Machine-Learning-Guided Peptide Drug Discovery: Development of GLP-1 Receptor Agonists with Improved Drug Properties.

Peptide-based drug discovery has surged with the development of peptide hormone-derived analogs for the treatment of diabetes and obesity. Machine learning (ML)-enabled quantitative structure-activity relationship (QSAR) approaches have shown great promise in small molecule drug discovery but have been less successful in peptide drug discovery due to limited data availability. We have developed a peptide drug discovery platform called streaMLine, enabling rigorous design, synthesis, screening, and ML-driven analysis of large peptide libraries.

NN1213 - A Potent, Long-Acting, and Selective Analog of Human Amylin.

Amylin, a member of the calcitonin family, acts via amylin receptors in the hindbrain and hypothalamus to suppress appetite. Native ligands of these receptors are peptides with short half-lives. Conjugating fatty acids to these peptides can increase their half-lives.

Inflammatory and interferon gene expression signatures in patients with mitochondrial disease.

Background: People with mitochondrial disease (MtD) are susceptible to metabolic decompensation and neurological symptom progression in response to an infection. Increasing evidence suggests that mitochondrial dysfunction may cause chronic inflammation, which may promote hyper-responsiveness to pathogens and neurodegeneration. We sought to examine transcriptional changes between MtD patients and healthy controls to identify common gene signatures of immune dysregulation in MtD.

A mechanosensory defect in a amyloid-beta glutamatergic neuron model is reversed following exposure to species extracts.

Previous research has described promising neuroprotective and/or antioxidant properties for extracts derived from a few (sage) species. Here, six new species were isolated during flowering times from plants native to Turkey. Extracts were prepared and then examined for their potential to rescue both anterior and posterior mechanosensory behavioral defects in a transgenic Alzheimer's disease model that expresses human amyloid-beta (Aβ) peptide (1-42) exclusively in the glutamatergic neurons.