Scinnohub Pharmaceutical Co. Ltd. has patented new 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors reported to be useful for the treatment of autoimmune diseases, fibrosis, ulcerative colitis and more.
Acute respiratory distress syndrome (ARDS) is a multifactorial disease, the pathogenesis of which involves environmental exposure and genetic predisposition.
Netherton syndrome (NS) is caused by mutations in the serine protease inhibitor Kazal type 5 gene (SPINK5), which encodes lympho-epithelial Kazal-type-related inhibitor (LEKTI).
JJP Biologics Sp. z o.o. has received clearance from the EMA to conduct a first-in-human study of its CD89 antagonist, JJP-1212, for IgA-mediated autoimmune and fibrotic diseases. A phase I study in healthy participants will be conducted in Poland.
Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), also known as PIP2, is a cellular membrane phospholipid generated by phosphatidylinositol phosphorylation that regulates the functions of several proteins.
It is known that transient receptor potential cation channel subfamily V member 3 (TRPV3) is crucial for the modulation of skin homeostasis by regulation of Ca2+.
Bristol Myers Squibb Co. has exercised its option for an exclusive global license for PRX-019, a potential treatment of neurodegenerative diseases with an undisclosed target, under an agreement with Prothena Corp. plc.
C-C chemokine receptor type 6 (CCR6) regulates the migration and recruitment of T cells in inflammatory and immunological processes and, as part of the CCR6-CCL20 axis together with its exclusive binding molecule CCL20, plays a critical role in maintaining immunological homeostasis during inflammation and infection.
Genetic deletion of protease-activated receptor 4 (PAR4) in experimental models has been linked to improvement in neurological dysfunction and reduction of infarct volume in the context of stroke. Moreover, pretreatment with PAR4 antagonists in models of traumatic brain injury has shown protection against secondary tissue injury and thrombo-inflammatory activation.
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