製品番号: HY-N0481

Roburic acid

1 Cited Publications

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Based on 1 publication(s) in Google Scholar

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.

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純度: 99.93%
CAS 番号: 6812-81-3
分子式: C₃₀H₄₈O₂
分子量:440.70

保管条件:

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)

Roburic acid 構造式

CAS 番号: 6812-81-3

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数量

Amount: USD 0.00

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生物活性
- 製品説明
- IC₅₀ & Target
- Cellular Effect
- 体外実験
- 体内実験
化学情報
Publications (1)
溶剤 & 溶解度
- 体外
- 体内
純度とドキュメンテーション
参考文献
Help & FAQs
関連分類
Bioz

生物活性

製品説明

IC₅₀ & Target

COX-1

5 μM (IC₅₀)

COX-2

9 μM (IC₅₀)

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TNF Receptor アイソフォーム固有の製品をすべて表示 :

NO Synthase アイソフォーム固有の製品をすべて表示 :

Interleukin Related アイソフォーム固有の製品をすべて表示 :

NF-κB アイソフォーム固有の製品をすべて表示 :

p38 MAPK アイソフォーム固有の製品をすべて表示 :

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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	[PMID: 24844534]

体外実験

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.

Real Time qPCR^[2]

Cell Line:

RANKL-stimulated bone marrow macrophages (BMMs)
Concentration:

5 and 10 μM
Incubation Time:

6 days
Result:

Dose-dependently decreased the mRNA levels of osteoclast-related genes (c-Fos, Acp5, Nfatc1, Atp6v0d2, Ctsk, Mmp9) that were upregulated by RANKL.

Western Blot Analysis^[2]

Cell Line:

RANKL-stimulated bone marrow macrophages (BMMs)
Concentration:

10 μM
Incubation Time:

10, 20, 30, 60 min (short-term); 1, 3, 5 days (long-term)
Result:

Restricted TRAF6 expression, ERK1/2 phosphorylation, and IκB-α degradation in RANKL-stimulated BMMs.

Western Blot Analysis^[2]

Cell Line:

RANKL-stimulated bone marrow macrophages (BMMs)
Concentration:

10 μM
Incubation Time:

1, 3, 5 days
Result:

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.

Cell Viability Assay^[3]

Cell Line:

HCT-116, HCT-15, HT29, Colo205 human colorectal cancer cell lines
Concentration:

0, 1, 2, 4, 6, 8, 10, 15 and 20 μM
Incubation Time:

48 h
Result:

Inhibited cell viability in all tested cell lines with IC50 values of 3.90 μM (HCT-116), 4.77 μM (HCT-15), 5.35 μM (HT29), and 14.54 μM (Colo205).

Cell Proliferation Assay^[3]

Cell Line:

HCT-116, HCT-15 human colorectal cancer cells
Concentration:

4, 8 and 16 μM
Incubation Time:

8 days
Result:

Significantly inhibited colony formation in a concentration-dependent manner.

Cell Proliferation Assay^[3]

Cell Line:

HCT-116, HCT-15 human colorectal cancer cells
Concentration:

4, 8 and 16 μM; 10 μM (EdU)
Incubation Time:

24 h (roburic acid treatment; 2 h EdU incubation)
Result:

Markedly suppressed DNA synthesis in both cell lines.

Cell Cycle Analysis^[3]

Cell Line:

HCT-116, HCT-15 human colorectal cancer cells
Concentration:

4, 8 and 16 μM
Incubation Time:

24 h
Result:

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.

Apoptosis Analysis^[3]

Cell Line:

HCT-116, HCT-15 human colorectal cancer cells
Concentration:

4, 8 and 16 μM
Incubation Time:

24 h (serum-free medium)
Result:

Led to a significant, concentration-dependent increase in the number of Annexin V-FITC-positive (apoptotic) cells in both cell lines.

Western Blot Analysis^[3]

Cell Line:

HCT-116, HCT-15 human colorectal cancer cells
Concentration:

8 μM; 10 ng/mL (TNF)
Incubation Time:

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.

Immunofluorescence^[3]

Cell Line:

HCT-116, HCT-15 human colorectal cancer cells
Concentration:

8 μM; 10 ng/mL (TNF)
Incubation Time:

4 h (pretreatment; 30 min TNF stimulation)
Result:

Significantly inhibited TNF-induced p65 nuclear translocation in both cell lines.

Cell Viability Assay^[5]

Cell Line:

RAW264.7 macrophage cells
Concentration:

5, 10, 20 and 50 μM
Incubation Time:

24 h
Result:

Inhibited less than 20% of cell proliferation at concentrations up to 20 μM; showed greater inhibition at 50 μM relative to untreated cells.

Western Blot Analysis^[5]

Cell Line:

LPS-stimulated RAW264.7 macrophage cells
Concentration:

5, 10 and 20 μM
Incubation Time:

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.

ELISA Assay^[5]

Cell Line:

LPS-stimulated RAW264.7 macrophage cells
Concentration:

5, 10 and 20 μM
Incubation Time:

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.

Western Blot Analysis^[5]

Cell Line:

LPS-stimulated RAW264.7 macrophage cells
Concentration:

5, 10 and 20 μM
Incubation Time:

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.

Western Blot Analysis^[5]

Cell Line:

LPS-stimulated RAW264.7 macrophage cells
Concentration:

5, 10 and 20 μM
Incubation Time:

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.

Western Blot Analysis^[5]

Cell Line:

LPS-stimulated RAW264.7 macrophage cells
Concentration:

5, 10 and 20 μM
Incubation Time:

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.

体内実験

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.

Animal Model:

Sprague-Dawley (male, 180-220 g, adjuvant-induced arthritis model)^[1]
Dosage:

5 mg/kg
Administration:

i.v.; on days 17, 20, 23, 26
Result:

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).

Animal Model:

C57BL/6J mice (10-week-old female, ovariectomized)^[2]
Dosage:

10 mg/kg
Administration:

i.p.; once every 2 days; 7 weeks
Result:

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.

Animal Model:

BALB/c nude (male, 5 weeks old, subcutaneous colorectal cancer xenograft model)^[3]
Dosage:

5, 10 mg/kg
Administration:

i.p.; once daily; 18 days
Result:

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.

化学情報

CAS 番号 6812-81-3
性状 Solid
分子量 440.70
分子式 C₃₀H₄₈O₂
Color White to off-white
SMILES

C[C@](C1=CC2)(CC[C@]3(C)[C@@]1([H])[C@@H](C)[C@H](C)CC3)[C@@](CC[C@H]4C(C)=C)(C)[C@@]2([H])[C@@]4(C)CCC(O)=O
Structure Classification
- Terpenoids
- Triterpenes
Initial Source
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

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)

Publications (1)

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Journal Impact Factor

Int J Mol Sci

Cycloastragenol Improves Fatty Acid Metabolism Through NHR-49/FAT-7 Suppression and Potent AAK-2 Activation in Caenorhabditis elegans Obesity Model. [Abstract]

2026 Jan 13;27(2):772. PMID: 41596421

溶剤 & 溶解度

体外:

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)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

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

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.

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希釈計算機

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体内:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

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 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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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).

Working solution concentration: 0.22 mg/mL

純度とドキュメンテーション

バッチを選択:

純度: 99.98%

Assay: 99.98%

ee.: 99.98%

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参考文献

[1]. Jia N, et al. Metabolic reprogramming of proinflammatory macrophages by target delivered roburic acid effectively ameliorates rheumatoid arthritis symptoms. Signal Transduct Target Ther. 2023;8(1):280. Published 2023 Jul 28. [Content Brief]

[2]. Wang G, et al. Roburic acid attenuates osteoclastogenesis and bone resorption by targeting RANKL-induced intracellular signaling pathways. J Cell Physiol. 2022;237(3):1790-1803. [Content Brief]

[3]. Xu H, et al. Roburic Acid Targets TNF to Inhibit the NF-κB Signaling Pathway and Suppress Human Colorectal Cancer Cell Growth. Front Immunol. 2022;13:853165. Published 2022 Feb 9. [Content Brief]

[4]. Cao H, et al. Discovery of cyclooxygenase inhibitors from medicinal plants used to treat inflammation. Pharmacol Res. 2010 Jun;61(6):519-24.
[Content Brief]

[5]. Chen Y, et al. Roburic Acid Suppresses NO and IL-6 Production via Targeting NF-κB and MAPK Pathway in RAW264.7 Cells. Inflammation. 2017;40(6):1959-1966. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.2691 mL	11.3456 mL	22.6912 mL	56.7279 mL
	5 mM	0.4538 mL	2.2691 mL	4.5382 mL	11.3456 mL
	10 mM	0.2269 mL	1.1346 mL	2.2691 mL	5.6728 mL
	15 mM	0.1513 mL	0.7564 mL	1.5127 mL	3.7819 mL
	20 mM	0.1135 mL	0.5673 mL	1.1346 mL	2.8364 mL
	25 mM	0.0908 mL	0.4538 mL	0.9076 mL	2.2691 mL
	30 mM	0.0756 mL	0.3782 mL	0.7564 mL	1.8909 mL
	40 mM	0.0567 mL	0.2836 mL	0.5673 mL	1.4182 mL
	50 mM	0.0454 mL	0.2269 mL	0.4538 mL	1.1346 mL
	60 mM	0.0378 mL	0.1891 mL	0.3782 mL	0.9455 mL

Roburic acid

1 Cited Publications

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Roburic acid

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