Currently, most patients with urinary tract infections (UTIs) require long-term antibiotic treatment, which poses risks of resistance development and alters the patients' microbiota. Therefore, vaccines that raise safe, effective and long-lasting immune responses across populations for UTI prevention constitute a critical medical need. However, developing such vaccination strategies remains challenging because the responses need to be specific to a broad range of UTI-causing bacteria and include both blood and mucosal responses in the urogenital tract.

CD40-targeting therapies have been proposed as an interesting alternative to overcome resistance to immune checkpoint inhibitors. In particular, bispecific CD40 antibodies can target CD40 more efficiently and safely than monospecific therapies. In a recent publication, researchers at Alligator Bioscience AB and collaborators demonstrate that bispecific antibodies targeting CD40 and tumor-associated antigens (TAA) can enhance priming of tumor-specific T cells in vivo.

Scientists in Edinburgh are planning a clinical trial of licensed drugs in the prevention of chronic kidney disease (CKD) following acute kidney injury (AKI), after uncovering a new mechanism linking the pathology of one with the other. It has only recently been recognized that AKI is linked to CKD and cardiovascular disease, and to date the molecular pathways that control the transition are not well-mapped. As a result, there are no therapies for preventing acute injury progressing to chronic disease.

The California Institute for Regenerative Medicine (CIRM) has awarded Calidi Biotherapeutics Inc. a US$3.1 million grant to support continued development of the company's Supernova-1 (SNV-1) preclinical program through IND application. The grant was awarded to Calidi to support IND-enabling studies, finalize manufacturing and the completion of Calidi's IND application for the SNV-1 program.

Programmable genome insertion of long DNA sequences, useful for both gene therapy and basic research, commonly relies on cellular responses to double-strand breaks (DSBs) using programmable nucleases, such as CRISPR-Cas9, for induction of repair pathways such as non-homologous end joining (NHEJ). To overcome the current limitations of gene integration approaches, scientists from the Massachusetts Institute of Technology and colleagues developed a new strategy based on advances in programmable CRISPR-based gene editing, such as prime editing, together with the application of precise site-specific integrases.