Unmet Need: Necrotizing enterocolitis (NEC) is the acute onset of inflammation in the gut of babies, and is the leading cause of premature infant mortality from gastrointestinal disease. The mortality of NEC is over 30%, and those infants who do survive suffer significant deficiency due to the effects of a damaged intestine, as well as profound cognitive impairment, due to the recently discovered effects of gut inflammation on the developing brain. With no current treatment options available, there is an urgent need for the development of prevention and/or treatment strategies against NEC. Disclosed herein are novel compositions to activate aryl hydrocarbon receptor (AHR) as a strategy to attenuate NEC by limiting TLR4 signaling.
Technical Details: Researchers at Johns Hopkins University and the University of Pittsburgh have developed small molecule compounds to limit inflammatory signaling as a prevention/treatment strategy against NEC. Compound “C169” activates the aryl hydrocarbon receptor (AHR), which leads to decreased signaling from Toll-like receptor 4 (TLR4), the main driver of pathogenesis in NEC. As shown in mice and resected NEC tissue from premature infants, treatment with C169 leads to decreased TLR4 signaling in the gut. In addition, when administered to pregnant mice, C169 prevented development of NEC in premature pups.
Value Proposition:
· Novel small molecule agonist to treat NEC
· Capable of administration to the mother, thus achieving mother-to-fetal transmission as a NEC prevention strategy in the setting of premature labor.
· Broad application to other gastrointestinal inflammatory disorders
Looking for Partners to: Develop & commercialize the technology as a novel compound for the treatment and/or prevention of NEC.
Stage of Development: Pre-Clinical
Data Availability: In vivo mouse data
Inventors: David Hackam, Chhinder P. Sodhi, Peng Lu, Peter Wipf, David Kornfilt
Patent Status: Pending
