RNA interactome capture (RIC) was used by researchers from The Barcelona Institute of Science and Technology and their collaborators to examine the melanoma RNA-binding proteomes (RBPomes) of two melanoma cell lines: nontumoral melanocytic Mel-ST and metastatic SK-Mel-147.
Yangtze River Pharmaceutical Group and Shanghai Haiyan Pharmaceutical Technology have discovered substituted pyrazolo[1,5-a]pyrimidine-7-amine derivatives acting as cyclin-dependent kinase 9 (CDK9) inhibitors reported to be useful for the treatment of cancer.
Cold Spring Harbor Laboratory, Vichem Chemie Research and The Feinstein Institute for Medical Research have described dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A (DYRK1A) inhibitors reported to be useful for the treatment of cancer, Down syndrome, mild cognitive impairment and Alzheimer's disease.
Ryvu Therapeutics has outlined its plans over the next 2 years to advance one preclinical program into phase I trials, strengthen its synthetic lethality platform and accelerate its early pipeline. The company is currently leading multiple initiatives in the area of synthetic lethality.
In cancer, aberrant signaling pathways can evade therapy; activation of oncogenic PI3K and MAPK signaling has inspired researchers to develop molecularly targeted drugs, such as LP-182 (University of Michigan), a multitargeted kinase inhibitor that researchers have tested in vitro and in vivo for the treatment of myelofibrosis.
Working to overcome the short circulatory half-lives of platinum drugs in vivo, researchers at Shenzhen University and the City University of Hong Kong have explored the use of a platinum(IV) prodrug to bind erythrocytes.
Jemincare and its wholly owned subsidiary Shanghai Jemincare Pharmaceutical have signed an exclusive worldwide license agreement with Roche and Genentech for the development and commercialization of the androgen receptor degrader JMKX-002992.
Halia Therapeutics has presented serine/threonine-protein kinase Nek7 inhibitors reported to be useful for the treatment of cancer, asthma, obesity, type 2 diabetes, hepatitis, peritonitis, neurodegeneration and psoriasis, among others.
The development of cancer after p53 inactivation is determined by a series of genomic changes that occur in four steps. The loss of heterozygosity of TP53 (the gene encoding p53 in humans, named Trp53 in mice) is followed by an accumulation of deletions, genome doubling, and the emergence of gains and amplifications.
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