Antimicrobial resistance (AMR) is predicted to cause 10 million deaths every year by 2050. Since its identification more than 50 years ago, pleuromutilin has served as a scaffold for the development of new types of antibiotics.
Triple-negative breast cancer (TNBC) remains one of the most aggressive and challenging subtypes to treat due to the lack of targeted therapies. Therefore, identifying molecular drivers of TNBC progression and metastasis is crucial for the development of new treatment strategies.
The nuclear protein charged amino acid-rich leucine zipper 1 (Crlz-1) has been shown to play a role in the rapid proliferative stages of B-cell development, being targeted by the canonical Wnt/β-catenin signaling pathway.
In8bio Inc. has unveiled INB-600, its next-generation γδ T-cell-based T-cell engager (TCE) platform designed to address one of the shortcomings of current existing γδ TCEs, specifically insufficient numbers of γδ T cell effector cells to deliver clinical impact. The platform could have applications across oncology as well as autoimmune diseases.
Tyrosine kinase 2 (TYK2), expressed in astrocytes and microglia, is involved in the activation of pathways triggered by proinflammatory cytokines, such as IL-23, IL-12 and type I interferons (IFNs), within the central nervous system (CNS). Dysregulated activation of astrocytes and microglia may contribute to the neuroinflammation associated with progressive forms of multiple sclerosis (MS).
Laekna Inc. has obtained FDA clearance of its IND application for LAE-120, an allosteric and highly potent USP1 inhibitor, for the treatment of advanced solid tumors.
Although radiotherapy is widely used in cancer treatment, its effects on the tumor microenvironment (TME) can be immunosuppressive as well as immunostimulatory. Fibroblast activation protein (FAP) is expressed by cancer-associated fibroblasts (CAFs) in several tumors, with higher levels linked to a weakened immune response to immune checkpoint blockade in patients.
Researchers at the University of California San Diego have uncovered a key mechanism underlying the treatment resistance of melanoma with the BRAF V600E mutation through pathways involved in focal adhesion and extracellular matrix (ECM) remodeling. These two processes remodel the tumor cell environment in melanoma through the RAF/MEK cell signaling pathway. However, the combined use of FAK inhibitors with a RAF-MEK clamp overcame this resistance.
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