At the recently concluded Digestive Disease Week, researchers from Kymera Therapeutics Inc. presented preclinical efficacy data on KT-579, a selective oral IRF5 degrader, in models of IBD.
The combination of impaired epithelial barrier function, mucosal inflammation and elevated oxidative stress is determinant for the pathogenesis of ulcerative colitis (UC). NF-E2-related factor 2 (NRF2) is an important transcription factor for modulating antioxidant defenses, inhibiting inflammatory pathways and regenerating the epithelial barrier. Montai Therapeutics Inc. has developed a potent and selective NRF2 agonist compound, MTAI-1025, for the management of UC using its proprietary CONECTA platform.
A major challenge in tissue engineering is not only achieving the correct cellular organization of an engineered tissue, but also expanding it to a clinically useful size after implantation. Researchers from the Wyss Institute at Harvard University have developed a synthetic biology platform that genetically programs tissues to grow large organ implants on demand. Building on a 2017 study suggesting engineered liver tissues could respond to regenerative signals released after injury, the researchers set out to identify and harness those cues.
“If we could figure out what those signals were, we could synthetically drive these factors locally in an implant to control its growth ourselves,” first author Amy Stoddard told BioWorld. Stoddard is a postdoctoral researcher at the Wyss Institute.
Researchers from Elpiscience Biopharmaceuticals Inc. hypothesized that dual targeting of the TL1A/DR3 and IL-23 signaling pathways with a single bispecific antibody would exert superior efficacy by reshaping the immune landscape in disorders such as inflammatory bowel disease (IBD). The company has developed a bispecific antibody targeting both TL1A/DR3 and IL-23p19 – ES-302 – for the treatment of IBD.
Mayinglong Pharmaceutical Group Co. Ltd. has reported new 5-HT4 receptor agonists that are potentially useful for the treatment of gastroesophageal reflux disease, constipation, irritable bowel syndrome, dyspepsia, delayed gastric emptying (gastroparesis), intestinal pseudo-obstruction, diabetic gastroparesis and postoperative Ileus.
Hubei Bio-Pharmaceutical Industrial Technological Institute Inc. has identified new molecular glue degrader compounds acting as proto-oncogene Vav (VAV1)/protein cereblon (CRBN) interaction inducers for degradation of VAV1 reported to be useful for the treatment of inflammatory bowel disease.
The development of glucagon-like peptide 1 receptor (GLP-1R) agonists, such as semaglutide and tirzepatide, has been a game changer in the clinical management of overweight and obesity, but there is interpersonal variability in efficacy of these medications for weight loss, as well as in the incidence of undesired side effects. Investigators from the 23andMe Research Institute have shed some light on how variations in the GLP-1R and GIP receptor (GIPR) genes impact their effectiveness and the occurrence of side effects.
The tumor necrosis factor (TNF)-α-induced protein 8-like 2 (TIPE2), predominantly expressed in bone marrow-derived cells or lymphoid tissues, is an essential regulator of immune homeostasis. TIPE2 acts as a key negative modulator of inflammatory signaling through the suppression of toll-like receptor (TLR) activity, with TIPE2-deficient mice exhibiting spontaneous systemic inflammation and premature death.
Proqr Therapeutics NV has highlighted the continued progression and expansion of its early-stage pipeline of RNA editing therapies, including programs in cholestatic diseases, Hurler syndrome, metabolic dysfunction-associated steatohepatitis and Rett syndrome.
In recent work, researchers from Shanghai Jiaotong University School of Medicine and Shanghai Colorectal Cancer Research Center reported that the transcription factor hematopoietically expressed homeobox (HHEX) promotes tumorigenesis in colitis-associated colorectal cancer. In a new paper, the team aimed to further characterize the biological function and potentially dysregulated mechanisms of HHEX during intestinal inflammation, which remained largely unexplored.