SynthoPlate
why mimic platelets to control bleeding?
Platelets are cells in the blood that constantly monitor for injury. When they identify an area of injury, they bind to the injury site through interaction of their surface receptors with injury site-specific proteins, like collagen and von Willebrand Factor. After adhesion to the injury site, platelets activate and change their shape and expression of other surface receptors, like GPIIb-IIIa. Upon activation, platelets become cross-linked through binding of blood protein fibrinogen. As the platelets pile up and plug the injury site, stabilization of the clot is achieved through the formation of a fibrin mesh.
Inability to clot and excess bleeding can happen when platelets are low in number (thrombocytopenia) or defective in function. Annually, over 2 million units of donor platelets are transfused in the clinic to treat bleeding in the United States. However, donor platelets suffer from the following limitations leading to 20% of collected platelets being discarded:
Limited availability
Short supply due to dependence on donors
Blood banking systems not available at all hospitals
Short shelf-life (5-7 days after donation)
Special storage requirements
Donor-to-recipient type-matching and risk of transplant rejection
Risk of bacterial infection
Introducing our synthetic platelet technology
To address the shortcomings of donor platelet products, Haima is developing SynthoPlate, a platelet inspired, IV injectable drug that stops bleeding in patients with low platelet counts or platelet dysfunction.
SynthoPlate is an IV-injectable hemostatic agent that mimics and amplifies platelet’s adhesion and aggregation functions. SynthoPlate is fully synthetic, available for large scale manufacture, easily portable, and requires no need for blood type matching.
Uses for SynthoPlate
Research Publications
A factor VIII-derived peptide enables von Willebrand factor (VWF)-binding of artificial platelet nanoconstructs without interfering with VWF-adhesion of natural platelets. Nanoscale 2014.
Peptide-decorated liposomes promote arrest and aggregation of activated platelets under flow on vascular injury relevant protein surfaces in vitro. Biomacromolecules 2012.