Biolojic Design Ltd. has earned an additional milestone payment from its collaboration partner, Teva Pharmaceutical Industries Ltd., for TEV‘325 (TEV-56308, formerly BD-9), a multibody targeting IL-13 and thymic stromal lymphopoietin (TSLP) for autoimmune disease
Gilead Sciences Inc. said after U.S. market close March 23 that it will acquire privately held Ouro Medicines LLC and its autoimmune BCMA/CD3 bispecific T-cell engager, gamgertamig, in a deal valued at $2.17 billion.
For a company founded only four years ago, Quotient Therapeutics Inc. entered its third major deal, this time with Merck & Co. Inc. to find novel drug targets for inflammatory bowel disease (IBD) using its somatic genomics platform technology.
Shanghai Qilu Pharmaceutical Research and Development Centre Ltd. has prepared and tested molecular glue degraders comprising E3 ubiquitin-protein ligases acting as proto-oncogene Vav (VAV1) degradation inducers reported to be useful for the treatment of inflammation and autoimmune diseases.
A new way of understanding Alzheimer’s disease, based on biological inflection points that mark decisive moments in the progression of the disorder, could change how new drugs are developed to achieve more effective therapies. This new perspective could rethink strategies that depend not so much on the target itself, but on the precise moment at which it is addressed.
Work at Boehringer Ingelheim Pharma GmbH & Co. KG has led to the synthesis of pyrazolo[5,1-f][1,2,4]triazin-4-ones acting as NADPH oxidase 4 (NOX4) inhibitors. As such, they are described as potentially useful for the treatment of liver disease, portal hypertension, viral infection, cancer, interstitial lung diseases, retinopathy, inflammation and fibrosis.
Pulmonary fibrosis (PF) is a fatal lung disease characterized by excessive deposition of extracellular matrix proteins in the lung interstitium due to excessive fibroblast activation, which leads to tissue scarring and potential respiratory failure. Chinese researchers have published results of their investigations into circular RNAs and the pathogenesis of PF.
A new way of understanding Alzheimer’s disease, based on biological inflection points that mark decisive moments in the progression of the disorder, could change how new drugs are developed to achieve more effective therapies. This new perspective could rethink strategies that depend not so much on the target itself, but on the precise moment at which it is addressed.
Neurodegenerative disease and cognitive decline cannot be explained by a single process. Beta-amyloid plaques, hyperphosphorylated tau, alpha-synuclein, activated microglia and astrocytes, altered receptors such as TREM2, mitochondrial dysfunction, epigenetic changes and cerebrovascular alterations all seem to contribute to the development of dementia in Alzheimer’s disease (AD). While scientists attempt to address each of these elements, prevention is growing as a primary goal.
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