Pharmaceuticals & Biologics
Yale researchers have identified that the acute inflammatory response to biomaterials can be limited by inhibition of inflammasome-related pathways.
Mice that overexpress TGF-β have identified several novel targets (including β1 integrin) for therapeutic interventions in fibrotic lung diseases. Semaphorin 7A inhibition is also effective as a therapeutic treatment for fibrotic disease.
Yale researchers created an inactivated version of the thyphoid toxin, which can serve as the basis for the development of novel second-generation vaccines to treat typhoid fever.
GFB-204 is a novel compound that binds PDGF and VEGF and prevents binding to their respective receptors, and subsequently suppresses downstream signaling pathways.
Yale investigators have developed a new synthetic platelet to treat hemorrhage. The synthetic platelet resembles the shape of an activated platelet (star burst) and is made from FDA-approved materials, consisting of a nanosphere core and polyethylene glycol (PEG) arms. Our synthetic platelet is capable of forming a barrier to reduce membrane permeability and enhance the sealing on a disrupted blood vessel wall, which is extremely beneficial to promote synthetic platelet aggregation at the site of injury.
The recent discovery of a role for SEMA 7A in fibrosis using mouse models provides a new therapeutic target for the treatment of fibrosis in lung disease and may be suitable for the treatment of other fibrotic diseases.
Researchers at Yale University have identified a pharmacological mechanism whereby proliferation of oligodendrocytes can be stimulated by activation of ATP-dependent potassium channels (KATP channel) in the plasma membranes of oligodendrocytes. Small molecular weight candidate therapeutic compounds (e.g., Diazoxide) have been identified which activate the KATP channel and which have been shown not only to promote proliferation of oligodendrocyte precursor cells in culture but also to increase myelination in rat brain slices in vitro and to prevent hypomyelination and ventriculomegaly in vivo in newborn mice subjected to chronic sub-lethal hypoxia. One of the KATP channel activators shown to mediate the effect on myelination has also been used therapeutically in infants to treat hyperinsulinemic hypoglycemia.