Patent highlights April-May 2018.

  title={Patent highlights April-May 2018.},
  author={Hermann A. M. Mucke},
  journal={Pharmaceutical patent analyst},
  volume={7 5},
  • H. Mucke
  • Published 1 August 2018
  • Biology
  • Pharmaceutical patent analyst
Assignee: Université Laval, Québec (Canada) Inflammatory bowel diseases seem to be triggered by an intestinal epithelial dysfunction, probably in response to danger signals that might only suggest the presence of pathogens but nevertheless amplify and sustain the release of proinflammatory cytokines. There is considerable evidence that activation of purinergic receptors by nucleotides such as ATP and UTP, constitutes at least part of these signals and not only in the intestinal tract [1,2… 



Characterization of Human CD39+ Th17 Cells with Suppressor Activity and Modulation in Inflammatory Bowel Disease

A human Th17 subpopulation with suppressor activity, which expresses high levels of CD39 and consequently produces extracellular adenosine is described, which might have implications for the development of novel anti-inflammatory therapeutic approaches in these and potentially other immune disorders.

Purinergic Ligands as Potential Therapeutic Tools for the Treatment of Inflammation-Related Intestinal Diseases

The most promising purine-based therapeutic strategies for the treatment of inflammation-related gastrointestinal disorders are schematically summarized.

A bacterial metabolite ameliorates periodontal pathogen-induced gingival epithelial barrier disruption via GPR40 signaling

Results suggest that 10-Hydroxy-cis-12-octadecenoic acid exerts a protective function, through GPR40 signaling, against periodontopathic bacteria-induced gingival epithelial barrier impairment and contributes to the suppression of inflammatory responses in periodontal diseases.

Fasiglifam (TAK-875), a G Protein-Coupled Receptor 40 (GPR40) Agonist, May Induce Hepatotoxicity through Reactive Oxygen Species Generation in a GPR40-Dependent Manner

Histopathological examination of zebrafish exposed to TAK-875 revealed severe hepatotoxicity as manifested by degenerated hypertrophic hepatocytes with cytoplasmic vacuolation and acentric nuclei, confirming that Tak-875 may induce direct hepatot toxicity and that ROS generation may be involved in a GPR40-dependent manner.

Bismuth-Induced Inactivation of Ferric Uptake Regulator from Helicobacter pylori.

It is demonstrated that Bi(III) binds to HpFur protein specifically at the physiologically important S1 site, which further leads to protein oligomerization and loss of DNA binding capability, and present direct evidence that perturbation of iron metabolism in H. pylori by bismuth might serve as one of the mechanisms for the antimicrobial activity of bismUTH drugs.

Agonism of the 5-Hydroxytryptamine 1F Receptor Promotes Mitochondrial Biogenesis and Recovery from Acute Kidney Injury

Induction of MB through 5-HT1F receptor agonism represents a new target and approach to treat mitochondrial organ dysfunction and promotes recovery from AKI injury.

The role of microbial amyloid in neurodegeneration

The term “mapranosis” is proposed to describe the process of microbiota-associated proteopathy and neuroinflammation, which is a promising area for therapeutic intervention because there are many ways to alter the authors' microbial partners and their products, including amyloid proteins.

Bismuth antimicrobial drugs serve as broad-spectrum metallo-β-lactamase inhibitors

The authors show that the anti-Helicobacter pylori drug colloidal bismuth subcitrate inhibits MBLs by displacing the zinc ions with Bi(III), which is of great interest for the development of antibiotics.

HMGB1 Protein: A Therapeutic Target Inside and Outside the Cell.