Resveratrol (SRT501; RM1812)   中文名称: 白藜芦醇

Natural phytoalexin; Autophagy; Adenylyl cyclase 0.8 nM (IC50); Mitophagy; IKKβ 1 μM (IC50); DNA polymerase α 3.3 μM (IC50); DNA polymerase δ 5 μM (IC50); Sirtuin

白藜芦醇（反式白藜芦醇；SRT501）是在多种植物来源中发现的众多多酚化学物质之一。在绝大多数情况下，白藜芦醇在微摩尔范围内表现出抑制/激活作用，这在药理学上可能是可行的，尽管纳摩尔范围内的目标也已被描述[1]。 MCF-7 细胞接种于补充有 5% FBS 和增加剂量的白藜芦醇的 DME-F12 培养基中。对照细胞仅用相同体积的载体（0.1%乙醇）处理。白藜芦醇以剂量依赖性方式抑制 MCF-7 细胞的发育。添加 10 μM 白藜芦醇 6 天后，MCF-7 细胞生长受到 82% 的抑制，但添加 1 μM 时，仅抑制 10%。用 10 μM 白藜芦醇处理的细胞的倍增时间为 60 小时，而对照细胞每 30 小时倍增一次。台盼蓝排除试验表明，在 10 μM 或更低的浓度下，白藜芦醇不会损害细胞活力（90% 的活细胞），但在 100 μM 的剂量下，白藜芦醇给药 6 天后，只有 50% 的细胞存活。此外，根据 ApoAlert 膜联蛋白 V 细胞凋亡试剂盒的评估，MCF-7 细胞与 10 μM 剂量的白藜芦醇一起孵育后并未发生细胞凋亡 [2]。白藜芦醇通过上调内皮一氧化氮合酶 (eNOS) 的表达、增强 eNOS 酶活性并阻断 eNOS 解偶联来促进内皮细胞中一氧化氮 (NO) 的产生 [7]。

在体内，白藜芦醇已被证明可以增加血浆抗氧化能力并减少脂质过氧化；然而，很难评估这些影响是直接的，还是内源性抗氧化酶上调的结果。[1]
尽管大多数体内研究强烈支持白藜芦醇的化学预防作用，但也有明显的例外，没有观察到任何益处。例如，每天每公斤体重1-5毫克的白藜芦醇不能影响小鼠乳腺癌的生长或转移，尽管体外实验结果很有希望17。剂量、给药方式、肿瘤来源和饮食的其他成分都可能影响白藜芦醇的治疗效果。总的来说，体内研究清楚地显示了这种分子在治疗癌症方面的巨大前景。目前正在进行几项人体口服白藜芦醇的I期临床试验，剂量高达每天7.5 g，包括美国密歇根大学和莱斯特大学的国家癌症研究所资助的研究。[1]
在体内，白藜芦醇已被证明可以增加内皮和诱导型一氧化氮合酶（eNOS和iNOS）的表达[1]
由于白藜芦醇是体内环加氧酶活性的有效抑制剂20,22,28，其抗炎特性已被研究。[1]
白藜芦醇(反式白藜芦醇；SRT501) 50 mg/kg(195.5±124.8 mm3；P<0.05)或100 mg/kg使平均肿瘤体积减小（81.7±70.5 mm3）；P < 0.001)。肿瘤的体积与体积有很强的相关性。

胰岛素样生长因子1酶联免疫吸附试验[2]
采用Human IGF-I/IGF-1 DuoSet ELISA法测定细胞上清中IGF-1的浓度。测量时，将小胶质细胞（HMC3）接种于6孔板中（80000个细胞/1 mL培养基/孔），用resveratrol/白藜芦醇/（100µM）处理24小时。然后，收集细胞上清液并根据制造商说明进行处理。

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葡萄糖摄取定量[2]
为了分析葡萄糖摄取，将小胶质细胞（HMC3）接种于白色96孔板（5000个细胞/100µL培养基/孔）。在resveratrol/白藜芦醇/（100µM）处理24小时后，根据制造商的说明，使用非放射性葡萄糖摄取- glo™测定法，以技术重复的方式测量培养基中的葡萄糖摄取。使用TECAN GENios微孔板读卡器读板。

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tmre -线粒体膜电位测定[2]
根据制造商的说明，使用tmre线粒体膜电位测定试剂盒检测线粒体活性。小胶质细胞（HMC3）接种于24孔板（7500个细胞/250µL培养基/孔）。使用Keyence BZx800荧光显微镜，在resveratrol/白藜芦醇/（100µM）处理24 h后进行成像。利用ImageJ对每个实验中两个区域的荧光强度进行量化

炎性小体活性测定[2]
为了定量炎性小体活性，将小胶质细胞（HMC3）接种于白色96孔板（8000个细胞/100µL培养基/孔）。在resveratrol/白藜芦醇/（100µM）处理6小时后，根据制造商的说明，使用Caspase-Glo®1炎性体测定法（Caspase-Glo®1 inflammasome Assay）测量技术重复的炎性体活性。使用TECAN GENios微孔板读卡器读板。

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扫描电子显微镜（SEM）[2]
将小胶质细胞（HMC3）接种于24 mm × 12 mm的盖上，盖于6孔板中（60,000个细胞/1 mL培养基/孔）。resveratrol/白藜芦醇/（100µM）处理24小时后，用PBS洗涤细胞，在3%戊二醛中固定30分钟。下一步，用PBS洗涤样品，并在2%锇溶液中保存20分钟。随后，通过将样品置于增加乙醇浓度（30-100%）中去除所有水分，并使用CPD 030进行临界点干燥。最后，用SCD 050溅射涂层机对样品进行涂层50 s，并使用JSM-IT200成像。

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扩散[2]
在resveratrol/白藜芦醇/（100µM）处理24小时后，用T20自动细胞计数器计数6孔板（80000个细胞/1 mL培养基/孔）中接种的小胶质细胞（HMC3）的增殖。增殖以初始播种细胞数的n倍计算。

The purpose of this study was to investigate the protective effect of low-dose trans-resveratrol (trans-RSV) on diabetes-induced retinal ganglion cell (RGC) degeneration and its possible mechanism. Methods: A streptozotocin-induced diabetic mouse model was established and treated with or without trans-RSV intragastric administration (10 mg/kg body weight/day) for 12 weeks. Oscillatory potentials (Ops) of the dark-adapted electroretinogram (ERG) were recorded. The number of RGCs was detected by Tuj1 and TUNEL staining. The apoptosis markers in the retina were analyzed by Western blot. The cross sections of optic nerves were observed by transmission electron microscopy. In addition, mouse neuroblastoma N2a cells were injured by high-glucose (HG) treatment. Cell viability and apoptosis were measured with or without low-dose trans-RSV treatment. The intracellular localization of tyrosyl transfer-RNA synthetase (TyrRS) was observed in both mouse retinas and N2a cells. The effects of low-dose trans-RSV on the binding of TyrRS to the transcription factor c-Jun and the binding of c-Jun to pro-apoptotic genes were analyzed by co-IP and ChIP assays in HEK 293 cells. Results: Trans-RSV relieved electrophysiological injury of retinas and inhibited RGC apoptosis in diabetic mice. It also protected N2a cells from HG-induced apoptosis. Additionally, it promoted TyrRS nuclear translocation in both diabetic mouse retinas and HG-treated N2a cells. Trans-RSV promoted TyrRS binding to c-Jun, inhibited the phosphorylation of Ser-63 of c-Jun, and downregulated pro-apoptotic gene transcription. Conclusions: Low-dose trans-RSV can ameliorate diabetes-induced RGC degeneration via the TyrRS/c-Jun pathway. It can promote TyrRS nuclear translocation and bind to c-Jun, downregulating c-Jun phosphorylation and downstream pro-apoptotic genes.https://pubmed.ncbi.nlm.nih.gov/37261387/

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Dissolved insodium lactate buffer (50 mM, pH 4.0); 100 mg/kg; i.p. injection

Human ovarian xenografts PA-1

Absorption, Distribution and Excretion
High absorption but very low bioavailability.
... Glycosylated resveratrol is more stable and more soluble and readily absorbed in the human gastrointestinal tract ... In humans, following its absorption, it is readily metabolized in the liver ... to water-soluble trans-resveratrol-3-O-glucuronide and trans-resveratrol-3-O-sulfate, accounting for its predominant urine excretion ... Compared to other known polyphenols, such as quercetin and catechin, trans-resveratrol is well absorbed much more efficiently following oral administration to humans ...
... Resveratrol is absorbed from the gastrointestinal tract following its ingestion ...
... Preclinical studies in rats, using HPLC methods, have suggested that intragastric administration of 20 mg/kg trans-resveratrol generated peak values of 1.2 uM in plasma ... In a separate study, male rats treated with 300, 1000, and 3000 mg/kg body weight per day were reported to achieve plasma concentrations of 576, 991, and 2728 ng/mL, respectively, and whereas in females, it was 333, 704, and 1137 ng/mL ... A plasma concentration of approximately 1.1 ug/mL was determined to be approximately 5 uM ... A single oral administration of (14)C-trans-resveratrol to male Balb/c mice showed preferential binding of radio-labeled resveratrol in the stomach, liver, kidney, intestine, bile, and urine, and penetrated the tissues of the liver and kidney ... Both the parent compound and the Phase-II metabolites were also detected in these tissues ... In humans, 24.6% of the oral dose administered appeared in the urine, including metabolites ... whereas after intragastric administration to rodents, only 1.5% of resveratrol reached the plasma compartment ...
In a human melanoma xenograft model ... The resveratrol content in the skin of these mice, measured 5 min after a bolus of 75 mg/kg introduced, was found to be 21 nmol/g and 4.67 nmol/g in glucuronide-conjugate forms. A measurable amount of resveratrol was found in the tumors, although it was less than the amount found in the skin ...
For more Absorption, Distribution and Excretion (Complete) data for RESVERATROL (12 total), please visit the HSDB record page.

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Metabolism / Metabolites
Hepatic. Rapidly metabolized and excreted.
... This study ... examined the absorption, bioavailability, and metabolism of (14)C-resveratrol after oral and iv doses in six human volunteers. The absorption of a dietary relevant 25-mg oral dose was at least 70%, with peak plasma levels of resveratrol and metabolites of 491 + or - 90 ng/mL (about 2 uM) and a plasma half-life of 9.2 + or - 0.6 hr. However, only trace amounts of unchanged resveratrol (<5 ng/mL) could be detected in plasma. Most of the oral dose was recovered in urine, and liquid chromatography/mass spectrometry analysis identified three metabolic pathways, ie, sulfate and glucuronic acid conjugation of the phenolic groups and, interestingly, hydrogenation of the aliphatic double bond, the latter likely produced by the intestinal microflora. Extremely rapid sulfate conjugation by the intestine/liver appears to be the rate-limiting step in resveratrol's bioavailability.
In plants, it mostly exists in glycosylated piceid forms (3-O-B-D-glucosides). Other minor conjugated forms containing 1 to 2 methyl groups (pterostilbene), a sulfate group (trans-resveratrol-3-sulfate) or a fatty acid have also been identified. Glycosylation is known to protect resveratrol from oxidative degradation, and glycosylated resveratrol is more stable ... In humans, following its absorption, it is readily metabolized in the liver by Phase-2 drug-metabolizing enzymes to water-soluble trans-resveratrol-3-O-glucuronide and trans-resveratrol-3-O-sulfate, accounting for its predominant urine excretion ...
... Resveratrol was metabolized in humans into two metabolites, which were characterized as resveratrol-3-O- and 4'-O-glucuronides ...
... In two 8-week long feeding experiments with rats, a low-resveratrol diet containing 50 mg resveratrol per kg body weight (bw) and day and a high-resveratrol diet with 300 mg per kg bw and day were administered. ... The level of resveratrol and its metabolites in the feces, urine, plasma, liver, and kidneys was identified and quantitated by high-performance liquid chromatography-diode array detection (HPLC-DAD) using synthesized resveratrol conjugate standards. ... The formation of trans-resveratrol-3-sulfate, trans-resveratrol-4'-sulfate, trans-resveratrol-3,5-disulfate, trans-resveratrol-3,4'-disulfate, trans-resveratrol-3,4',5-trisulfate, trans-resveratrol-3-O-beta-D-glucuronide, and resveratrol aglycone was detected by HPLC analysis, depending on the biological material. ...
Resveratrol has known human metabolites that include Resveratrol 3-O-glucuronide.

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Biological Half-Life
Pharmacokinetics of trans-resveratrol in its aglycone (RES(AGL)) and glucuronide (RES(GLU)) forms were studied following intravenous (15 mg/kg i.v.) and oral (50 mg/kg p.o.) administration of trans-resveratrol in a solution of beta-cyclodextrin to intact rats ... After i.v. administration, plasma concentrations of RES(AGL) declined with a rapid elimination half-life (T(1/2), 0.13 hr), followed by sudden increases in plasma concentrations 4 to 8 hr after drug administration. These plasma concentrations resulted in a significant prolongation of the terminal elimination half-life of RES(AGL) (T(1/2TER), 1.31 hr). RES(AGL) and RES(GLU) also displayed sudden increases in plasma concentrations 4 to 8 hr after oral administration, with T(1/2TER) of 1.48 and 1.58 hr, respectively ...
Resveratrol ... has a plasma half-life of 8 to 14 min; the metabolites /(trans-resveratrol-3-O-glucuronide and trans-resveratrol-3-O-sulfate)/ have a plasma half-life of about 9.2 hours ...
... A dietary relevant 25-mg oral dose /of (14)C-resveratrol in six human volunteers resulted in/ ... a plasma half-life of 9.2 + or - 0.6 hr ...
A 25-mg oral dose /of (14)C-resveratrol had/ a plasma half-life of 9.2 + or - 0.6 hr. ...
Trans-resveratrol half-life /in human plasma/ was 1-3 hr following single-doses and 2-5 hr following repeated dosing.

Hepatotoxicity
Liver injury attributable to resveratrol has not been reported. In trials of resveratrol in human subjects, there have been no reports of serum enzyme elevations or clinically apparent liver injury. Thus, hepatotoxicity due to resveratrol must be rare, if it occurs at all.
Likelihood score: E (unlikely cause of clinically apparent liver injury).
Drug Class: Herbal and Dietary Supplements

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Resveratrol (3,4',5-trans-trihydroxystilbene) is an antioxidant found in numerous plant species and in red wine. Resveratrol has no specific lactation-related uses. In general, it is used to prevent heart disease, cancer, and other diseases associated with aging, although high-quality studies are lacking. Resveratrol appears to be relatively free from adverse reactions. However, no data exist on the excretion of resveratrol into breastmilk or on the safety and efficacy of resveratrol in nursing mothers or infants. Resveratrol supplements usually contain hundreds of times the amounts found in wine or other foods, so their safety during breastfeeding cannot be assured. It is probably best to avoid the use of red wine as a source of resveratrol during breastfeeding. Refer to the LactMed record on Alcohol for details.
Dietary supplements do not require extensive pre-marketing approval from the U.S. Food and Drug Administration. Manufacturers are responsible to ensure the safety, but do not need to prove the safety and effectiveness of dietary supplements before they are marketed. Dietary supplements may contain multiple ingredients, and differences are often found between labeled and actual ingredients or their amounts. A manufacturer may contract with an independent organization to verify the quality of a product or its ingredients, but that does not certify the safety or effectiveness of a product. Because of the above issues, clinical testing results on one product may not be applicable to other products. More detailed information about dietary supplements is available elsewhere on the LactMed Web site.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Strong affinity towards protein binding.

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Interactions
... /Resveratrol exhibited/ dose-dependent inhibition of the mutagenic response induced by treatment of Salmonella typhimurium strain TM 677 with 7,12-dimethyl-benzanthracene (DMBA) ...
... Resveratrol ... enhanced the anti-tumor effect of 5-FU ...
In neuronal-like cells, such as the human neuroblastoma SH-SY5Y resveratrol was shown to inhibit caspase 7 activation, as well as degradation of poly-(ADP-ribose)-polymerase, which occur in cells exposed to paclitaxel, an anti-cancer drug ... Resveratrol was shown to induce S-phase arrest, preventing SH-SY5Y from entering mitosis, the phase of the cell cycle in which paclitaxel exerts its activity ... Phosphorylation of Bcl-2 and JNK/SAPK, which specifically occurs after paclitaxel exposure, was reversed by resveratrol ...
The combined effects of resveratrol have been tested with Ara-C or tiazofurin, both antimetabolites, and showed synergistic growth inhibition and apoptosis induction in HL-60 cells ...
For more Interactions (Complete) data for RESVERATROL (22 total), please visit the HSDB record page.

[1]. Nat Rev Drug Discov. 2006 Jun;5(6):493-506.
[2]. Antioxidants (Basel). 2023 Jun 9;12(6):1248.

Therapeutic Uses
Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Antimutagenic Agents; Antineoplastic Agents, Phytogenic; Antioxidants; Enzyme Inhibitors; Platelet Aggregation Inhibitors
/EXPL THER/ The antioxidant potency of three natural polyphenols, resveratrol, curcumin, and genistein, was compared by using the two human models: oxymodified with H2O2 and homocysteine (Hcy) G proteins in the postmortem frontal cortex (FC) membranes of age-matched control and Alzheimer's disease (AD) subjects; and Cu(2+)-induced oxidation of plasma low-density lipoproteins (LDL). In Co, 3-10 uM polyphenols dose-dependently depressed the G protein 25% stimulation induced by 10 uM H2O2 or 500 uM Hcy. Resveratrol revealed significantly higher antioxidativity than curcumin or genistein. In AD, the antioxidativity of polyphenols showed no significant differences. Polyphenols (1 uM) significantly increased the LDL oxidation lag time (oxyresistance) as compared with control, the effect of resveratrol being most potent. Due to the dual antioxidant mechanism, the investigated polyphenols, particularly resveratrol, should have preferences for the preventive-therapeutic use in age-related oxidative stress-based pathologies.
/EXPL THER/ Arthritis, an inflammation of the joints, is usually a chronic disease that results from dysregulation of pro-inflammatory cytokines (e.g. tumor necrosis factor and interleukin-1beta) and pro-inflammatory enzymes that mediate the production of prostaglandins (e.g. cyclooxygenase-2) and leukotrienes (e.g. lipooxygenase), together with the expression of adhesion molecules and matrix metalloproteinases, and hyperproliferation of synovial fibroblasts. All of these factors are regulated by the activation of the transcription factor nuclear factor-kappaB. Thus, agents that suppress the expression of tumor necrosis factor-alpha, interleukin-1beta, cyclooxygenase-2, lipooxygenase, matrix metalloproteinases or adhesion molecules, or suppress the activation of NF-kappaB, all have potential for the treatment of arthritis. Numerous agents derived from plants can suppress these cell signaling intermediates, including curcumin (from turmeric), resveratrol (red grapes, cranberries and peanuts), tea polyphenols, genistein (soy), quercetin (onions), silymarin (artichoke), guggulsterone (guggul), boswellic acid (salai guggul) and withanolides (ashwagandha). Indeed, several preclinical and clinical studies suggest that these agents have potential for arthritis treatment. Although gold compounds are no longer employed for the treatment of arthritis, the large number of inexpensive natural products that can modulate inflammatory responses, but lack side effects, constitute 'goldmines' for the treatment of arthritis.
/EXPL THER/ Resveratrol, a red wine polyphenol, is known to protect against cardiovascular diseases and cancers, as well as to promote antiaging effects in numerous organisms. It also modulates pathomechanisms of debilitating neurological disorders, such as strokes, ischemia, and Huntington's disease. The role of resveratrol in Alzheimer's disease is still unclear, although some recent studies on red wine bioactive compounds suggest that resveratrol modulates multiple mechanisms of Alzheimer's disease pathology ...
For more Therapeutic Uses (Complete) data for RESVERATROL (12 total), please visit the HSDB record page.

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Drug Warnings
Pregnant women and nursing mothers should avoid the use of resveratrol-containing supplements. They should also avoid the use of wine as a resveratrol source. Purple grape juice is a good and safe source of resveratrol, as well as other polyphenolic antioxidants.
Resveratrol is contraindicated in those hypersensitive to any component of resveratrol-containing product.

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Pharmacodynamics
Resveratrol, a phytoalexin, has been found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner, although this is only one of its many pharmaceutical properties. In some countries where there is higher consumption of red wine, there appears to be a lower incidence of heart disease. Other benefits of resveratrol include its anti-inflammatory and antioxidant effects. In preclinical studies, Resveratrol has been found to have potential anticancer properties.

C14H12O3

228.24

228.078

C, 73.67; H, 5.30; O, 21.03

501-36-0

Resveratrol;501-36-0

445154

White to off-white solid powder

1.4±0.1 g/cm3

449.1±14.0 °C at 760 mmHg

253-255°C

222.3±14.7 °C

0.0±1.1 mmHg at 25°C

1.763

3.14

60.69

3

3

2

17

246

0

C1=CC(=CC=C1/C=C/C2=CC(=CC(=C2)O)O)O

LUKBXSAWLPMMSZ-OWOJBTEDSA-N

InChI=1S/C14H12O3/c15-12-5-3-10(4-6-12)1-2-11-7-13(16)9-14(17)8-11/h1-9,15-17H/b2-1+

(E)-5-(4-hydroxystyryl)benzene-1,3-diol

SRT-501; RM-1812; SRT 501; RM 1812; SRT501; RM1812; trans-Resveratrol; CA1201; CA-1201; CA 1201; Resvida; Vineatrol 20M.

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: 5 mg/mL (21.91 mM) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶。
例如，若需制备1 mL的工作液，将 100 μL 50.0 mg/mL 澄清乙醇储备液加入到 400 μL PEG300 中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: 5 mg/mL (21.91 mM) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶.
例如，若需制备1 mL的工作液，可将 100 μL 50.0 mg/mL 澄清乙醇储备液加入到 900 μL 20% SBE-β-CD 生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 5 mg/mL (21.91 mM) (饱和度未知) in 10% EtOH + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 50.0 mg/mL 澄清 EtOH 储备液添加到 900 μL 玉米油中并充分混合。

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配方 4 中的溶解度: ≥ 2.5 mg/mL (10.95 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL 澄清的 DMSO 储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL 生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 5 中的溶解度: ≥ 2.5 mg/mL (10.95 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100μL 25.0mg/mL澄清的DMSO储备液加入到900μL 20％SBE-β-CD生理盐水中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 6 中的溶解度: ≥ 2.5 mg/mL (10.95 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 7 中的溶解度: ≥ 2.5 mg/mL (10.95 mM) (饱和度未知) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 8 中的溶解度: ≥ 2.5 mg/mL (10.95 mM) (饱和度未知) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 9 中的溶解度: 2% DMSO+30% PEG 300+ddH2O: 5mg/mL

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配方 10 中的溶解度: 12.5 mg/mL (54.77 mM) in 50% PEG300 50% Saline (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 11 中的溶解度: 16.67 mg/mL (73.04 mM) in 0.5% CMC-Na/saline water (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。