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Rubiadin is an orally active polyketide-derived compound and free radical scavenger that inhibits the activation of the NF-κB pathway. Rubiadin inhibits osteoclast formation, bone resorption, lipid peroxidation, HBV DNA replication and cancer cell proliferation; reduces pro-inflammatory cytokine levels; induces cancer cell apoptosis; and possesses antifungal, antimalarial, antibacterial and anticonvulsant activities. Rubiadin can be used in the research of osteoporosis, acute inflammation, chronic inflammation, carbon tetrachloride-induced liver injury, Alzheimer's disease, breast cancer, iron overload disorders, hepatitis B virus infection, colon cancer, liver cancer, T-lymphocytic leukemia, cervical cancer, diabetic nephropathy, epileptic seizures, fungal infections, malaria and bacterial infections.
For research use only. We do not sell to patients.
Rubiadin is an orally active polyketide-derived compound and free radical scavenger that inhibits the activation of the NF-κB pathway. Rubiadin inhibits osteoclast formation, bone resorption, lipid peroxidation, HBV DNA replication and cancer cell proliferation; reduces pro-inflammatory cytokine levels; induces cancer cell apoptosis; and possesses antifungal, antimalarial, antibacterial and anticonvulsant activities. Rubiadin can be used in the research of osteoporosis, acute inflammation, chronic inflammation, carbon tetrachloride-induced liver injury, Alzheimer's disease, breast cancer, iron overload disorders, hepatitis B virus infection, colon cancer, liver cancer, T-lymphocytic leukemia, cervical cancer, diabetic nephropathy, epileptic seizures, fungal infections, malaria and bacterial infections[1][2][3][4][5][6][7][8][9].
Cellular Effect
Cell Line
Type
Value
Description
References
DU-145
IC50
32 μM
Compound: 10, rubiadin
Cytotoxicity against Homo sapiens (human) DU145 cells assessed as inhibition of cell survival after 96 hr by MTT assay
Cytotoxicity against Homo sapiens (human) DU145 cells assessed as inhibition of cell survival after 96 hr by MTT assay
Rubiadin (5-20 μM; 3 h pre-incubation, then 24 h continued incubation) protects N2a cells against Aβ1−42-induced cytotoxicity, significantly enhancing cell viability relative to Aβ1−42-only treated cells[4]. Rubiadin (5-20 μM; 3 h pre-incubation, then 24 h continued incubation) suppresses activation of the IKK/IκB/NF-κB pathway in Aβ1-42-induced N2a cells by reducing phosphorylation of key pathway components[4]. Rubiadin (1-100 μM; 24 h post-irradiation) induces light dose-dependent cytotoxicity in MCF-7c3 human breast cancer cells, with an LD50 of 0.66 J/cm2, reducing viability by 76% at 100 μM and 1 J/cm2[5]. Rubiadin (0.4-40 μM; 24 h) does not impair the viability of human HepG2 cells[6]. Rubiadin (0.4-40 μM; 24 h, dose-dependent) and (20 μM; 3-24 h, time-dependent) upregulates hepcidin mRNA and protein expression in human HepG2 cells in both a dose-dependent and time-dependent manner, with maximal 5-fold mRNA upregulation at 20 μM for 24 h[6]. Rubiadin (5, 10, 20, 40 μg/ml; 72 h) dose-dependently inhibits the proliferation of HepG2.2.15 cells with an IC50 of 17 μg/ml, and nontoxic concentrations (<8 μg/ml) support its use in anti-HBV activity assays[7]. Rubiadin (4, 6 μg/ml; 24, 48, 72 h) dose-dependently reduces the secretion of HBsAg, HBeAg, and HBcAg by HepG2.2.15 cells, with particularly potent inhibition of HBeAg and HBcAg at 72 h[7]. Rubiadin inhibits Candida tropicalis biofilm formation and induces oxidative stress under irradiation, and acts synergistically with Amphotericin B against the fungus[8]. Rubiadin inhibits Plasmodium falciparum viability with an IC50 of 13.00 μg/mL, reducing schizont counts in a dose-dependent manner[8]. Rubiadin exhibits moderate experimental DPPH radical scavenging activity in aqueous physiological media (pH 7.4), with an IC50 of 91.00 ± 1.03 μM[9]. Rubiadin exhibits moderate experimental ABTS•+ radical scavenging activity in aqueous physiological media (pH 7.4), with an IC50 of 73.44 ± 1.17 μM[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
3 h pre-incubation, then 24 h continued incubation
Result:
Reduced the expression levels of pro-inflammatory cytokines IL-1β, IL-6, TNF-α. Increased the expression of anti-inflammatory cytokine IL-4. Decreased phosphorylated Tau protein expression in Aβ1₋42-exposed N2a cells.\nSignificantly inhibited the phosphorylation of IKK, IκB, and NF-κB in Aβ1₋42-exposed N2a cells.
24 h (untreated cells); 24 h (FAC-pretreated cells)
Result:
Dose-dependently decreased protein expression of TfR1, Fpn1 and FtL in untreated HepG2 cells, with significant reductions at 20 and 40 μM for TfR1 and Fpn1, and at 8, 20, and 40 μM for FtL; had no significant effect on divalen DMT1 or FtH expression.\nFurther decreased TfR1 protein expression and reversed FAC-induced elevation of FtL protein expression in FAC-pretreated HepG2 cells; had no significant effect on Fpn1, DMT1, or FtH expression in FAC-pretreated cells.
Dose-dependently decreased extracellular levels of hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and hepatitis B core antigen (HBcAg). Reduced HBeAg secretion by 26.31% and HBcAg secretion by 29.26% at 72 h, with more efficient inhibition than the positive control.
Resulted in G0/G1 phase percentages of 75.2% (4 μg/ml) and 78.1% (6 μg/ml), with no statistically significant difference from the untreated control (73.3%). Induced no cell cycle arrest.
In Vivo
Rubiadin (0.3-0.5 mg/kg; i.p.; single dose) exhibits significant acute anti-inflammatory activity, with a 61% inhibition of peak carrageenan-induced paw edema and a significant reduction in paw tissue TNF-α levels in male Wistar albino rats[2]. Rubiadin (50-200 mg/kg; p.o.; daily; 14 days) exhibits dose-dependent hepatoprotective activity against CCl4-induced hepatic damage in Sprague-Dawley rats, with highly significant efficacy at 100 and 200 mg/kg that approaches the activity of the reference drug silymarin[3]. Rubiadin (20 mg/kg; intragastric; daily; 8 weeks) improves spatial and non-spatial memory, reduces cerebral Aβ deposition, mitigates neuroinflammation, and inhibits NF-κB pathway activation in APP/PS1 Alzheimer's disease model mice[4]. Rubiadin (1 mg/kg; i.p.; every other day; 6 weeks) reduces serum iron, total iron-binding capacity, and transferrin saturation in normal 8-week-old C57BL/6 male mice[6]. Rubiadin (5-20 mg/kg; i.p.; daily; 4 weeks) alleviates iron overload in high-iron diet-fed C57BL/6 male mice by reversing splenomegaly, reducing serum iron parameters and duodenal iron content, and enhancing hepatic hepcidin expression and SMAD1/5/9 phosphorylation[6]. Rubiadin (100-250 mg/kg; p.o.; daily; 3 days) exhibits anticonvulsant effects in Swiss albino mice, reducing seizure severity in both pentylene tetrazole and maximal electro shock models when administered orally at 100 and 250 mg/kg for 3 days[8]. Rubiadin (0.04%; dietary; daily; 23 weeks) acts as a carcinogenic metabolite in F344 rats, enhancing renal preneoplastic lesions, liver cell foci, and intestinal dysplasias when administered at 0.04% in the diet for 23 weeks[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Produced paw edema inhibition percentages of 24% (0.5 hr), 17.5% (1 hr), 8.3% (2 hr), 21% (3 hr), and 13% (4 hr) at 0.3 mg/kg. Produced paw edema inhibition percentages of 48% (0.5 hr), 40% (1 hr), 45% (2 hr), 61% (3 hr), and 54% (4 hr) at 0.5 mg/kg, with 61% inhibition at peak edema time being statistically significant. Caused a statistically significant decrease in paw tissue TNF-α levels at 0.5 mg/kg compared to controls. Significantly reduced paw tissue edema and histopathological damage compared to controls at both doses.
Produced 34.71% inhibition of granuloma formation and 19.76% inhibition of transudate formation at 0.3 mg/kg. Produced 46.12% inhibition of granuloma formation and 38.13% inhibition of transudate formation at 0.5 mg/kg, with both values statistically. Caused a statistically significant decrease in serum IL-1β levels at 0.5 mg/kg compared to controls.
Animal Model:
C57BL/6 (6-week-old, male; high-iron diet-induced iron overload)[6]
Dosage:
5 mg/kg; 20 mg/kg
Administration:
i.p.; daily; 4 weeks
Result:
Did not significantly affect mouse body weight.\nSignificantly reversed splenomegaly, reduced elevated serum iron, total iron-binding capacity, and transferrin saturation caused by the high-iron diet, and reversed the elevated duodenal iron content caused by the high-iron diet.\nFurther increased hepatic hepcidin mRNA expression, hepatic hepcidin protein expression, and hepatic SMAD1/5/9 phosphorylation levels relative to the high-iron diet alone.
DMSO : ≥ 6.25 mg/mL (24.58 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
*"≥" means soluble, but saturation unknown.
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
3.9333 mL
19.6665 mL
39.3329 mL
5 mM
0.7867 mL
3.9333 mL
7.8666 mL
10 mM
0.3933 mL
1.9666 mL
3.9333 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 (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
*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 (protect from 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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