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Pomiferin, a flavonoid from the fruits of Maclura pomifera, acts as an potential inhibitor of HDAC, with an IC50 of 1.05 μM, and also potently inhibits mTOR (IC50, 6.2 &#181M).

Pomiferin is an potential inhibitor of HDAC, with an IC50 of 1.05 μM. Pomiferin shows cytotoxic effects on human tumor cell lines, with GI50s of 1.32 ± 0.02 μM (HCT-15 cells), 2.92 ± 0.09 μM (MDA-MB-231 cells), 3.18 ± 0.05 μM (ACHN cells), 3.34 ± 0.11 μM (LOX-IMVI cells), 3.95 ± 0.05 μM (PC-3 cells), 5.14 ± 0.06 μM (NCI-H23 cells), and 123 μM (Hepatocyte cells)[1]. Pomiferin is a highly specific mTOR inhibitor, with an IC50 of 6.2 &#181M. Pomiferin triacetate only affects two PI3Kα mutants, E542K and E545K. Pomiferin triacetate (0.3125-20 &#181M) stabilizes Pdcd4 from TPA-induced degradation in HEK293 cells. Pomiferin triacetate (20 &#181M) inhibits IGF-1-induced signaling downstream of Akt activation[2].

Pomiferin (5, 10 and 20 mg/kg, p.o.) shows protective effects on the treatment of reperfusion injury. Pomiferin also increases SOD activities and total antioxidative capacity, and decreases malondialdehyde in rats[3].

[1]. Son IH, et al. Pomiferin, histone deacetylase inhibitor isolated from the fruits of Maclura pomifera. Bioorg Med Chem Lett. 2007 Sep 1;17(17):4753-5. [2]. Bajer MM, et al. Characterization of pomiferin triacetate as a novel mTOR and translation inhibitor. Biochem Pharmacol. 2014 Apr 1;88(3):313-21. [3]. Barto?íková L, et al. Effect of pomiferin administration on kidney ischaemia-reperfusion injury in rats. Interdiscip Toxicol. 2010 Jun;3(2):76-81.

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