To enhance service speed and avoid tariff delays, we've opened a US warehouse. All US orders ship directly from our US facility.
| Cas No.: | 6754-58-1 |
| SMILES: | O=C(C1=C(OC)C=C(O)C(C/C=C(C)\C)=C1O)/C=C/C2=CC=C(O)C=C2 |
| Formula: | C21H22O5 |
| M.Wt: | 354.4 |
| Purity: | >98% |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Xanthohumol is one of the principal flavonoids isolated from hops, the inhibitor of diacylglycerol acetyltransferase (DGAT), COX-1 and COX-2, and shows anti-cancer and anti-angiogenic activities. |
| In Vitro: | Xanthohumol significantly attenuates ADP-induced blood platelet aggregation, and significantly reduces the expression of fibrinogen receptor (activated form of GPIIbIIIa) on platelets' surface[1]. Xanthohumol (5-50 nM) reduces the frequency of spontaneously occurring Ca2+ sparks and Ca2+ waves in control myocytes and in cells subjected to Ca2+ overload caused by: (1) exposure to low K+ solutions, (2) periods of high frequency electrical stimulation, (3) exposures to isoproterenol or (4) caffeine. Xanthohumol (50-100 nM) reduces the rate of relaxation of electrically- or caffeine-triggered Ca2+ transients, without suppressing ICa, but this effect is small and reversed by isoproterenol at physiological temperatures. Xanthohumol also suppresses the Ca2+ content of the SR, and its rate of recirculation[2]. Treatment of endothelial cells with Xanthohumol leads to increased AMPK phosphorylation and activity. Functional studies using biochemical approaches confirm that AMPK mediates Xanthohumol anti-angiogenic activity. AMPK activation by Xanthohumol is mediated by CAMMKβ, but not LKB1. Analysis of the downstream mechanisms shows that Xanthohumol-induced AMPK activation reduces nitric oxide (NO) levels in endothelial cells by decreasing eNOS phosphorylation. Finally, AKT pathway is inactivated by Xanthohumol as part of its anti-angiogenic activity, but independently from AMPK, suggesting that these two signaling pathways proceed autonomously[3]. Xanthohumol significantly reduces cell viability and induces apoptosis via pro-caspase-3/8 cleavage and poly(ADP ribose) polymerase (PARP) degradation. Pro-caspase-9 cleavage, Bcl2 family expression changes, mitochondrial dysfunction, and intracellular ROS generation also participate in Xanthohumol-induced glioma cell death. Xanthohumol's inhibition of the IGFBP2/AKT/Bcl2 pathway via miR-204-3p targeting plays a critical role in mediating glioma cell death[4]. |
| Cell Assay: | In vitro cell proliferation/viability is measured by the MTT test at different time points. 1000 cells/well are plated into 96-multiwell plates in complete medium. Following adhesion, medium is replaced with fresh medium containing the different treatments or vehicle (DMSO in medium). Xanthohumol and EGCG are used in a concentration range from 2.5 to 40 μM, up to 96 hours. 3 hours before each time point, MTT reagent (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) is added to the wells and plates are incubated at 37°C. At the indicated time points, absorbance at 540 nm is then measured by a FLUOstar spectrophotometer. |
| References: | [1]. Luzak B, et al. Xanthohumol from hop cones (Humulus lupulus L.) prevents ADP-induced platelet reactivity. Arch Physiol Biochem. 2016 Nov 18:1-7. [2]. Arnaiz-Cot JJ, et al. Xanthohumol modulates calcium signaling in rat ventricular myocytes: Possible Antiarrhythmic properties. J Pharmacol Exp Ther. 2016 Nov 4. pii: jpet.116.236588. [3]. Gallo C, et al. Hop derived flavonoid xanthohumol inhibits endothelial cell functions via AMPK activation. Oncotarget. 2016 Aug 1. [4]. Chen PH, et al. The miR-204-3p-targeted IGFBP2 pathway is involved in xanthohumol-induced glioma cell apoptotic death. Neuropharmacology. 2016 Nov;110(Pt A):362-75. |