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| Cas No.: | 1143-70-0 |
| SMILES: | O=C1C2=CC(O)=CC=C2C3=CC=C(O)C=C3O1 |
| Formula: | C13H8O4 |
| M.Wt: | 228.2 |
| Purity: | >98% |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Urolithin A is an intestinal metabolite of ellagic acid with antioxidant and antiproliferative effects; inhibits T24 and Caco-2 cell growth with IC50 values of 43.9 and 49 μM, respectively. |
| Target: | IC50: 43.9 μM (T24 cell)[1], 49 μM (Caco-2cell)[2] |
| In Vivo: | The volume of paw edema is reduced at 1 h after oral administration of urolithin A. In addition, plasma in treated mice exhibited significant oxygen radical antioxidant capacity (ORAC) scores with high plasma levels of the unconjugated form at 1 h after oral administration of urolithin A[4]. |
| In Vitro: | Urolithins could mainly inhibit prostate cancer and colon cancer cell growth. Urolithin A increases mRNA and protein expression of Phospho-p38 MAPK, and decreases mRNA and protein expression of MEKK1 and Phospho-c-Jun in T24 cells. Caspase-3 is also activated and PPAR-γ protein expression increased in drug-induced apoptosis[1]. Urolithin A exerts a dose- and time-dependent significant arrest at G2/M and S phases after treatments with 50 and 100 μM at 24 and 48 h compared to control cells. It induces cell apoptosis with 50 and 100 μM [2]. Urolithin A shows potent antiproliferative activity on HepG2 cells. When cell death is induced by Urolithin A, the expression of β-catenin, c-Myc and Cyclin D1 are decreased and TCF/LEF transcriptional activation is notably down-regulated. Urolithin A also increases protein expression of p53, p38-MAPK and caspase-3, but suppresses expression of NF-κB p65 and other inflammatory mediators[3]. |
| Cell Assay: | Human colon cancer cells HT-29 are treated for 24 and 48 h at 100 and 50 μM of Urolithin A and Iso Urolithin A aglycones and their glucuronide conjugates. Cell viability and proliferation are measured using a TC10 automated cell counter with the addition of Trypan blue for viability determination. IC50 values are determined by MTT assay[2]. |
| Animal Administration: | Mice: Paw edema is induced in the right hind paw of ICR mice by the subcutaneous injection of 1% λ-carrageenan in pysiological saline (50 μL). The inflammation level is quantified by the volume of paw edema. Urolithin A dissolved in 0.5% carboxymethylcellulose suspension is orally administered to the mice at 1 or 6 h before carrageenan injection. The anti-inflammatory effects of urolithin A on carrageenan-induced edema in mice are analyzed[4]. |
| References: | [1]. Qiu Z, et al. In vitro antioxidant and antiproliferative effects of ellagic acid and its colonic metabolite, urolithins, on human bladder cancer T24 cells. Food Chem Toxicol. 2013 Sep;59:428-37. [2]. González-Sarrías A, et al. Antiproliferative activity of the ellagic acid-derived gut microbiota isourolithin A and comparison with its urolithin A isomer: the role of cell metabolism.Eur J Nutr. 2017 Mar;56(2):831-841. [3]. Wang Y, et al. In vitro antiproliferative and antioxidant effects of urolithin A, the colonic metabolite of ellagic acid, on hepatocellular carcinomas HepG2 cells. Toxicol In Vitro. 2015 Aug;29(5):1107-15. [4]. Ishimoto H, et al. In vivo anti-inflammatory and antioxidant properties of ellagitannin metabolite urolithin A. Bioorg Med Chem Lett. 2011 Oct 1;21(19):5901-4. |
MSDS
COA
| LOT NO. | DOWNLOAD |
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| 2018-0101 |
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| 2018-0101 |
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