Researchers have discovered that inhibition of RIP1 kinase blocks the progression of multiple sclerosis in an immune-induced demyelination mouse model (EAE) but not a chemically-induced one (CPZ). RIPA-56 (Focus Biomolecules Cat# 10-4611) blocked disease progression at a step of monocyte elevation downstream of T-cell activation and myelin-specific antibody generation but upstream of blood-brain barrier breakdown. This represents a previously unknown function of RIP1 kinase and offers a potential new therapeutic opportunity for treatment of immune system mediated demyelinating diseases such as multiple sclerosis.
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