ArticleACR open rheumatology2026
The ERβ Agonist, OSU-ERβ-012, Mitigates Inflammation in a Chimeric Model of Systemic Lupus Erythematosus.
Article in ACR open rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveSystemic lupus erythematosus (SLE) is an autoimmune disease characterized by multiple organ damage, affecting women between the ages of 15 and 45 years at a 9:1 rate as compared to men. The etiology of SLE is complex and elusive; however, the susceptibility of women during the years in which estrogen levels are at their highest suggests a significant contribution to the development of SLE. Previously, our group and others have shown that estrogen receptor α (ERα) carrying immune cells are mediators of the proinflammatory effects of estrogen as compared to cells that lack this receptor. ERβ, the other estrogen responsive transcription factor, has been postulated to have an antagonistic effect to ERα, which mediates the anti-inflammatory effects of estrogen.
methodsIn the pursuit of a drug that is tailored to have a favorable selective estrogenic effect, The Ohio State University Drug Development Institute discovered a novel carborane-based selective ER modulator, OSU-ERβ-012. This ERβ agonist exhibits potent binding of human ERβ (Ki = 2.0 nM) and functional selectivity for ERβ over ERα of at least 200-fold. We tested the effectiveness of OSU-ERβ-012 in treating lupus-humanized NSG mice by examining serum for the presence of inflammatory cytokines and histopathology of hearts and kidneys.
resultsThe humanized mice exhibited increased expression of inflammatory cytokines, pericarditis, and increased glomerular size, which were all mitigated by the treatment with OSU-ERβ-012.
conclusionOSU-ERβ-012 is an effective therapeutic in this NSG mouse model with humanized SLE because it inhibits the proinflammatory renal and cardiac phenotype.
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