The boronic acid transition state inhibitors S-02030 and MB-076 were strategically designed to be active against cephalosporinases and carbapenemases, especially KPC (Klebsiella pneumoniae carbapenemase).
Researchers from Hebei Normal University and affiliated organizations presented the discovery and preclinical characterization of a novel B lymphoma Mo-MLV insertion region 1 (Bmi-1) expression inhibitor, APD-94, designed as an agent that could potentially overcome drug resistance in patients with colorectal cancer.
The Gates Foundation, Novo Nordisk Foundation and Wellcome have announced the launch of the Gram-Negative Antibiotic Discovery Innovator (Gr-ADI), a $50 million investment that will focus on combatting antimicrobial resistance (AMR) caused by a specific range of bacteria that are among the leading contributors to AMR-associated deaths.
Understanding the mechanisms of resistance to cancer treatments is necessary to find effective therapies at different stages of the disease. Scientists at UT Southwestern Medical Center studied the most frequent mutation in pancreatic ductal adenocarcinoma (PDAC), identified an escape route to a therapy in clinical trials, blocked it with another experimental compound and reduced tumors in mice.
In a recently published study, researchers based at Université Paris-Saclay identified OXA-1186, a novel carbapenemase related to the previously known OXA-198 enzyme, in a clinical isolate of Citrobacter freundii. This discovery underscores the ongoing challenge of antibiotic resistance in bacterial pathogens.
Cancer therapies can eliminate specific tumors based on their genetic content. However, some cancer cells survive. How do they do it? Part of the answer lies in extrachromosomal DNA (ecDNA), an ace up the tumors’ sleeve to adapt and evade attack. Three simultaneous studies in the journal Nature lay all the cards on the table, revealing ecDNAs’ content, their origin, their inheritance, their influence in cancer, and a way to combat them.
Cancer therapies can eliminate specific tumors based on their genetic content. However, some cancer cells survive. How do they do it? Part of the answer lies in extrachromosomal DNA (ecDNA), an ace up the tumors’ sleeve to adapt and evade attack. Three simultaneous studies in the journal Nature lay all the cards on the table, revealing ecDNAs’ content, their origin, their inheritance, their influence in cancer, and a way to combat them.
Cancer therapies can eliminate specific tumors based on their genetic content. However, some cancer cells survive. How do they do it? Part of the answer lies in extrachromosomal DNA (ecDNA), an ace up the tumors’ sleeve to adapt and evade attack. Three simultaneous studies in the journal Nature lay all the cards on the table, revealing ecDNAs’ content, their origin, their inheritance, their influence in cancer, and a way to combat them.
Genome & Co. Ltd. has reported preclinical findings of its anti-CNTN4 antibody, GENA-104A16, and anti-APP antibody, 5A7 — stressing the contactin-4 (CNTN4) and amyloid precursor protein (APP) axis as a potential target for immuno-oncology. In the latest murine experiments, investigators led by Genome executives and researchers of Gwangju Institute of Science and Technology (GIST) found that blocking the interaction between CNTN4 and APP promoted cancer-destroying responses in mice, suggesting the pathway as a target for immunotherapy.
The inappropriate use of antibiotics over long periods of time has led to increasing bacterial drug resistance. Quinolones are among the most effective and widely used antibacterials, and there are ongoing efforts to develop new quinolone-based drugs able to overcome emerging bacterial drug resistance.
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