
8-Prenylnaringeninestrogen receptor inhibitor |
Sample solution is provided at 25 µL, 10mM.
































Quality Control & MSDS
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- Purity = 98.00%
- COA (Certificate Of Analysis)
- MSDS (Material Safety Data Sheet)
Chemical structure


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Cas No. | 53846-50-7 | SDF | Download SDF |
Synonyms | Flavaprenin,8-PN | ||
Chemical Name | (2S)-2,3-dihydro-5,7-dihydroxy-2-(4-hydroxyphenyl)-8-(3-methyl-2-buten-1-yl)-4H-1-benzopyran-4-one | ||
Canonical SMILES | O=C1C[C@@H](C2=CC=C(O)C=C2)OC3=C(C/C=C(C)/C)C(O)=CC(O)=C31 | ||
Formula | C20H20O5 | M.Wt | 340.4 |
Solubility | Soluble in DMSO | Storage | Store at -20°C |
Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
IC50: 57 and 68 nM for ERα and ERβ, respectively
8-Prenylnaringenin is an estrogen receptor inhibitor.
The two estrogen receptors ERα and ERβ belong to the nuclear receptor superfamily and are ligand-regulated transcription factors accounting for mediating the physiological effects of the steroid hormone 17α-estradiol. ER is an established target for the development of synthetic ligands for therapeutic applications.
In vitro: Previous study identified 8-prenylnaringenin as a potent phytoestrogen in hops, which had an activity greater than other known plant estrogens. The estrogenic activity of 8-prenylnaringenin was reflected in its relative binding affinity to estrogen receptors from rat uteri. In addition, the presence of 8-prenylnaringenin in hops might explane the accounts of menstrual disturbances in female hop workers [1].
In vivo: Previous animal data demonstrated that 8-prenylnaringenin treatment could result in AMPK signaling pathway activation, therefore suppressing lipogenesis. The consumption of 8-prenylnaringenin was able to prevent body weight gain and improve plasma lipid profile, with significant improvement of insulin resistance and glucose tolerance. Moreove, it was found that 8-prenylnaringenin-enriched diet could ameliorate diabetic-associated metabolic disturbances via regulating glucose and lipid pathways [2].
Clinical trial: So far, no clinical study has been conducted.
References:[1] Milligan SR, Kalita JC, Heyerick A, Rong H, De Cooman L, De Keukeleire D.Identification of a potent phytoestrogen in hops (Humulus lupulus L.) and beer. J Clin Endocrinol Metab. 1999 Jun;84(6):2249-52.[2] Costa R et al. Xanthohumol and 8-prenylnaringenin ameliorate diabetic-related metabolic dysfunctions in mice. J Nutr Biochem. 2017 Apr 6;45:39-47.
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1.抗原性是指抗原与其所诱导产生的抗体或致敏淋巴细胞特异性结合的能力。抗原性的强弱与抗原分子的大小、化学成分、抗原决定簇的结构、抗原与被免疫动物亲缘关系的远近等有密切关系。通常认为抗原的分子量愈大、化学组成愈复杂、立体结构愈完整以及与被免疫动物的亲缘关系愈远,则抗原性愈强。
2.免疫原性是指能够刺激机体形成特异抗体或致敏淋巴细胞的能力。即指抗原能刺激特定的免疫细胞,使免疫细胞活化、增殖、分化,最终产生免疫效应物质抗体和致敏淋巴细胞的特性。也指抗原刺激机体后,机体免疫系统能形成抗体或致敏T淋巴细胞的特异性免疫反应。
可与MHCⅡ类分子结合的都是蛋白性抗原;多糖和脂类不易于MHCⅡ类分子连接,难以被TH细胞识别,因而多不是良好的免疫原;但有时可以诱导抗体性免疫应答。 抗原递呈(antigenpresentation)是辅佐细胞向辅助性T细胞展示抗原和MHCⅡ类分子的复合物,并使之与TCR结合的过程。这个过程是几乎所有淋巴细胞活化的必需步骤。抗原递呈之前,经处理后的抗原肽段已经连接在MHC分子顶端的槽中,这个复合物便是TCR的配体。TCR与配体结合的精确模式尚未清楚,一个合理的说法是TCR中α和β链的V段接触MHC分子的α螺旋(形成MHC分子顶端槽的肽段),使高可变的连接部(V-J及V-D-J)与抗原肽段相结合。这样保证了TCR识别抗原的特异性。
超抗原的递呈有独特的模式,它不需要胞内处理,可以直接与MHCⅡ类分子结合。超抗原不结合在MHCⅡ类分子的顶端槽中,而是结合在槽的外侧;与TCR结合时,不结合其α链,只结合β链的V节段。超抗原对TCR和MHCⅡ类分子的结合都非常牢固,象一支双向钩子将T细胞和辅佐细胞紧紧地连在一起,很容易使T细胞活化。另外,任何超抗原都只与含特殊β链V节段的TCR结合,这样的TCR约占外周T细胞总数的1%~10%,这一数字远远大于任何普通抗原所能识别的细胞数;所以某些产毒细胞感染时,容易发生急性期素休克综合征,就是超抗原刺激的结果。向左转|向右转
我们自身的细胞,蛋白也是抗原,但是自体在正常情况下没有针对自身的抗体。抗体产生的过程很复杂,我简单说一下:抗体由B细胞产生。本质是蛋白质。B细胞在成熟的过程中,编码抗体抗原识别区的那段基因会发生随机组合,这样就有可能会产生无数种抗体。但是如果一个B细胞产生了针对自身的抗体,那这个细胞就会和抚养它的细胞发生过于紧密的接触,被杀死。如果一个B细胞产生的抗体还不能识别任何抗原,那它就得不到足够的生长刺激,所以也不能存活。最后成熟的免疫细胞只占很小一部分。只有那些可以识别外源抗体的B细胞才能得到刺激,大量增殖。然后体内的抗体就增高了。
所以你的最后一句话不对。并不是人人都可以对任何抗原产生抗体的。比如青霉素过敏,过敏的人就是因为体内有针对青霉素的抗体IgE。而其他人就没有抗体。

