SCIENCE
Resolvin E1 is a BLT1 agonist that promotes immune homeostasis
A novel approach targeting the BLT1 receptor
Biased Agonism of RvE1 and LTB4 at BLT1
- Role of BLT1 in Human Health: BLT1, a key G protein-coupled receptor (GPCR) involved in regulating innate and adaptive immune responses, has two naturally-occurring ligands, RvE1 and LTB4. that have distinct biological outcomes, attributed to "biased agonism", a feature of many GPCRs. 1-3
- LTB4 at BLT1: LTB4 activation of BLT1 plays a critical role in triggering early inflammatory responses for host defense. However, when this pathway remains unchecked, it can contribute to the progression of chronic diseases and cancer. This has motivated development of anti-inflammatory drugs focused on inhibiting LTB4 synthesis or blocking the BLT1 receptor. However, these efforts have had limited success, in part due to the essential and complex role of BLT1 in immune regulation. 4-8
- RvE1 at BLT1: RvE1 promotes immune homeostasis by stimulating clearance of cellular debris and microbes from inflamed tissue, a process called phagocytosis. RvE1 acting through BLT1 also promotes tissue repair and competes with LTB4 at BLT1 to reduce its pro-inflammatory effects. This multi-faceted mechanism offers unique therapeutic potential in chronic diseases like IBD and cancer. 9-21
Inflammatory bowel disease
TP-317 has shown promising results in preclinical models of IBD, demonstrating multiple beneficial effects on intestinal health and immune function. This pro-resolution, barrier-protective mechanism distinguishes TP-317 from approved IBD therapies.
TP-317 Mechanism of Action in IBD
Promotes barrier integrity, a critical goal in IBD management to limit entry of pathogenic substances from the gut that exacerbate inflammation 10-13
Induces phagocytosis (clearance) of immune cell debris and microbes from inflamed tissue that perpetuate chronic inflammation if left uncleared 14
Downregulates inflammatory cytokines that are key drivers of the inflammatory cascade in IBD 9
Limits migration of immune cells from the microvasculature into the intestinal mucosa that drive inflammation 15-19
Solid tumor cancers
Harnessing the body’s natural defense to fight cancer must meet two pre-requisites. First, T-cells can function as cytotoxic T-cells with the ability to detect and kill tumor cells only when primed with tumor antigens presented by innate immune cells. Second, tumors cells must present their antigens to enable detection by cytotoxic T-cells. These pre-requisites are currently not effectively addressed by approved therapies including immune checkpoint inhibitors.
TP-317 enhances anti-tumor immunity by stimulating macrophages and dendritic cells to clear tumor debris from the tumor environment and to utilize the tumor material ingested in this process to present tumor antigens to T-cells. TP-317 also enhances presentation of antigens by the tumor cells themselves. This multi-faceted mechanism turns “immune cold” tumors into “immune hot” tumors and distinguishes TP-317’s ability to augment anti-tumor immunity. 13, 20-24
TP-317 Mechanism of Action in Solid Tumors
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