Increased expression and elevated levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 play a role in impaired cardiac function. These MMPs make for essential targets in the treatment of heart failure, specifically heart failure with preserved ejection fraction (HFpEF).
Researchers from Aligos Therapeutics Inc. have described the discovery of novel liver-targeted oral PD-L1 small-molecule inhibitors for the treatment of chronic hepatitis B and liver cancers.
Ono Pharmaceutical Co. Ltd. has entered a worldwide drug discovery collaboration agreement with Captor Therapeutics SA to develop novel small-molecule degrader drugs against a currently undrugged target of interest in neurodegenerative diseases.
Calcium/calmodulin-dependent protein kinase II (CaMKII) is involved in the regulation of calcium and its hyperactivation can lead to cardiac issues, particularly with rhythm and contraction.
CD39 has an essential role in converting extracellular adenosine triphosphate (ATP; pro-inflammatory) into adenosine monophosphate (AMP; anti-inflammatory). Preventing the action of CD39 in the tumor microenvironment would increase levels of ATP, causing myeloid cell activation and improvement of tumor control.
Stimulating the brain via implanted electrodes is used to treat both movement disorders such as Parkinson’s disease, and some psychiatric conditions such as obsessive compulsive disorder. But researchers are also working on ways to make such implanted electrodes listen instead of talk – and translate neuronal signals for people that have lost the ability speak, or the ability to move. At the Neurophysiology: Decoding and Neural Processing II session of the 2022 Annual Meeting of the Society for Neuroscience in San Diego, researchers from the Wyss Center for Bio and Neuroengineering (Switzerland) presented a device implanted in the brain that allowed restoration of movement and speech.
Investigators working at University of Texas Health Science Center, Houston, have discovered that the ubiquitin ligase UBR2 is up-regulated and sufficient for targeting the myosin heavy chain protein for the degradation characteristic of cancer cachexia. UBR2 knockout or pharmacological inhibition could prevent cachexia in mice. Confirmatory observations were noted in cancer cachexia patient-derived tissues.
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