Endogenous Metabolite

婴儿大脑的生长和功能的发育取决于二十二碳六烯酸（DHA）。成年人的正常大脑功能也需要DHA。食用富含 DHA 的饮食可以增强记忆和学习能力 [1]。大脑发育的每个阶段，包括神经细胞增殖、迁移、分化和突触发生，从根本上取决于 DHA。由于其独特的结构和众多的双键，DHA 可以赋予有利于细胞信号传导的特定膜特性。 DHA 水平降低与许多发育性疾病有关，包括阅读障碍、自闭症谱系障碍、注意力缺陷多动障碍、精神分裂症等 [2]。强大的 RXR 配体 DHA 可在低微摩尔浓度下诱导强 RXR 激活。 DHA 激活 RXRα 的 EC50 为 5–10 μM 脂肪酸 [3]。

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最近，有证据表明，小鼠大脑中存在一种不同的天然RXR配体，即高度富集的多不饱和脂肪酸（PUFA）二十二碳六烯酸（DHA）（Mata de Urquiza等人（2000）Science 2902140-2144）。然而，研究结果表明，有效激活RXR需要超生理水平的DHA。使用向转染细胞添加配体的改进方法，目前的研究表明，DHA是一种比以前观察到的更有效的RXR配体，在低微摩尔浓度下已经诱导了强烈的RXR激活。此外，研究表明，其他天然存在的PUFA可以以与DHA相似的效率激活RXR。在另外的实验中，脂肪酸配体与RXRα的结合是通过RXR配体结合结构域（LBD）与其配体之间的非共价复合物的电喷雾质谱直接证明的。所提供的数据显示了RXR LBD与许多PUFA（包括DHA和花生四烯酸）之间的非共价相互作用，证实了转染细胞中的结果[3]。

在十周的过程中，服用二十二碳六烯酸显着增加了大脑皮层和海马体中二十二碳六烯酸的含量，并显着减少了参考记忆错误的数量，而没有增加工作记忆错误的数量。十二碳六烯酸与花生四烯酸的比例[4]。在帕金森病实验小鼠模型中，DHA 疗法具有神经保护作用。 MPTP 小鼠的大脑显示出脂质氧化水平略低的趋势[5]。

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Wistar大鼠被喂食鱼油缺乏的饮食三代。将第三代年轻（5周龄）雄性大鼠随机分为两组。在10周内，一组口服溶解在5%阿拉伯胶溶液中的二十二碳六烯酸/DHA，剂量为300mg/kg/天；另一组仅接受了类似数量的车辆。开始给药五周后，用部分（八个中的四个）诱饵的八臂径向迷宫测试大鼠与两种记忆相关的学习能力，即参考记忆和工作记忆。参考记忆是应该保留到下一次试验的信息。工作记忆是在短时间内消失的信息。进入非平衡臂和重复进入受访臂分别被定义为参考记忆错误和工作记忆错误。在10周内服用二十二碳六烯酸显著减少了参考记忆错误的次数，而不影响工作记忆错误的数量，并显著增加了海马和大脑皮层中的二十二碳六碳六烯酸含量和二十二碳六烯酸/花生四烯酸比率。此外，该比率与参考记忆错误的数量呈显著负相关。这些结果表明，长期服用二十二碳六烯酸有助于提高参考记忆相关的学习能力，海马或大脑皮层或两者中的二十二碳六烯酸/花生四烯酸比值可能是学习能力的指标。[4]

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本研究旨在研究二十二碳六烯酸（DHA）对帕金森病（PD）实验小鼠模型中发生的氧化应激的影响。通过四次腹腔注射1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）（4×20mg/kg，间隔12小时）建立PD的实验模型。连续4周每天通过强饲法给予二十二碳六烯酸（36mg/kg/天）。通过极点试验评估小鼠的运动活动，并通过酪氨酸羟化酶（TH）免疫阳性细胞的免疫组织化学分析确定多巴胺能损伤。通过分光光度法测定大脑中抗氧化酶的活性，并测量硫代巴比妥酸反应物质（TBARS）的浓度作为氧化损伤的指标。与对照组相比，MPTP治疗的小鼠中凋亡的多巴胺能细胞数量显著增加。尽管DHA显著降低了MPTP治疗小鼠的细胞死亡数量，但它并没有改善实验性PD模型中观察到的运动活性下降。与MPTP组相比，二十二碳六烯酸显著降低了MPTP+DHA组的细胞死亡量。MPTP治疗后，脑内TBARS水平显著升高。各组脑谷胱甘肽过氧化物酶（GPx）和过氧化氢酶（CAT）活性均无变化。与对照组相比，MPTP治疗组的脑超氧化物歧化酶（SOD）活性降低，但DHA治疗对MPTP+DHA组的SOD活性没有影响。我们目前的数据显示，DHA治疗对帕金森病的实验性小鼠模型具有神经保护作用。MPTP小鼠的脑脂质氧化有下降趋势，但并不显著[5]。

RXRαLBD配体的脂质提取和ES分析——[3]
将上述亲和捕获实验中的脱盐蛋白质组分解冻，并使用Lipidex-1000凝胶提取结合的脂质。使用前，Lipidex-1000用以下物质洗涤：1）50%甲醇，2）100%甲醇，3）水，然后以50%（v/v）浆液的形式储存在水中。每次提取时，将300μl Lipidex-1000浆液转移到1.5ml Eppendorf管中，离心后去除多余的水。将1毫升上述亲和捕获实验中解冻的脱盐蛋白质部分和2μl中1432.2 ng[14C]DHA加入凝胶床中（[14C]DHA在乙醇中，比活55 mCi/mmol）。通过计数1μl乙醇溶液来测定[14C]DHA的浓度，并使用比活度值计算为716.1 ng/μl。使用乙酸将浆液酸化至pH 2-3，并在37°C下孵育30分钟。除去上清液，用1.2ml水洗涤Lipidex床，弃去。用3×0.5ml甲醇提取结合在Lipidex床上的脂质。在氮气流下蒸发甲醇相，将残余物溶解在0.1ml甲醇中。通过负离子纳米ES质谱分析所得样品。未标记的提取DHA的量是根据未标记和标记的DHA离子的强度比（即m/z 327/329，DHA[m-H]−：m/z 327和[14C]DHA[m-H−：m/s 329）和添加的[14C]DHA的量（1432.2 ng）计算的。根据327+2同位素离子对329离子强度的贡献以及[14C]DHA标准中未标记的DHA，使用以下方程式校正m/z 327/329强度比：
其中RS是样品中未标记（327）与标记（329）离子的比率，RL是标记标准中未标记与标记离子的比率（测量值为0.167），RU是未标记参考化合物的“标记”（即[M-H]−+2同位素离子）与未标记离子的比率（理论上计算DHA为0.0264）。
提取的油酸和花生四烯酸的量是通过其各自脱质子分子的相对强度（分别为m/z 281和303）与脱质子的DHA进行比较来确定的。为了测定原始脑条件培养基的脂肪酸组成，使用上述Lipidex-1000程序提取1ml脑条件培养液。m/z 281、303和327处的离子通过其各自的二锂化加合物（[m-H+2Li]+）的低能碰撞诱导解离进行鉴定。

Docosahexaenoic acid administration [4]
G3 male rats were weaned on to the F-1® and randomly divided into two groups of eight rats each. One group (DHA group) was perorally administered DHA-95E emulsified in 5% gum Arabic solution at 300 mg/kg/day; the other group (control group) was administered a similar volume of vehicle alone. The administration was started when the G3 rats were five weeks of age and maintained until all the experiments ended.

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The eight-arm radial maze task [4]
An eight-arm radial maze, used for the estimation of learning ability, set at 60 cm elevation above floor level, consisted of an octagonal center platform surrounded by eight equally spaced radial arms (50 cm long×11 cm wide). Food cups, 1.5 cm deep and 2.5 cm in diameter, were located at the end of each arm. The maze was placed in a closed room with a number of visual cues: fluorescent ceiling lights, curtained door and windows, a chair for the observer and some boxes. The experimenter maintained a constant position beside the maze and observed the behavior of the rats.
Three weeks after starting the DHA administration, each rat was placed on a limited-food schedule designed to maintain weight at 80–85% of the free-feeding weight and was handled 5 min daily for five consecutive days. Then, for five days, the rats were familiarized with the apparatus, where 45 mg of reward pellets (made with F-1®) was scattered throughout the maze.

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Experimental design [5]
Mice were randomly divided into four experimental groups as follows: control (n = 15); DHA-treated (DHA) (n = 15); MPTP-injected (MPTP) (n = 15), and DHA-treated + MPTP-injected (MPTP + DHA) (n = 15). DHA/Docosahexaenoic acid was dissolved in corn oil at a concentration of 0.046 M and was given to the treatment groups for 30 days (36 mg/kg/day) by gavage (Hacioglu et al., 2006, Hacioglu et al., 2007, Kremer et al., 1990, Simopoulos, 1989, Tanriover et al., 2010). To eliminate the effects of a daily gavage and vehicle, other groups received a similar volume of corn oil alone. Food and water were provided ad libitum throughout the experiments.

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Treatment of mice with MPTP [5]
On the 23rd day of gavage treatment, animals in the MPTP and MPTP + DHA groups received intraperitoneal (i.p.) injections of either freshly prepared 20 mg/kg MPTP hydrochloride dissolved in saline or an equivalent volume of saline (pH 7.4) every 12 h with a total of four doses (Date et al., 1990). All four animal groups continued on their normal diets for an additional week after treatment.

Absorption, Distribution and Excretion
Like other omega-3 fatty acids, DHA is hydrolyzed from the intestines and delivered through the lymphatic circulation. Plasma DHA concentrations increase in a dose-dependent and saturable manner.
DHA is the most abundant n−3 fatty acid in membranes and is present in all organs. It is also the most variable among organs and is particularly abundant in neural tissue, such as brain and retina, where it is several hundred-fold more abundant than EPA.

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Metabolism / Metabolites
DHA can be metabolized into DHA-derived specialized pro-resolving mediators (SPMs), DHA epoxides, electrophilic oxo-derivatives (EFOX) of DHA, neuroprostanes, ethanolamines, acylglycerols, docosahexaenoyl amides of amino acids or neurotransmitters, and branched DHA esters of hydroxy fatty acids, among others. It is converted to 17-hydroperoxy-DHA derivatives via COX-2 and 15-LOX and 5-LOX activity. These derivatives are further converted into D-series resolvins and protectins with potent anti-inflammatory potential and potent neuroprotective effect. DHA may also be metabolized to 19,20-epoxydocosapentaenoic acids (EDPs) and isomers via CYP2C9 activity. Epoxy metabolites are reported to mediate anti-tumor activity by inhibiting angiogenesis, tumor growth, and metastasis.

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Biological Half-Life
Approximately 20 hours.

[1]. Health benefits of docosahexaenoic acid (DHA). Pharmacol Res. 1999 Sep;40(3):211-25.

[2]. Essential role of docosahexaenoic acid towards development of a smarter brain. Neurochem Int. 2015 Oct;89:51-62.

[3]. Polyunsaturated fatty acids including docosahexaenoic and arachidonic acid bind to the retinoid Xreceptor alpha ligand-binding domain. Mol Cell Proteomics. 2004 Jul;3(7):692-703.

[4]. Chronic administration of docosahexaenoic acid improves reference memory-related learning ability in young rats. Neuroscience. 1999;93(1):237-41.

[5]. The influence and the mechanism of docosahexaenoic acid on a mouse model of Parkinson's disease. Neurochem Int. 2011 Oct;59(5):664-70.

All-cis-docosa-4,7,10,13,16,19-hexaenoic acid is a docosahexaenoic acid having six cis-double bonds at positions 4, 7, 10, 13, 16 and 19. It has a role as a nutraceutical, an antineoplastic agent, a human metabolite, a Daphnia tenebrosa metabolite, a mouse metabolite and an algal metabolite. It is a docosahexaenoic acid and an omega-3 fatty acid. It is a conjugate acid of a (4Z,7Z,10Z,13Z,16Z,19Z)-docosahexaenoate.
A mixture of fish oil and primrose oil, doconexent is used as a high-docosahexaenoic acid (DHA) supplement. DHA is a 22 carbon chain with 6 cis double bonds with anti-inflammatory effects. It can be biosythesized from alpha-linolenic acid or commercially manufactured from microalgae. It is an omega-3 fatty acid and primary structural component of the human brain, cerebral cortex, skin, and retina thus plays an important role in their development and function. The amino-phospholipid DHA is found at a high concentration across several brain subcellular fractions, including nerve terminals, microsomes, synaptic vesicles, and synaptosomal plasma membranes.
Docosahexaenoic acid has been reported in Homo sapiens, Sarcophyton trocheliophorum, and other organisms with data available.
Doconexent is a polyunsaturated very long-chain fatty acid with a 22-carbon backbone and 6 double bonds, originating from the 3rd, 6th, 9th, 12th, 15th and 18th positions from the methyl end.
Docosahexaenoic Acid is a polyunsaturated very long-chain fatty acid with a 22-carbon backbone and 6 double bonds. Four separate isomers can be called by this name.
C22-unsaturated fatty acids found predominantly in FISH OILS.
See also: Fish Oil (is active moiety of); Cod Liver Oil (part of); Krill oil (part of) ... View More ...

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Drug Indication
Used as a high-docosahexaenoic acid (DHA) oral supplement.
Treatment of Retinitis Pigmentosa

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Mechanism of Action
DHA and its conversion to other lipid signalling moleccules compete with the arachidonic acid cascade from endogenous phospholipids and shift the inflammatory state to being more anti-inflammatory. DHA inhibits endotoxin-stimulated production of IL-6 and IL-8 in human endothelial cells. Derivatives of DHA are anti-inflammatory lipid mediators. Lipid mediators resolvin D1 and protectin D1 all inhibit transendothelial migration of neutrophils, so preventing neutrophilic infiltration at sites of inflammation, resolvin D1 inhibits IL-1β production, and protectin D1 inhibits TNF and IL-1β production. Monoxydroxy derivative of DHA converted by LOX inhibit thromboxane-induced platelet aggregation. DHA supplementation has also shown to reduce the levels of serum C-reactive protein (CRP) and other circulating markers of inflammation such as neutrophils in hypertriglyceridemic men. DHA acts as a ligand at peroxisome proliferator-activated receptor (PPAR) gamma and alpha that regulate lipid signalling molecule-mediated transduction pathways and modulate inflammation. As a natural ligand, DHA induces a protective effect in retinal tissues by activating retinoid x receptors and subsequent ERK/MAPK signaling pathway in photoreceptors to promote their survival and differentiation, stimulating the expression of antiapoptotic proteins such as Bcl-2 and preserving mitochondrial membrane potential.

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Pharmacodynamics
DHA in the central nervous system is found in the phospholipid bilayers where it modulates the physical environment and increase the free volume within the membrane bilayer. It influences the G-protein coupled receptor activity and affects transmembrane transport and cell interaction with the exterior world. It is also reported to promote apoptosis, neuronal differentiation and ion channel activity. Like other polyunsaturated fatty acids, DHA acts as a ligand at PPARs that plays an anti-inflammatory effect and regulate inflammatory gene expression and NFκB activation. DHA also gives rise to resolvins and related compounds (e.g., protectins) through pathways involving cyclooxygenase and lipoxygenase enzymes to resolve the inflammatory responses.

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Docosahexaenoic acid (DHA) is essential for the growth and functional development of the brain in infants. DHA is also required for maintenance of normal brain function in adults. The inclusion of plentiful DHA in the diet improves learning ability, whereas deficiencies of DHA are associated with deficits in learning. DHA is taken up by the brain in preference to other fatty acids. The turnover of DHA in the brain is very fast, more so than is generally realized. The visual acuity of healthy, full-term, formula-fed infants is increased when their formula includes DHA. During the last 50 years, many infants have been fed formula diets lacking DHA and other omega-3 fatty acids. DHA deficiencies are associated with foetal alcohol syndrome, attention deficit hyperactivity disorder, cystic fibrosis, phenylketonuria, unipolar depression, aggressive hostility, and adrenoleukodystrophy. Decreases in DHA in the brain are associated with cognitive decline during aging and with onset of sporadic Alzheimer disease. The leading cause of death in western nations is cardiovascular disease. Epidemiological studies have shown a strong correlation between fish consumption and reduction in sudden death from myocardial infarction. The reduction is approximately 50% with 200 mg day(-1)of DHA from fish. DHA is the active component in fish. Not only does fish oil reduce triglycerides in the blood and decrease thrombosis, but it also prevents cardiac arrhythmias. The association of DHA deficiency with depression is the reason for the robust positive correlation between depression and myocardial infarction. Patients with cardiovascular disease or Type II diabetes are often advised to adopt a low-fat diet with a high proportion of carbohydrate. A study with women shows that this type of diet increases plasma triglycerides and the severity of Type II diabetes and coronary heart disease. DHA is present in fatty fish (salmon, tuna, mackerel) and mother's milk. DHA is present at low levels in meat and eggs, but is not usually present in infant formulas. EPA, another long-chain n-3 fatty acid, is also present in fatty fish. The shorter chain n-3 fatty acid, alpha-linolenic acid, is not converted very well to DHA in man. These longchain n-3 fatty acids (also known as omega-3 fatty acids) are now becoming available in some foods, especially infant formula and eggs in Europe and Japan. Fish oil decreases the proliferation of tumour cells, whereas arachidonic acid, a longchain n-6 fatty acid, increases their proliferation. These opposite effects are also seen with inflammation, particularly with rheumatoid arthritis, and with asthma. DHA has a positive effect on diseases such as hypertension, arthritis, atherosclerosis, depression, adult-onset diabetes mellitus, myocardial infarction, thrombosis, and some cancers. [1]

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Evolution of the high order brain function in humans can be attributed to intake of poly unsaturated fatty acids (PUFAs) of which the ω-3 fatty acid, docosahexaenoic acid (DHA) has special significance. DHA is abundantly present in the human brain and is an essential requirement in every step of brain development like neural cell proliferation, migration, differentiation, synaptogenesis etc. The multiple double bonds and unique structure allow DHA to impart special membrane characteristics for effective cell signaling. Evidences indicate that DHA accumulate in areas of the brain associated with learning and memory. Many development disorders like dyslexia, autism spectrum disorder, attention deficit hyperactivity disorder, schizophrenia etc. are causally related to decreased level of DHA. The review discusses the various reports of DHA in these areas for a better understanding of the role of DHA in overall brain development. Studies involving laboratory animals and clinical findings in cases as well as during trials have been taken into consideration. Additionally the currently available dietary source of DHA for supplementation as nutraceutics with general caution for overuse has been examined.[2]

C₂₂H₃₂O₂

328.4883

328.24

6217-54-5

Docosahexaenoic acid-d5;1197205-71-2;Docosahexaenoic acid-13C22

445580

Colorless to light yellow liquid

0.9±0.1 g/cm3

446.7±24.0 °C at 760 mmHg

-44ºC

343.4±18.0 °C

0.0±2.3 mmHg at 25°C

1.521

6.78

37.3

1

2

14

24

462

0

O([H])C(C([H])([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])/C(/[H])=C(/[H])\C([H])([H])/C(/[H])=C(/[H])\C([H])([H])/C(/[H])=C(/[H])\C([H])([H])/C(/[H])=C(/[H])\C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])[H])=O

MBMBGCFOFBJSGT-KUBAVDMBSA-N

InChI=1S/C22H32O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-20-21-22(23)24/h3-4,6-7,9-10,12-13,15-16,18-19H,2,5,8,11,14,17,20-21H2,1H3,(H,23,24)/b4-3-,7-6-,10-9-,13-12-,16-15-,19-18-

cis-4,7,10,13,16,19-Docosahexaenoic acid

DHA; Cervonic Acid; Docosahexaenoic acid; Doconexent; Doconexento; Doconexentum; Doxonexent; AquaGrow Advantage; Martek DHA HM; 6217-54-5; Doconexent

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： (1). 本产品在运输和储存过程中需避光。  (2). 请将本产品存放在密封且受保护的环境中（例如氮气保护），避免吸湿/受潮。

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

DMSO : ~100 mg/mL (~304.42 mM)
Ethanol : ~50 mg/mL (~152.21 mM)

配方 1 中的溶解度: ≥ 5 mg/mL (15.22 mM) (饱和度未知) 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。
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 (15.22 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), 悬浊液; 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 (15.22 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 (7.61 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 (7.61 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 (7.61 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 (7.61 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 (7.61 mM) 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), 悬浊液; 超声助溶。
*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: 33.33 mg/mL (101.46 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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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。