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.
OCR5570 is a novel combination therapy that prevents chemotherapy-induced peripheral neuropathy (CIPN) through its co-administration or co-formulation with the patients chemotherapeutic treatment while maintaining the anti-cancer ability of the chemotherapy. OCR5570 is based on a newly identified molecular cascade that explains taxane induced peripheral neuropathy. OCR5570 interferes with these pathological cascades and ultimately results in the prevention of CIPN. This invention is a novel use of known drugs that have been shown to exhibit low toxicity, especially in the context of oncology, and have been approved for commercial use for chronic administration. This invention is the first pharmacologic agent that offers the ability to prevent CIPN.
Dr. Arnsten has discovered in animal studies that exposure to uncontrollable stress impairs prefrontal cortical function via activation of protein kinase C, and that administration of chelerythrine or a chelerythrine analog in accordance with the invention inhibits harmful protein kinase C activation.
Yale researchers have discovered a novel method of stimulating arterial collateral growth by simultaneous activation of both the Raf1/ERK and PI3K/Akt signaling pathway, a result not typically seen in adult cells, mimicking embryonic arteriogenesis. Specifically, ERK activation is achieved by introducing RAF1 mutant resistant to inhibition by PI3K/Akt signaling. Representative microCT images show increased artery development after treatment with GS4898 (an ERK activator), similar results are expected from ongoing mouse experiments with simultaneous activation of both Raf1/ERK and PI3K/Akt signaling.