This study explores the development and efficacy of small-molecule inhibitors that target the oligomerization of the Stimulator of Interferon Genes (STING) protein. By preventing STING oligomerization, these inhibitors aim to modulate the immune response associated with STING activation, offering potential therapeutic avenues for conditions characterized by excessive inflammation.
The small-molecule inhibitors effectively prevented STING oligomerization, leading to a significant reduction in type I interferon production and pro-inflammatory cytokines. In the Trex1 D18N mouse model, treatment with these inhibitors ameliorated systemic inflammation and improved survival rates, highlighting their therapeutic potential in STING-mediated autoimmune diseases.
The study utilized a Trex1 D18N Knockin mouse model developed by genOway, in which the endogenous Trex1 gene carries the D18N point mutation. This mutation leads to chronic activation of the STING pathway, resulting in a lupus-like autoimmune phenotype, making it a suitable model for evaluating STING-targeted therapies.
Autoimmunity, STING pathway, Inflammation, Small-molecule inhibitors, Lupus-like disease
Knockin mouse model, Trex1 D18N mutation, STING oligomerization inhibition, Point mutation, Autoimmune disease modeling
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
