Our Research
Selexys has completed research on its anti-adhesion technologies and is in preclinical development of antibody-based therapeutics for treating inflammation. If you would like to learn more about our products or discuss partnering or license opportunities, please contact us.
Product Pipeline
Our product development is supported by discoveries made by our co-founding scientists and supported by over $25 million in grants and awards over the past 12 years from the National Heart Lung and Blood Institute at NIH. But this is only part of the story. The NIH and the Pharmaceutical Industry have also spent decades and hundreds of millions in research and development to understand inflammation and the roll played by P-selectin mediated cell adhesion. This body of work is well documented in over 5,000 publications (PubMed: P-selectin). For Selexys, this history and the continued robust academic and industrial publication record in this area represent a strong testament to the potential for treating inflammatory and thrombotic disease by blocking P-selectin function. You can learn more about this by reading About the Company or contact us.
Selexys has a pipeline of drug candidates that block P-selectin function and prevent white blood cells from initiating inflammation. These programs are designed to address major areas of inflammatory and thrombotic diseases. Each program has a unique application to meet the needs of a specific inflammatory condition. These initial applications can be expanded into other large inflammatory and thrombotic indications as we successfully demonstrate the efficacy or our antibodies.
Product Pipeline
Humanized antibodies to PSGL-1
Selexys has engineering humanized forms of our function blocking mouse monoclonal antibodies to PSGL-1. These antibodies are being developed for the treatment of inflammatory bowel diseases such as Crohn's.
Humanized antibodies to P-selectin
Selexys has engineered humanized antibodies to P-selectin that are in preclinical evaluation. These antibodies are being developed for treatment of crisis precipitated by vasoocclusion in sickle cell disease as a lead indication. Sickle cell is an orphan drug indication with major unmet medical needs.
Small molecule P-selectin inhibitors
Glysopep (GSP) is a small molecule inhibitor of P-selectin based on the N-terminal domain of PSGL-1. GSP has been shown to block and reverse white blood cell adhesion in vitro and in vivo. Selexys is developing GSP for acute inflammatory indications where a modifiable half-life would be useful. GSP also has application as a drug delivery and imaging agent. This technology is available for licensing or co-development.
PSGL-1
Selexys has rights to key patents for the use of PSGL-1 to treat ischemia reperfusion and other inflammatory disorders. This technology is available for licensing or co-development.
Soluble P-selectin
Soluble P-selectin has pro-coagulant properties that have application in thrombotic disorders that lead to excessive bleeding in surgical settings and for treatment of hemophilia. The company has composition and use patents for soluble P-selectin. This technology is available for licensing or co-development opportunities.
How Selexys Drugs Block White Blood Cell Adhesion
Fig. 1 - Resting State
P-selectin is the therapeutic target for our antibody-based drugs. As shown in Fig. 1, P-selectin is stored in vesicles within endothelial cells that line blood vessels. It is also present within circulating blood platelets, which participate in both blood clotting and inflammation. In a normal non-inflammatory resting state P-selectin is not accessible to PSGL-1 and white blood cells circulate freely in the blood.
Fig. 2 - Inflammatory State
When endothelial cells lining the blood vessel become activated in inflammatory disease, P-selectin is moved to the endothelial cell surface as shown in Fig. 2. This makes P-selectin accessible to its receptor PSGL-1. As white blood cells flow past P-selectin, their PSGL-1 molecules bind to P-selectin on the endothelial cells. This causes the white blood cells to begin adhering to the blood vessel surface. In some diseases platelets are also activated and P-selectin is moved to the platelet surface where white blood cells can also bind. Thus, white blood cells can adhere to both platelets and endothelial cells on blood vessel surfaces. Importantly, this binding is very specific to the site of inflammation. This is the FIRST cellular event in the inflammatory cascade. White blood cells then migrate into the surrounding matrix through a process called extravasation. This sets into motion other complex inflammatory mediators that ultimately destroy tissues and organs. These downstream events are complex and involve numerous parallel signaling pathways that are difficult to modulate with a single drug. The precise targeting of P-selectin allows Selexys to mediate the initial cellular event in inflammation and diminish or prevent downstream signaling, a significant competitive advantage for our anti-adhesion approach.
 Fig. 3 - Antibody to P-selectin |
 Fig. 4 - Antibody to PSGL-1 |
Blocking P-selectin function is intended to prevent or reduce tissue injury in inflammatory diseases. When a Selexys antibody to P-selectin is injected intravenously it quickly binds to P-selectin (Fig. 3). This prevents PSGL-1 from binding to P-selectin and the white blood cells do not adhere to the blood vessel wall and cannot migrate into the tissue to cause damage. Inflammation can be prevented or reduced. Likewise, administration of a Selexys antibody to PSGL-1 would have a similar effect by binding to and occupying PSGL-1 and preventing it from binding to P-selectin (Fig. 4). Each of these preclinical products have distinct applications which can impact inflammatory and thrombotic diseases.