153  0 Kommentare Twist Bioscience Publishes Preclinical Data in Diabetes Validating GLP-1R Antagonist Antibody as Potential Treatment for Congenital Hyperinsulinism

Twist Bioscience Corporation (NASDAQ: TWST), a company enabling customers to succeed through its offering of high-quality synthetic DNA using its silicon platform, today announced publication of preclinical data supporting the potential use of the highly potent and optimized GLP-1R antagonist antibody, TB-222-023, as a treatment for congenital hyperinsulinism (CHI). This pediatric genetic disorder has estimates of prevalence ranging from 1 in 25,000 to 1 in 50,000 live births in the U.S., which could translate into a steady-state treatable population of up to 2,500 cases in the U.S. It is caused by excessive pancreatic beta cell insulin secretion, resulting in hypoglycemia that can cause brain damage or death without treatment.

The Diabetes publication entitled, “Optimization of a glucagon-like peptide 1 receptor antagonist antibody for treatment of hyperinsulinism”, presents the results from several preclinical experiments using TB-222-023 as part of a research collaboration between Twist and the laboratory of Diva D. De León-Crutchlow, MD, Chief of the Division of Endocrinology and Diabetes and Director of the Congenital Hyperinsulinism Center at Children's Hospital of Philadelphia.

“Patients with congenital hyperinsulinism have few treatment options. The promising results from our studies described in the Diabetes paper demonstrate that targeting GLP-1R with an antibody antagonist, such as TB-222-023, could be an effective strategy for the treatment of this very serious condition,” said De León-Crutchlow.

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Twist researchers had previously identified a highly potent and specific GLP-1R antagonist antibody, TB-001-003, from synthetic antibody libraries designed to target G protein-coupled receptors. Subsequently, this lead was optimized further for greater activity against GLP-1R using the Twist Antibody Optimization (TAO) library platform. One antagonist, TB-222-023, was identified and shown to be more potent than exendin-(9-39), a clinical stage GLP-1R antagonist peptide. The results of the studies conducted at Children's Hospital of Philadelphia showed that TB-222-023 effectively decreased insulin secretion in primary isolated pancreatic islets from a mouse model of hyperinsulinism, Sur1^-/- mice, and in islets from an infant with hyperinsulinism. TB-222-023 also increased plasma glucose and decreased the insulin to glucose ratio in Sur1^-/- mice.