Rubiadin

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]}. In Vitro: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 Aβ_1-42-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/cm^2[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]. 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].