Chinese researchers from Huazhong University of Science and Technology have developed a novel carbonic anhydrase IX (CAIX)-targeting radiotracer, [68Ga]NXK-44, for the imaging of hypoxic tumors and renal cell carcinoma (RCC).

Researchers from Grey Wolf Therapeutics Ltd. presented the preclinical characterization of GRWD-0715, a selective ERAP1 inhibitor developed as a disease-modifying therapeutic approach aimed at preventing CD8+ T-cell activation and the subsequent tissue inflammation and damage associated with autoimmune conditions.

ASC-47 is a thyroid hormone receptor β agonist, muscle-preserving weight loss compound for treating obesity developed by Ascletis Pharma Inc. ASC-47 demonstrated a half-life of 26 and 40 days in healthy subjects and in patients with obesity, respectively.

Agonists of immune checkpoint modulators for treating autoimmune and inflammatory disorders have shown high potential in immunotherapy. P-selectin glycoprotein ligand 1 (PSGL-1) is known to exert immune checkpoint regulator functions in T cells aside from its classic role as an adhesion molecule involved in leukocyte trafficking.

Researchers at Washington University reported the preclinical validation of [18F]FQ-NeuroROS, a redox-sensitive reporter probe for imaging neuroinflammation in preclinical models of multiple sclerosis (MS). MS is a chronic autoimmune disorder of the central nervous system (CNS), characterized by inflammatory cell infiltration, demyelination and axonal damage.

A healthy life for a healthy heart is a popular saying. However, even when following good habits, heart health can be already compromised from the very earliest stages of development. Maternal cells reach the embryo through the placenta contributing to its normal formation. So, just as the mother helps form a functional heart, she can also induce a condition that may not appear until adulthood.

Therapies based on glucagon-like peptide 1 (GLP-1) are the most effective for treating obesity to date, but their efficacy and tolerability are limited by gastrointestinal side effects and compensatory reduction of energy expenditure.

NKG2A is an inhibitory immune checkpoint receptor expressed on cytotoxic T cells and natural killer (NK) cells. Its upregulation in the tumor microenvironment (TME) contributes to the functional exhaustion of T cells, enabling tumor cells to evade immune surveillance. Therapeutic targeting of NKG2A represents a promising strategy to restore T-cell activity and enhance antitumor immunity.

Synthetic mitochondrial protonophores uncouple ATP production, increasing tricarboxylic acid (TCA) cycle activity and fat oxidation to meet energy demands. This approach promotes weight loss and may also enhance glycemic control and lipid metabolism.