The first-in-class orally available AT2R agonist C21 (buloxibutid) demonstrates safety and disease-modifying potential for idiopathic pulmonary fibrosis in early phase clinical trials.
Do angiotensin type II receptor (AT2R) agonists improve outcomes in patients with idiopathic pulmonary fibrosis?
AT2R agonists, particularly C21 (buloxibutid), represent a promising novel therapeutic class with disease-modifying potential for idiopathic pulmonary fibrosis.
Introduction Current standard-of-care for idiopathic pulmonary fibrosis is limited to nintedanib and pirfenidone, which only slow the progressive loss of lung function and have significant adverse effects that are intolerable to many patients. There is therefore a significant unmet need for alternative treatments for this incurable disease.Areas covered This review describes emerging evidence implicating dysregulation of the renin-angiotensin system in IPF pathogenesis, and both pre-clinical and recent clinical data supporting activation of the anti-fibrotic AT2R as a promising therapeutic strategy. The efficacy of AT2R agonists across pre-clinical models of both IPF and relevant lung diseases is discussed, with a particular focus on favorable findings with the AT2R agonist C21 (buloxibutid), leading to its current clinical trials for IPF.Expert opinion Rapid translation of C21 (now named buloxibutid), the first-in-class orally available AT2R agonist, to early phase clinical trials for IPF have established its safety and disease-modifying potential. Ongoing development of novel, more highly selective AT2R agonists may deliver the same clinical benefit as C21 with reduced off-target effects. The AT2R drug class offers great promise as novel therapeutics, potentially extending beyond IPF to other inflammatory and fibrotic lung diseases.
Young et al. (Fri,) conducted a review in idiopathic pulmonary fibrosis. Angiotensin type II receptor agonists (C21/buloxibutid) was evaluated. The first-in-class orally available AT2R agonist C21 (buloxibutid) demonstrates safety and disease-modifying potential for idiopathic pulmonary fibrosis in early phase clinical trials.