β-Aminoarteether (SM934 free base), an orally active derivative of Artemisinin, serves a pivotal role in the research of inflammation and autoimmune disorders, including those related to lupus diseases.

β-Aminoarteether (SM934; 10 μM; 24 hours) directly increases IL-10 production and reduces IL-12/23p40 production in primary peritoneal macrophages upon IFN-γ stimulation [1]. Additionally, in vitro, β-Aminoarteether (SM934) inhibits Th1 and Th17 polarization without affecting Treg differentiation [1].

Treatment with β-Aminoarteether (SM934; orally administered at doses of 1-10 mg/kg daily for 3 months) substantially slowed the advancement of glomerulonephritis and enhanced survival rates in female NZB/W F1 mice aged six and a half months [1]. Additionally, β-Aminoarteether therapy bolstered the production of IL-10 by macrophages derived from these mice [1]. This indicates a promising therapeutic potential for managing glomerulonephritis in this mouse model.