Researchers at Stanford and the University of Helsinki discovered that a human secretoglobin protein found in sweat gland cells acts as a novel host defense mechanism against Lyme disease.
Wound healing is a huge clinical problem. Problematic outcomes of skin wounds can range from under-healing (e.g., chronic/non-healing wounds) to over-healing (e.g., scarring).
Stanford scientists have developed a set of preclinical assays that are specifically designed to detect empathogenic effects of a drug that may indicate applications for that molecule in treating psychiatric diseases like PTSD.
The blood-brain barrier is a huge challenge when it comes to the delivery of therapeutic proteins to treat genetic diseases, injury, and neurodegenerative diseases.
Stanford inventors have developed a method of using CRISPR/Cas9 or similar gene editing technologies to genetically edit an individual's own myeloid cells for specific gene targets, which are critical to wound repair, and applying these edited cells in a hydrogel to promote ra
Researchers at Stanford University have identified a small molecule tryptase inhibitor for treatment of severe allergies. Mast cells are a part of the innate and adaptive immune response. Mast Cell activation results in release of granules containing tryptases.
Ion channel dysfunctions lead to a wide array of illnesses including epilepsy, cardiac arrhythmia and type II diabetes. However, the number of clinically approved drugs for restoring normal ion channel function is limited.
Stanford researchers in the laboratory of Dr. Daria Mochly-Rosen have developed novel small molecules for modulating ALDH2 (mitochondrial aldehyde dehydrogenase-2).
Stanford researchers developed a first-in-class small-molecule inhibitor of the CLC-2 ion channel for research and drug development. CLC-2 is part of the CLC family of chloride ion channels, which regulate the flux of chloride ions across cell membranes.
Disease indication - Cancer, specifically:
-highly mutated cancers, including the ~20% of cancer with BAF complex mutations
-combination therapy with ATR inhibitors