Researchers from Totus Medicines Inc. presented preclinical data for the potent and selective covalent inhibitor of phosphoinositide 3-kinase α (PI3Kα), TOS-358, which is being developed for the treatment of cancer.
Researchers from Black Diamond Therapeutics Inc. presented the discovery and preclinical characterization of a novel brain-penetrant BRAF class I/II/III mutation inhibitor, BDTX-4933.
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.
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.
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.
Novartis AG has synthesized heteroaryl aminopropanol derivatives acting as leukotriene A4 hydrolase (LTA4H; LTA4) inhibitors reported to be useful for the treatment of cancer, chronic obstructive pulmonary disease (COPD), psoriasis, sepsis, periodontal and autoimmune disease, cardiovascular and inflammatory disorders, among others.
Immune checkpoint inhibitor (ICI) treatment reduced levels of estrogen and important heart-protective proteins, researchers reported in the Nov. 2, 2022, online edition of Science Translational Medicine. Hormone therapies could target this endocrine-cardiac-immune pathway and mitigate myocarditis risk without affecting treatment responses.
X-chromosome inactivation (XCI) is not unique to female cells and may confer some survival advantage to male cancer cells, according to scientists at the Dana-Farber Cancer Institute at Harvard. The noncoding RNA XIST (acronym for X-inactive specific transcript), which in female mammals (of genotype XX) inactivates one of the X chromosomes, preventing the overexpression of the genes of the repeated chromosome from early stages of embryonic development, also acts somatically in some male cancers, compensating for the loss of the entire chromosome.
“We found that a small percentage of male cancers are expressing XIST, which normally is expressed in female cancers. And the percentage of male cancers that express XIST is variable depending on the cancer type,” Srinivas Viswanathan, researcher in the Department of Medical Oncology at the Dana-Farber Cancer Institute at Harvard and assistant professor of Medicine at Harvard Medical School, told BioWorld.
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