beta-D-glycopyranoside, zygophyloside E, and lupeol. Structural topographies associated with different pharmacokinetic properties have been systematically assessed.
 
  Glycosylation on quinovic acid is found to be noteworthy for the improvement of pharmacokinetic and toxicological properties, which leads to the prediction that zygophyloside E can be further tailored down to get the lead DPP-IV inhibitor.
 
  This assessment provides useful insight into the future development of novel drugs for the treatment of diabetes mellitus.
 This assessment provides useful insight into the future development of novel drugs for the treatment of diabetes mellitus.
  Rheum palmatum L． (RpL) is a traditional Chinese medicine commonly used in clinical. However, there was no systematic research to elucidate the mechanisms of RpL acting on COPD.
 
  To explore the potential mechanisms against COPD based on network pharmacology.
 
  The active compounds of RpL were retrieved from TCMSP database, and their corresponding targets were obtained through TCMSP and STITCH databases. COPD-related targets were identified from the TTD, GeneCards and MalaCards database. Drug-disease genes were obtained through intersection analysis, and the correlation between these genes and COPD was analyzed. After that, a protein-protein interaction network was constructed and enrichment analysis was performed. Then, key targets were obtained according to the network topology attributes analysis. Finally, the Auto dock vina 1.1.2 was used for molecular docking to verify the binding ability between the active compounds and key targets.
 
  There were 8 active compounds and 90 corresponding targets were identified in RpL. A total of 4502 COPDrelated targets were obtained from databases. After cross-analysis, 81 drug-disease targets were obtained. Drug-disease targets mainly regulated apoptosis and inflammatory responses and participated in related signal pathways. Besides, 28 key genes were obtained from the network topology analysis. TP53, TNF, NFKB1, VEGFA, MMP9, and MMP1 were selected to dock with the compounds. The results of molecular docking showed that the above targets have different affinities with the 8 active compounds of RpL.
 
  The mechanisms of RpL acting on COPD were mainly related to the regulation of apoptosis, inflammatory response, and airway remodeling.
 The mechanisms of RpL acting on COPD were mainly related to the regulation of apoptosis, inflammatory response, and airway remodeling.The Alzheimer disease is a age related neurodegenerative disease. The factors causing alzheimer disease are numerous. Research on humans and rodent models predicted various causative factors involved in Alzheimer disease progression. Among them, neuroinflammation, oxidative stress and apoptosis play a major role because of accumulation of extracellular amyloid beta peptides. Here, the clearance of amyloid beta peptide plays a major role because of the imbalance in the production and clearance of the amyloid beta peptide. Additionally, neuroinflammation by microglia, astrocytes, cytokines, chemokines and the complement system also have a major role in Alzheimer disease. The physiological clearance pathways involved in amyloid beta peptide are glymphatic, vascular and immune pathways. Amyloid precursor protein, low density lipoprotein receptor-related protein 1, receptor for advanced glycation end product, apolipoprotein E, clusterin, aquaporin 4, auto-antibodies, complement system, cytokines and microglia are involved in amyloid beta peptide clearance pathways across the blood brain barrier. The plaque formation in the brain by alternative splicing of amyloid precursor protein and production of misfolded protein results in amyloid beta agglomeration. This insoluble amyloid beta leads to neurodegenerative cascade and neuronal cell death occurs. Studies had shown disturbed sleep may be a risk factor for dementia and cognitive decline. In this review, the therapeutic targets for alzheimer disease via focussing on pathways for amyloid beta clearance are discussed.
  Depression is a mental illness caused by the imbalance of important neurotransmitters such as serotonin (5-HT) and norepinephrine (NE). It is a serious neurological disorder that could be treated by antidepressant drugs.
 
  There are two major classes such as TCAs and phenoxyphenylpropylamines which have been proven to be broad-spectrum antidepressant compounds. Several attempts were made to design, synthesize and discover potent antidepressant compounds having the least toxicity and most selectivity towards serotonin and norepinephrine transporters. But there is hardly any drug design based on quantitative structure-activity relationship (QSAR) and pharmacophore modeling attempted yet.
 
  In the present study, many TCAs (dibenzoazepine) and phenoxyphenylpropylamine derivatives are taken into consideration for pharmacophore feature generation followed by pharmacophoric distant related descriptors based QSAR modeling. Further, several five new congeners have been designed which are subjected to the prediction of biological activities in terms of serotonin receptor affinity utilizing validated QSAR models developed by us.