Transthera Sciences (Nanjing) Inc. has announced the initiation of IND-enabling studies for TT-02332, a potent, selective and highly CNS-penetrating NLRP3 inflammasome inhibitor.
1910 Genetics Inc. has divulged non-receptor tyrosine-protein kinase TYK2 (JH2 domain) inhibitors reported to be useful for the treatment of allergy, cancer, inflammation, autoimmune disease, metabolic diseases, endocrine and neurological disorders.
Novel pyrimidinyl and triazinyl sulfonamide derivatives acting as uracil nucleotide/cysteinyl leukotriene receptor (GPR17; P2Y-like) antagonists have been reported in an F. Hoffmann-La Roche Ltd. and Hoffmann-La Roche Inc. patent.
A Nanjing Suzhong Pharmaceutical Research Co. Ltd. and Suzhong Pharmaceutical Group Co. Ltd. patent describes phenyl-substituted dihydronaphthyridine compounds acting as mineralocorticoid receptor (MR) antagonists potentially useful for the treatment of aldosteronism, cirrhosis, diabetic nephropathy, heart failure, hypertension, myocardial infarction, renal failure and stroke.
Rpxds Co. Ltd. has identified new α-ketoglutarate-dependent dioxygenase FTO inhibitors acting as serum LDL-, cholesterol- and triglyceride-lowering agents and thus reported to be useful for the treatment of obesity, Alzheimer’s disease and obesity-related disorders.
Immunoglobulin G (IgG), an antibody that participates in the response to infection, could have a specific role in metabolism. During aging, it accumulates in certain tissues inducing metabolic dysfunction and fibrosis of fat tissue. This effect could be prevented through an intracellular receptor that contributes to the delivery of IgG. A team of researchers from Columbia University and Peking University (PKU) demonstrated that reducing excess IgG improved the metabolic health of aged mice and increased their life expectancy.
Pompe disease is a disorder caused by deficiency of the lysosomal acid α-glucosidase (GAA) enzyme, which leads to the accumulation of glycogen within the lysosomes, overall in skeletal and cardiac muscle.
Pompe disease is caused by a deficiency in the lysosomal enzyme acid α-glucosidase (GAA) that leads to accumulation of glycogen in the lysosomes, mainly seen in skeletal and cardiac muscles. Researchers from Duke University have developed a new murine model of Pompe disease, which recapitulates human infantile-onset disease. This model harbors the c.1826dupA mutation in the murine Gaa gene, which resembles the human GAA c.1826dupA (p.Y609*) mutation seen in infantile-onset Pompe disease.
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