Emulate Inc. has launched a new adeno-associated virus (AAV) transduction application for the Liver-Chip that enables gene therapy researchers to test the delivery efficiency and safety of AAV vectors in a validated, human-relevant model of the liver and get results in weeks.
Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are two devastating neurodegenerative diseases, with clinical, pathological and genetic overlap, without effective therapy.
Researchers from Anacor Pharmaceuticals Inc. and Pfizer Inc. have published preclinical data for the novel benzoxaborole prodrug AN-15368, being developed for the treatment of Chagas disease.
Netris Pharma SAS has entered into a scientific collaboration agreement with Orano SA and the Centre Léon Bérard (CLB) to develop novel antibody-radio conjugates for the treatment of cancer.
Therapeutic Solutions International Inc. has announced promising data on the use of Campbellcell for treatment of bipolar disorder by the company's suicide prevention-based spin-off Campbell Neurosciences Inc.
SBT-101 (Swanbio Therapeutics Inc.) is an adeno-associated virus serotype 9 (AAV9)-based gene therapy that delivers a functional copy of the ABCD1 gene and is under development for the treatment of adrenomyeloneuropathy (AMN).
As therapeutics development in Alzheimer’s disease (AD) is broadening its search for therapeutic targets, one of the alternatives to amyloid-β, or at least to its direct targeting by monoclonal antibodies, that is coming into focus is triggering receptor expressed on myeloid cells 2 (TREM2). From a drug development standpoint, amyloid-β remains a mystery. Scientific evidence clearly suggests that amyloid misprocessing is an underlying factor in the development of AD, and it is certainly a reasonable hypothesis that reducing amyloid plaque should fight the disease.
Scientists from the University of Lisbon have described how telomeres can establish the maximum damage that a cancer cell can suffer. Above this threshold, the cell would stop dividing and die. The damage comes from the transcription of the telomeres themselves of an RNA molecule called TERRA. When TERRA’s levels increase, the cell can no longer multiply. This mechanism occurs in ALT (alternative lengthening of telomeres) cells, which do not elongate their telomeres through telomerase.
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