Roburic acid

Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a K_i of 7.066 μM against human TNF, an IC₅₀ of 9 μM against human COX-2, and an IC₅₀ of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases^{[1][2][3][4][5]}. IC50 & Target:IC50: 5 μM (COX-1), 9 μM (COX-2)^[1] In Vitro:Roburic acid (1-10 μM; 6 days) inhibits RANKL-induced osteoclastogenesis in BMMs, with the most potent effect in the early stage (Day 1-3), and does so without cell toxicity at tested concentrations^[2].
Roburic acid (10 μM; 7 days) has no effect on osteoblast differentiation in MC3T3-E1 cells^[2].
Roburic acid (5-10 μM) arrests RANKL-induced F-actin belt formation in BMM-derived osteoclasts^[2].
Roburic acid (5-10 μM; 2 days) suppresses RANKL-induced osteoclast resorption activity in BMMs^[2].
Roburic acid (5-10 μM; 6 days) dose-dependently downregulates the expression of osteoclast-related genes in RANKL-stimulated BMMs^[2].
Roburic acid (1-10 μM; 7 h) inhibits RANKL-induced NF-κB activity in RAW264.7 cells^[2].
Roburic acid (10 μM; 10 min-5 days) inhibits RANKL-induced TRAF6 expression, ERK phosphorylation, and IκB-α degradation in BMMs^[2].
Roburic acid (1-10 μM; 48 h) enhances RANKL-suppressed Nrf2/ARE activity in RAW264.7 cells in a dose-dependent manner^[2].
Roburic acid (10 μM; 1-3 days) upregulates HO-1 protein expression in RANKL-stimulated BMMs^[2].
Roburic acid (10 μM; 1-5 days) reduces the expression of NFATc1 and its target proteins (Integrin αV, c-Fos, CTSK) in RANKL-stimulated BMMs^[2].
Roburic acid (10 μM; 25 h) abates RANKL-stimulated calcium oscillations in BMMs^[2].
Roburic acid (1-10 μM; 24 h) inhibits RANKL-induced NFATc1 activity in RAW264.7 cells^[2].
Roburic acid (10-40 μM; 4 h) inhibits TNF-induced NF-κB activation in 293-TNF Res (NF-κB) cells^[3].
Roburic acid (0-20 μM; 48 h) inhibits the viability of HCT-116, HCT-15, HT29, and Colo205 human colorectal cancer cells with IC₅₀ values of 3.90, 4.77, 5.35, and 14.54 μM, respectively^[3].
Roburic acid (4-16 μM; 8 days) inhibits colony formation in HCT-116 and HCT-15 human colorectal cancer cells^[3].
Roburic acid (4-16 μM; 26 h) suppresses DNA synthesis in HCT-116 and HCT-15 human colorectal cancer cells^[3].
Roburic acid (4-16 μM; 24 h) triggers G₀/G₁ cell cycle arrest in HCT-116 and HCT-15 human colorectal cancer cells^[3].
Roburic acid (4-16 μM; 24 h) induces apoptosis in HCT-116 and HCT-15 human colorectal cancer cells^[3].
Roburic acid (8 μM) inhibits TNF-induced NF-κB signaling in HCT-116 and HCT-15 human colorectal cancer cells^[3].
Roburic acid (8 μM; 4.5 h) inhibits TNF-induced p65 nuclear translocation in HCT-116 and HCT-15 human colorectal cancer cells^[3].
Roburic acid (5-20 μM; 25 h) dose-dependently inhibits LPS (HY-D1056)-induced NO, iNOS and IL-6 expression and NF-κB p65 nuclear translocation in RAW264.7 cells^[5].
Roburic acid (5-20 μM; 1.5 h) dose-dependently inhibits LPS-induced phosphorylation of IKKα/β, p38 and JNK MAPKs in RAW264.7 cells^[5]. In Vivo:Roburic acid (5 mg/kg; i.v., for 4 doses) provides moderate amelioration of rheumatoid arthritis symptoms, inflammation, and bone erosion in adjuvant-induced arthritis rats^[1].
Roburic acid (10 mg/kg; i.p.; once every 2 days; 7 weeks) alleviates OVX-induced bone loss in mice by improving trabecular bone parameters^[2].
Roburic acid (5-10 mg/kg; i.p.; once daily; 18 days) suppresses colorectal cancer tumor growth in xenograft mice by blocking NF-κB signaling, with significant reductions in tumor volume and weight^[3].