Precision medicine startup Solu Therapeutics has raised $31 million in an oversubscribed seed round to advance a therapeutic candidate based on technology that identifies cell surface, tumor-associated targets that antibodies alone fail to latch onto. The company was founded by venture capital firm Longwood Fund and has high hopes for its cytotoxicity targeting chimera platform. “[It] has the potential to unlock new tumor-associated antigens and develop molecules that deplete pathogenic immune cells and extend the half-life of small-molecule antagonists and agonists,” CEO and co-founder of Solu, David Donabedian, told BioWorld.
Lung adenocarcinoma (LUAD) represents 35% to 40% of all lung cancers, making it the most common non-small-cell lung cancer in the U.S. Despite continual treatment advances, lung cancer remains the leading cause of cancer-related mortality worldwide. Accordingly, there is an ongoing urgent need to identify targets and associated therapeutics.
Giardia lamblia is a protozoan pathogen that colonizes the gastrointestinal tract and results in giardiasis. Recently, researchers from the University of California San Diego aimed to identify potent proteasome inhibitors that selectively target G. lamblia, as potential antigiardiasis therapeutics with low toxicity.
Protein tyrosine phosphatase nonreceptor type 22 (PTPN22) has been previously linked to several chronic inflammatory disorders and it has been established that PTPN22 regulates T-cell receptor signaling. Recent studies have also shown that PTPN22 plays a role in thrombosis, suggesting its potential use as target for cardiovascular diseases. In the current study, researchers from Southern Medical University and affiliated organizations aimed to assess the role of PTPN22 in the pathogenesis of calcific aortic valve disease (CAVD).
Researchers from the University of Texas and University of Tennessee set out to determine if the long noncoding RNA (lncRNA) MALAT1 (metastasis associated lung adenocarcinoma transcript 1), which is known to regulate a subset of genes involved in synaptic plasticity, cognitive function and memory, plays an important role in Alzheimer’s disease (AD) pathology.
Duchenne muscular dystrophy (DMD) is an X-linked genetic disorder affecting roughly 1 in 3,500 males. DMD is due to mutations in the dystrophin gene, which encodes for an exceptionally large 427 kD protein. DMD is characterized by repeated degeneration and regeneration of muscle fibers, but ultimately replacement of muscle with fibrotic and adipose tissue. Despite advances in gene therapy and improvements in quality of life, most patients still die by 30 years of age due to cardiopulmonary failure.
Osteosarcomas (OS) are the most common malignant bone tumor. The disease originates within the fastest growing areas of the long bones of children and young adults, where the histologic hallmark of OS is malignant bone formation (osteoid). Improvements in treatments have proven difficult to date with metastatic OS remaining a bleak prognosis routinely leading to lung metastases to ultimately cause death.
Identification of the mechanisms of innate immune sensors is fundamental to the understanding of health and disease. The pattern recognition receptor (PRR) subfamily of nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) work by recognizing either pathogen-associated molecular patterns (PAMPs), endogenous damage-associated molecular patterns (DAMPs) or associated molecular...
Chronic kidney disease (CKD) is the 10th leading cause of death in the United States because of the increased risk for cardiovascular mortality. The major functional cell type of the kidney, tubular epithelial cells (TECs), possess a limited ability to regenerate tissues. Infections can cause proximal G2/M cell cycle arrest, senescence and paracrine secretion of the profibrotic cytokines transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF), which stimulate extracellular matrix production ultimately leading to loss of the epithelial phenotype in TECs. Identification of targets controlling the G2/M cell cycle arrest in TECs may enable the development of therapeutics that can prevent CKD progression.