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Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki 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.
For research use only. We do not sell to patients.
Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki 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
COX-1
5 μM (IC50)
COX-2
9 μM (IC50)
Cellular Effect
Cell Line
Type
Value
Description
References
A549
IC50
> 10 μM
Compound: 11
Inhibition of microsomal PGES1 isolated from IL-1beta-stimulated human A549 cells preincubated for 15 mins followed by substrate addition measured after 1 min by RP-HPLC analysis
Inhibition of microsomal PGES1 isolated from IL-1beta-stimulated human A549 cells preincubated for 15 mins followed by substrate addition measured after 1 min by RP-HPLC analysis
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].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Boosted HO-1 protein expression that was downgraded by RANKL from Day 1 to 3.\nAttenuated the expression of NFATc1, Integrin αV, c-Fos, and CTSK in RANKL-stimulated BMMs.
Significantly increased the percentage of G0/G1 phase cells and decreased the percentages of S and G2 phase cells in both cell lines in a concentration-dependent manner.
4 h (pretreatment; followed by TNF stimulation for indicated times)
Result:
Inhibited TNF-induced phosphorylation of IKKα/β, IκBα, and p65, degradation of IκBα, and expression of NF-κB-target genes (XIAP, Mcl-1, Survivin, Cyclin D1, c-Myc) in both cell lines.
1 h pre-treatment, followed by 24 h LPS stimulation
Result:
Suppressed LPS-induced iNOS protein expression in a dose-dependent manner; showed the most significant, statistically significant reduction at 20 μM relative to LPS-only treated cells.
1 h pre-treatment, followed by 24 h LPS stimulation
Result:
Attenuated LPS-promoted IL-6 production in a dose-dependent manner; showed the most potent, statistically significant inhibition at 20 μM relative to LPS-only treated cells.
1 h pre-incubation, followed by 30 min LPS stimulation
Result:
Increased cytosolic p65 levels and decreased nuclear p65 levels in a dose-dependent manner, indicating inhibition of LPS-induced NF-κB p65 translocation to the nucleus.
1 h pre-treatment, followed by 15 min LPS stimulation (phosphorylation); 1 h pre-treatment, followed by 30 min LPS stimulation (degradation)
Result:
Suppressed LPS-induced phosphorylation and degradation of IκBα in a dose-dependent manner; showed the most significant inhibition at 20 μM relative to LPS-only treated cells, with statistical significance.
1 h pre-treatment, followed by 30 min LPS stimulation
Result:
Inhibited LPS-induced phosphorylation of IKKα/β in a dose-dependent manner; showed the most potent, statistically significant inhibition at 20 μM relative to LPS-only treated cells.\n Suppressed LPS-induced phosphorylation of p38 and JNK in a dose-dependent manner; showed the most significant inhibition at 20 μM relative to LPS-only treated cells, with statistical significance.
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].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Slightly reduced paw swelling and arthritis score. Limited reduction in inflammatory cell infiltration and synovial hyperplasia. Moderated relief of cartilage and bone tissue disappearance; moderate reduction in spleen and thymus indices. Limited downregulation of IL-1β, IL-6, and TNF-α secretion in ankle joints; moderate reduction in osteoclast number. Limited increase in ALP expression, moderate lowering of RANKL/OPG ratio; moderate improvement in bone mineral density (BMD), limited reduction in trabecular separation (Tb.Sp), and moderate increase in trabecular bone thickness (Tb.Th).
Significantly increased trabecular bone parameters including bone volume/tissue volume (BV/TV), bone surface/tissue volume (BS/TV), trabecular number (Tb.N), and trabecular pattern factor (Tb.Pf) compared to the OVX group; Reduced bone deterioration observed via representative micro-CT images.
Significantly decreased tumor volume and weight of HCT-116 and HCT-15 xenografts. Inhibited phosphorylation of p65 in tumor tissues. Promoted cleavage of Caspase3 in tumor tissues; suppressed protein expression of Bcl-xL, XIAP, and Cyclin D1 in tumor tissues. Downregulated expression of p-p65 and Ki-67 in treated tumors; increased level of cleaved Caspase3 in treated tumors.
Room temperature in continental US; may vary elsewhere.
Storage
4°C, sealed storage, away from moisture and light
*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Solvent & Solubility
In Vitro:
DMSO : 33.33 mg/mL (75.63 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
2.2691 mL
11.3456 mL
22.6912 mL
5 mM
0.4538 mL
2.2691 mL
4.5382 mL
10 mM
0.2269 mL
1.1346 mL
2.2691 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Protocol 1
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (5.67 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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