Every article, presentation, spotlight, and news item we've tagged to Regenerative Therapies.
Showing 145–150 of 150
Somatostatin overexpression in neurons reduces microglial activation and inflammatory signaling while enhancing amyloid-β clearance in an Alzheimer's mouse model. Existing drugs targeting this pathway suggest translational potential for addressing neuroinflammation in cognitive decline.
BGE-102, an oral NLRP3 inhibitor, demonstrated rapid and substantial reductions in high-sensitivity C-reactive protein (85–86% median reduction) and inflammatory markers in a Phase 1 trial, with 87–93% of treated participants normalizing hsCRP levels and no serious adverse events reported. This early evidence suggests a therapeutic approach to systemic inflammation that may have relevance to age-related disease prevention.
Lysoway Therapeutics has initiated Phase 1 testing of LW-1017, a small-molecule TRPML1 agonist designed to restore autophagy-lysosomal function in neurodegenerative diseases including Alzheimer's and Parkinson's. The compound represents a potential intervention targeting cellular waste clearance mechanisms that decline with age.
BioAge Labs reported positive interim Phase 1 data for BGE-102, an oral NLRP3 inhibitor, demonstrating significant reductions in inflammatory cardiovascular biomarkers (hsCRP 86%, IL-6 58%, fibrinogen 30%) and brain penetration. The company is advancing toward Phase 2a trials in cardiovascular disease and expanding into ophthalmology for diabetic macular edema, positioning the compound as a multi-indication anti-inflammatory therapy.
United Therapeutics received FDA Regenerative Medicine Advanced Therapy designation for Miroliver ELAP, a bioengineered external liver assist device combining a decellularized porcine scaffold seeded with human endothelial and hepatic cells. This designation accelerates development of a bridge therapy for acute liver failure, where 30% of patients currently die due to organ shortage despite potential for spontaneous recovery.
Exosomes in the gut lumen change composition with age, with those from older mice directly impairing barrier integrity and insulin sensitivity in younger recipients, while young exosomes reverse these effects in older mice. This identifies a specific molecular mechanism linking intestinal barrier dysfunction to metabolic aging.
