{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hall DB"],"funding":["NIDDK NIH HHS","National Institutes of Health"],"pagination":["ziae045"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11078046"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(6)"],"pubmed_abstract":["Hypoparathyroidism, a deficiency of parathyroid hormone (PTH), results in hypocalcemia, hyperphosphatemia, and hypercalciuria. The disease is poorly controlled by calcium and vitamin D supplements or native PTH(1-84) replacement therapy. A version of PTH is being developed using D-VITylation technology, whereby vitamin D is conjugated to a therapeutic peptide, which confers a long plasma half-life by virtue of binding to the abundant vitamin D binding protein (DBP). D-VITylation of PTH caused no reduction in activity at the PTHR1 receptor, and resulted in a plasma elimination half-life of 7-15 h in rats and 24-32 h in cynomolgus monkeys. Analysis of steady-state pharmacokinetics as a function of dose showed flat profiles with smaller peak:trough ratios at low doses, indicative of slower su"],"journal":["JBMR plus"],"pubmed_title":["Preclinical development of EXT608, an investigational parathyroid hormone derivative with extended half-life for the treatment of hypoparathyroidism."],"pmcid":["PMC11078046"],"funding_grant_id":["R44DK107231","R44 DK107231"],"pubmed_authors":["Hales LM","Soliman TM","Hall DB","Kostyla CH"],"additional_accession":[]},"is_claimable":false,"name":"Preclinical development of EXT608, an investigational parathyroid hormone derivative with extended half-life for the treatment of hypoparathyroidism.","description":"Hypoparathyroidism, a deficiency of parathyroid hormone (PTH), results in hypocalcemia, hyperphosphatemia, and hypercalciuria. The disease is poorly controlled by calcium and vitamin D supplements or native PTH(1-84) replacement therapy. A version of PTH is being developed using D-VITylation technology, whereby vitamin D is conjugated to a therapeutic peptide, which confers a long plasma half-life by virtue of binding to the abundant vitamin D binding protein (DBP). D-VITylation of PTH caused no reduction in activity at the PTHR1 receptor, and resulted in a plasma elimination half-life of 7-15 h in rats and 24-32 h in cynomolgus monkeys. Analysis of steady-state pharmacokinetics as a function of dose showed flat profiles with smaller peak:trough ratios at low doses, indicative of slower su","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-03-16T08:14:02.341Z","creation":"2025-08-14T03:05:48.507Z"},"accession":"S-EPMC11078046","cross_references":{"pubmed":["38721043"],"doi":["10.1093/jbmrpl/ziae045"]}}