Rubiadin-1-methyl ether

Rubiadin-1-methyl ether is an orally potent NF-κB p65 inhibitor and autophagy inhibitor. Rubiadin-1-methyl ether inhibits RANKL-induced phosphorylation and nuclear translocation of p65, suppresses BECN1 transcription, blocks LC3 conversion and autophagosome formation, thereby reducing the levels of BECN1 mRNA and Beclin1 protein. Rubiadin-1-methyl ether inhibits osteoclastogenesis, cell proliferation, macrophage M2 polarization and the TGF-β1 signaling pathway, and effectively alleviates pulmonary inflammation. Rubiadin-1-methyl ether is widely used in research on osteoporosis, pulmonary fibrosis, idiopathic pulmonary fibrosis, acute lung injury and other related diseases^[1][2][3]. IC50 & Target:NF-κB^[1] In Vitro:Rubiadin-1-methyl ether (0.1-10 mM; 6, 12, 24 h) inhibits the proliferation of bone marrow-derived osteoclast precursors (OCPs) in a concentration-dependent manner when incubated for 6, 12, or 24 h in the presence of RANKL and M-CSF^[1].
Rubiadin-1-methyl ether (0.1-10 mM; 4 days) inhibits RANKL- and M-CSF-induced differentiation of bone marrow-derived osteoclast precursors (OCPs) into mature and large osteoclasts in a concentration-dependent manner after 4 days of incubation^[1].
Rubiadin-1-methyl ether (0.1-10 mM; 4 days) downregulates the mRNA expression of osteoclast-related genes (CTSK, MMP9, TRAP) in bone marrow-derived osteoclast precursors (OCPs) in a concentration-dependent manner after 4 days of incubation with RANKL and M-CSF^[1].
Rubiadin-1-methyl ether (0.1-10 mM; 12 h) inhibits RANKL-induced LC3 conversion (a marker of autophagy) in bone marrow-derived osteoclast precursors (OCPs) in a concentration-dependent manner after 12 h of incubation^[1].
Rubiadin-1-methyl ether (0.1-10 mM; 12 h) inhibits RANKL-induced p65 phosphorylation in bone marrow-derived osteoclast precursors (OCPs) in a concentration-dependent manner after 12 h of incubation^[1].
Rubiadin-1-methyl ether (10 mM; 12 h) inhibits RANKL-induced LC3 conversion and LC3-puncta formation (markers of autophagy) in bone marrow-derived osteoclast precursors (OCPs) after 12 h of incubation, and this effect is reversed by the Beclin1 activator TAT-Beclin1^[1].
Rubiadin-1-methyl ether (10 mM; 12 h) reverses RANKL-induced p65 nuclear translocation in bone marrow-derived osteoclast precursors (OCPs) after 12 h of incubation, restoring cytoplasmic p65 levels to ~0.92-fold and reducing nuclear p65 levels to ~0.91-fold relative to control^[1].
Rubiadin-1-methyl ether (10 mM; 12 h) reduces RANKL-induced BECN1 mRNA and Beclin1 protein expression in bone marrow-derived osteoclast precursors (OCPs) after 12 h of incubation, and this effect is reversed by the Beclin1 activator TAT-Beclin1^[1].
Rubiadin-1-methyl ether (10 mM; 12 h) reduces RANKL-induced BECN1 mRNA and Beclin1 protein expression in bone marrow-derived osteoclast precursors (OCPs) after 12 h of incubation, and this effect is reversed by p65 overexpression^[1].
Rubiadin-1-methyl ether (10 mM; 12 h) inhibits RANKL-induced LC3 conversion and LC3-puncta formation (markers of autophagy) in bone marrow-derived osteoclast precursors (OCPs) after 12 h of incubation, and this effect is reversed by p65 overexpression^[1].
Rubiadin-1-methyl ether (1-300 μM; 24 h) has low cytotoxicity in RAW 264.7 murine macrophages, with a CC₁₀ of 30 μM^[3].
Rubiadin-1-methyl ether (3-30 μM; 24 h LPS stimulation) at 30 μM reverses the LPS-induced decrease in apoptosis rate in RAW 264.7 murine macrophages^[3]. In Vivo:Rubiadin-1-methyl ether (3-30 mg/kg; p.o.; single dose on day 14 post-induction) at 10 mg/kg exerts the most potent anti-pulmonary fibrosis efficacy, significantly reducing bleomycin-induced pulmonary inflammation, collagen deposition, and M2 macrophage polarization in mice^[2].
Rubiadin-1-methyl ether (3-30 mg/kg; p.o.; single dose 1 hour pre-LPS) exerts dose-dependent anti-inflammatory and immunomodulatory effects in LPS-induced acute lung injury in mice, with the highest dose of 30 mg/kg producing the most robust reductions in leukocyte infiltration, proinflammatory mediator levels, and lung tissue damage, alongside increased IL-10 production^[3].