Press release
Keros Therapeutics Presents Results from Preclinical Study of KER-012 in Pulmonary Arterial Hypertension at the American Thoracic Society International Conference
LEXINGTON, Mass., May 14, 2021 (GLOBE NEWSWIRE) -- Keros Therapeutics, Inc. (“Keros” or the “Company”) (Nasdaq: KROS), a clinical-stage biopharmaceutical
About this update from Keros Therapeutics, Inc.
[{"type":"text","content":"LEXINGTON, Mass., May 14, 2021 (GLOBE NEWSWIRE) -- Keros Therapeutics, Inc. (“Keros” or the “Company”) (Nasdaq: KROS), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of novel treatments for patients suffering from hematological and musculoskeletal disorders with high unmet medical need, today announced results from a preclinical study of KER-012 on pulmonary and cardiac dysfunction in an established rodent model of pulmonary arterial hypertension (“PAH”) at the virtual American Thoracic Society International Conference held May 14 through 19, 2021. Additional data from a previously conducted nonclinical study in cynomolgus monkeys was also included in the presentation. KER-012 prevented markers of inflammation and fibrosis, and vascular remodeling in a rodent PAH model and did not alter red blood cell number in rats or non-human primates. RKER-012, a Novel Activin Receptor Type IIB (ActRIIB) Ligand Trap, Reduced Cardiopulmonary Pathology in a Rodent Model of Pulmonary Arterial Hypertension Keros combined administration of SUGEN5416, a tyrosine kinase inhibitor of vascular endothelial growth factor receptors 1/2, with exposure to chronic hypoxia to recapitulate the biology in PAH. A research form of KER-012 (“RKER-012”) was tested in this SUGEN/hypoxia (“SH”) rat model of PAH. Adult male rats were subjected to SH and received either vehicle or 10 mg/kg RKER-012 twice weekly for four weeks. Rats maintained under normal oxygen conditions (“normoxic controls”) received only vehicle. Consistent with enhanced pulmonary vascular remodeling and cardiac fibrosis, vehicle-treated SH rats showed significantly greater right ventricle plasminogen activator inhibitor-1 (“PAI-1”) expression (+236.7%; p","length":2064,"tagName":"div"}]