Examples include the development of breathalyzers capable of diagnosing a COVID-19 infection and detectors, recognizing the airborne virus in open spaces, such as meeting rooms and hospital hallways.
Separate projects will concentrate on sensors that can pick up the virus via contact with human skin and potentially combining them with touchscreen and digital platforms for automatic detection.
NIH Director Francis Collins, M.D., said in a statement that to resolve an issue as complicated as COVID-19, they require ideas, tools, and technologies that challenge the way they conceive pandemic control.
GSK secures rights to Sosei Heptares drugs against untapped digestive disorder target
GlaxoSmithKline has struck a USD 481 Million agreement with Sosei Heptares to bag the rights to a promising therapy for inflammatory bowel disease (IBD) and related conditions. The deal confers GSK global rights to a portfolio of GPR35 agonists discovered by Sosei.
GPR35 is a G protein-coupled receptor (GPCR) that was recognized in the late 1990s. Information on the function of GPR35 was slow to develop because of the issues, including an initial lack of ligands, which regulate the receptor, and the inability to study its function in rodent models. Despite those barriers, the field has now progressed to the point that GPR35, which is highly expressed in the gastrointestinal tract, has been involved in the digestive system’s immune disorders such as IBD.
GSK has seen enough hope in the research to commit to giving Sosei up to USD 44 million in the form of an upfront payment, research funding, and near-term milestones to bag global rights to small-molecule agonists of GPR35. The deal is worth up to USD 437 million in longer-term milestones, plus tiered royalties.
The drugs covered by the agreement cover an advanced lead preclinical compound and a clutch of differentiated backup candidates. Sosei and GSK will collaborate during the research and early preclinical development stages of the R&D process. GSK will lead to clinical development and beyond.
Roche’s bispecific matches Regeneron’s Eylea in trials
Roche’s VEGFxAng2 bispecific antibody faricimab has resembled Regeneron’s leading Eylea in two phase 3 diabetic macular edema clinical trials. Faricimab was non-inferior to Eylea in spite of people on the experimental drug transitioning to a 16-week dosing window during the study.
Eylea is leading in the diabetic macular edema market due to its less troublesome dosing schedule than Roche and Novartis’s once-monthly rival Lucentis. Roche advanced faricimab into two phase 3 trials that pitted it against Regeneron and Bayer’s Eylea in a bid to step up its request to the incumbent diabetic macular edema drug.
Roche announced that both trials found faricimab was non-inferior to Eylea in terms of change in the best-corrected visual acuity (BCVA) from baseline after one year of treatment. Investigators evaluated BCVA using a standard vision testing tool highlighting rows of progressively smaller letters.
Patients on faricimab and Eylea both commenced the trial receiving injections every eight weeks. Subjects in the faricimab personalized dosing arms could change to longer gaps between injections during the study. More than half of the people in the personalized dosing arms were going 16 weeks between injections after one year.
The novel combos could conquer resistance to targeted drugs in leukemia, solid tumors
Drugs that target cancer-causing genes have proven effective in many tumor types. However, patients often become resistant to them. Combination therapies could answer this issue, and two academic groups lately released promising preclinical research on two such combos.
A team at Cincinnati Children’s Hospital Medical Center focused on resistance to mTOR inhibitors in patients with relapsed acute myeloid leukemia (AML). These drugs include rapamycin and several second-and third-generation mTOR inhibitors, are useful in many tumor types but have been ineffective in AML.
The researchers found that hemopoietic stem cells in bone marrow respond to mTOR loss by activating an alternate protein-signaling pathway that enables leukemia cells to avoid treatment. Inhibiting three other genes by combining mTOR blockers with drugs already in clinical trials could neutralize resistance, as reported in the journal Proceedings of the National Academy of Sciences.
The researchers used a new mouse model to study what happens when mTOR is excluded. They discovered that stem cells’ production in the bone marrow launches into overdrive, producing new blood cells that multiply using new signaling pathways.
