L-701324

NMDA receptor

在30分钟的固定应激或全身施用苯二氮卓/GABA（A）受体反向激动剂甲基-6,7-二甲氧基-4-乙基-β-卡博林-3-羧酸酯（DMCM）后，内侧前额叶皮层中的多巴胺代谢，如二羟基苯乙酸（DOPAC）浓度所反映的，显著增加。用苯二氮卓类/GABA（A）受体激动剂地西泮和唑吡坦预处理大鼠后，对应激的反应减弱。此外，用低效力部分激动剂R-（+）-3-氨基-1-羟基吡咯烷-2-酮（R-（+）-HA-966）和甘氨酸/NDA受体新型高亲和力全拮抗剂7-氯-4-羟基-3（3-苯氧基）苯基喹啉-2-（H）-酮（L-701324）预处理，可以减弱对应激和DMCM的反应。这些结果表明，甘氨酸/NDA受体复合物的拮抗剂在防止应激和GABA（A）受体反向激动剂激活大脑中皮层多巴胺系统的能力方面与苯二氮卓/GABA（A）接收器激动剂相当。讨论了甘氨酸/NDA受体拮抗剂、中脑皮层多巴胺系统和应激相关疾病之间的相互作用[3]。

在强迫游泳试验 (FST) 和悬尾试验 (TST) 中，L-701,324（5–10 mg/kg；腹腔注射；一次）显示出类似抗抑郁的潜力，且不影响小鼠的运动活动 [1]。在慢性不可预测的轻度应激 (CUMS) 抑郁模型中，L-701324（5-10 mg/kg；腹腔注射；每日一次，持续 2 周）显示出强烈的抗抑郁样作用，抑制 CUMS 诱导的欧洲生成，并减少 BDNF 信号级联反应。海马体[1]。 L-701324（2.5–5 mg/kg；口服；一次）减少无条件和无条件焦虑样行为，同时通过阻断 NMDA 受体上的 NMDA/甘氨酸敏感区域来抑制 NMDA 受体活性。包括有条件冲突行为的情况[2]。

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目前临床上使用的抗抑郁药存在疗效低、起效慢、不良反应多等局限性。开发单胺能药物之外的新型抗抑郁药已成为必要。L-701,324是一种强效的NMDA受体拮抗剂，本研究旨在探讨L-701,324对小鼠可能的抗抑郁作用。在这里，我们同时使用了各种方法，包括强迫游泳试验（FST）、尾部悬吊试验（TST）、慢性不可预测的轻度应激（CUMS）抑郁模型、蛋白质印迹和免疫荧光。单次注射L-701324在FST和TST中表现出抗抑郁样潜力，而不影响小鼠的运动活动。反复注射L-701324不仅可以预防CUMS诱导的小鼠抑郁样行为，还可以改善CUMS对海马BDNF信号级联和神经发生的下调作用。此外，BDNF系统的强效抑制剂K252a完全阻断了L-701324在小鼠体内的抗抑郁样活性。K252a给药还消除了L-701324对CUMS治疗小鼠海马BDNF信号级联和神经发生的激活作用。总的来说，这些数据表明L-701324在小鼠体内具有抗抑郁样活性，这至少部分是通过促进海马BDNF系统介导的。[1]

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在高架迷宫和Vogel冲突试验中检查了NMDA/甘氨酸位点拮抗剂7-氯-4-羟基-3-（3-苯氧基）苯基-2（1H）-喹诺酮（L-701324）和苯二氮卓类受体激动剂地西泮的作用。口服L-701324导致在开放臂中花费的时间百分比呈剂量依赖性增加（2.5和5.0 mg/kg，-30分钟），而进入+迷宫的臂总数或进入开放臂的百分比没有变化。相同剂量的L-701,324以剂量依赖的方式增加了Vogel冲突测试中的惩罚反应，对未受惩罚的饮酒行为没有影响。L-701324的抗焦虑样作用是在其本身对动物的运动活动没有影响的剂量下获得的。在正迷宫情况下，地西泮（2mg/kg，腹腔注射，-30分钟）比L-701324略有效，而在Vogel测试中，两种化合物的惩罚饮酒增加幅度相同。我们目前的研究结果表明，通过阻断NMDA受体上的NMDA/甘氨酸敏感位点来抑制NMDA受体活性，在非条件性和条件性冲突行为情境中都伴随着焦虑样行为的减少。[2]

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甘氨酸/NDA受体拮抗剂R-（+）-HA-966和L-701324对应激诱导的中脑DOPAC浓度增加的影响[3]
对大鼠进行R-（+）-HA-966（20mg/kg，i.p.）或L-701,324（5mg/kg，i.p..）预处理，可显著减轻30分钟固定应激后内侧前额叶皮层DOPAC浓度的增加，而不会影响DOPAC浓度本身（图3a-c）。相比之下，用L-701357（10mg/kg，i.p.）预处理，L-701324的非活性对映体，对内侧前额叶皮层中DOPAC浓度的基础或应激诱导的增加没有显著影响（图3d）。内侧前额叶皮层中的多巴胺浓度不受压力或药物治疗的影响（数据未显示）。

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甘氨酸/NDA受体拮抗剂L-701,324对苯二氮卓/GABA受体反向激动剂DMCM诱导的中脑DOPAC浓度增加的影响[3]
在给予GABAA受体反向激动剂DMCM（5mg/kg，i.p.）后，用L-701,324（5mg/kg）对大鼠进行预处理显著减轻了内侧前额叶皮层DOPAC浓度的增加。相比之下，用L-701357（10mg/kg，i.p.）预处理，L-701324的非活性区域异构体，不影响DMCM增加内侧前额叶皮层DOPAC浓度（图4）。内侧前额叶皮层中的多巴胺浓度不受DMCM或L-701324的影响（数据未显示）。

Animal/Disease Models: Male C57BL/6 J mice (7 weeks old) in chronic unpredictable mild stress (CUMS) [1]
Doses: 5 and 10 mg/kg
Route of Administration: intraperitoneal (ip) injection; one time/day, continuous 2-week
Experimental Results: diminished immobility in C57BL/6 J mice. The expression of BDNF, pTrkB and pCREB was increased in the hippocampus.

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Animal/Disease Models: Male C57BL/6 J mice, forced swimming test (FST) and tail suspension test (TST) (7 weeks old) [1]
Doses: 5 and 10 mg/kg
Route of Administration: intraperitoneal (ip) injection;
Experimental Results: diminished immobility of C57BL/6 J mice in FST and TST.

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Animal/Disease Models: Male SD (SD (Sprague-Dawley)) rat (280-300 g) [2]
Doses: 2.5 and 5 mg/kg
Route of Administration: Oral;
Route of Administration: Oral.
Experimental Results: Dose-dependent increase in percentage of time spent with arms open. Increased punishment responses in a dose-dependent manner in the Vogel conflict test.

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L-701,324 was dissolved in normal saline containing 1% DMSO (vehicle) and intraperitoneally (i.p) injected (10 mL/kg). The dosages of L-701,324 (5 and 10 mg/kg), fluoxetine (20 mg/kg) and K252a (25 μg/kg) were determined according to previous reports and our pilot study [1].

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Forced swim test (FST) [1]
Naïve C57BL/6 J mice were given a single i.p. injection of L-701,324, fluoxetine or vehicle 30 min before this test. Mice were individually placed in a transparent glass tank (containing 15 cm high pure water, 25 ± 1 °C) for 6 min. A stopwatch was used to record the duration of immobility for each mouse during the last 4 min. The water was replaced after each trial. Immobility was defined as the mouse was floating in the water without struggling or having only slight movements to keep its nose above the water. This test was recorded with the observer unaware of the experimental grouping.

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Tail suspension test (TST) [1]
Naïve C57BL/6 J mice were given a single i.p. injection of L-701,324, fluoxetine or vehicle 30 min before this test. The tail tip of each mouse was individually glued to a rail 60 cm above the floor, and hung for 6 min. The immobility (completely motionless) duration of each mouse during the 6-min period was recorded. This test was recorded with the observer unaware of the experimental grouping.

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Open field test (OFT) [1]
This test was carried out in a darkroom. Naïve C57BL/6 J mice were given a single i.p. injection of L-701,324, fluoxetine or vehicle 30 min before this test. Mice were individually placed in the floor of an open field apparatus (100 × 100 × 45 cm; 25 squares, 20 × 20 cm for each square) and allowed to explore freely for 5 min. The apparatus was illuminated with a red bulb (50 W) on the ceiling. The number of squares each mouse crossed during the 5-min period was recorded. This test was recorded with the observer unaware of the experimental grouping. After each trail, the floor was cleaned.

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Chronic unpredictable mild stress (CUMS) [1]
Briefly, 8 stressors were adopted in this study: damp bedding (24 h), cage tilting (12 h), restraint (1 h), shaking (30 min), 4 °C exposure (1 h), day/night inversion, food deprivation (23 h) or water deprivation (23 h). All these stressors were randomly given for 6 weeks, and administration of L-701,324/fluoxetine/vehicle was performed daily during the last 2 weeks. The control mice were left undisturbed except general handing (e.g. regular cage cleaning) and drug treatment. After CUMS, FST, TST and sucrose preference test were performed together to assay the depressive-like behaviors of animals.

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Elevated plus-maze experiments [2]
The plus-shaped maze was made of wood and positioned on a height of 50 cm above the ßoor in a quiet laboratory surrounding. Two opposite arms were open (50 ´ 10 cm) and the other two were enclosed with walls (50 ´ 10 ´ 40 cm). Experiments were carried out in a darkened and quiet room with a constant light of 15 W, located 80 cm above the maze and directed towards the apparatus. The light levels on the open and enclosed arms were equal. Three days before the experiment, each rat was handled every day for 5 min. Animals were brought in their home cage into a separate silent room for 60 min before the experiment. Before the start of the pluz-maze behavior recordings, each animal was placed into a novel environment, represented by a conventional Skinner box, for 5 min. The plus-maze experiment was initiated by placing the rat into the center of the plus-maze facing an open arm, after which the number of entries and time spent in each of the two arms were recorded for a period of 5 min by an independent observer with no knowledge of the drug treatment protocol. An “arm entry” was recorded when the rat entered the arm with all four paws into the arm. The maze was carefully cleaned with tap water after each test session and with a weak alcohol washing solution after Þnishing all the experimental sessions of the day. The open-arm activity was quantiÞed as a) time spent in the open arms, as well as b) number of entries into the open arms. The glycine receptor antagonist, L-701,324, was given per os (PO) 30 min prior to the test.

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Vogel’s conßict test [2]
The drinking training sessions and the conßict-suppressed drinking experiments (for protocol, see Möller et al. 1997) were conducted in two standard boxes for operant behavior but specially designed for shock-induced suppression of drinking in rats. The whole experimental period consisted of 3 days. In the morning of the Þrst day, the drinking water was removed from the home cage of the animals. During the second and third day, the subjects were placed in the test apparatus and allowed a 12-min period of free drinking with no electric shocks delivered. After this 2-day training period, most animals showed a stable baseline of number of licks recorded during the training session. A few animals refused to drink and were removed from the experiments. On the day of the experiments, the animals were randomly divided into a control group (receiving solvent), and an experimental group receiving the drug of interest. Thirty minutes after drug administration, the animals were placed into the apparatus and the experimental session was initiated as soon as the animals had completed 20 licks on the water bottle. After this, continued drinking triggered the delivery of electric shocks in cycles of 5 s, with 4-s intervals with a shock current set at 0.2 mA. The number of punished and unpunished “drinking episodes” was recorded during a 12-min period, and the number of punished drinking episodes was taken as a measure of suppressed drinking behavior. All recordings were carried out between 12 a.m. and 6 p.m. in order to avoid large diurnal variations in the results. The benzodiazepine receptors agonist, diazepam, was given in a dose of 2.0mg/kg intraperitoneally (IP), which previously has been found to produce a reliable anti-conßict actions in rats. The glycine receptor antagonist, L-701,324 was given PO in doses of 2.5 and 5.0mg/kg, 30min prior to the start of the behavioral recordings.

L-701,324 was given PO as a suspension prepared using a 0.5% solution of methyl cellulose.

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L-701,324 (1 and 5 mg/kg, i.p.), L-701,357 (10 mg/kg, i.p.) or vehicle (0.5% carboxy methylcellulose in 0.9% saline, 1 ml/kg, i.p.). Thirty minutes later rats were either injected with DMCM (5 mg/kg, i.p.) or vehicle (1 ml/kg, i.p.) and killed 30 min later or in the stress studies either left in the home cage or immobilised for 30 min and immediately killed. Brains were removed, the medial prefrontal cortex dissected, frozen on solid CO2, and stored at −70°C. All brain samples were analysed for dopamine and the acidic metabolite dihydroxyphenylacetic acid (DOPAC) by high pressure liquid chromatography (HPLC) with electrochemical detection (Hutson et al., 1991). Briefly, tissue samples were homogenised in 10 vols. of 0.4 M perchloric acid containing 0.1% cysteine, 0.01% sodium metabisulphite and 0.01% sodium ethylene diaminetetraacetic acid (NaEDTA) and centrifuged at 3000×g/10 min. The HPLC system comprised an HPLC Technology Techsphere 3μ ODS column (4.6 mm×7.5 cm). The mobile phase consisted of 0.07 M KH2PO4, 0.0035% NaEDTA, 0.023% octyl sodium sulphate and 12.5% methanol, pH 2.75 at a flow rate of 1 ml/min. Dopamine and metabolites were detected using an Antec electrochemical detector (Presearch) with the working electrode set at +0.65 V relative to a silver/silver chloride reference electrode. [3]

[1]. Antidepressant-like activity of L-701324 in mice: A behavioral and neurobiological characterization. Behav Brain Res. 2021 Feb 5;399:113038.

[2]. A characterization of anxiolytic-like actions induced by the novel NMDA/glycine site antagonist, L-701,324. Psychopharmacology (Berl). 1998 Jan;135(2):175-81.

[3]. L-701,324, a glycine/NMDA receptor antagonist, blocks the increase of cortical dopamine metabolism by stress and DMCM. Eur J Pharmacol. 1997 May 20;326(2-3):127-32.

7-Chloro-4-hydroxy-3-(3-phenoxyphenyl)-1H-quinoline-2-one belongs to the quinoline family of compounds.

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Dopamine metabolism in the medial prefrontal cortex (reflected by the concentration of dihydroxyphenylacetic acid (DOPAC)) was significantly increased after 30 minutes of fixed stress or systemic administration of the benzodiazepine/GABA(A) receptor inverse agonist methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylic acid ester (DMCM). Pretreatment of rats with the benzodiazepine/GABA(A) receptor agonists diazepam and zolpidem attenuated the stress response. Furthermore, pretreatment with the ineffective partial agonist R-(+)-3-amino-1-hydroxypyrrolidone-2-one (R-(+)-HA-966) and the novel high-affinity glycine/NMDA receptor complete antagonist 7-chloro-4-hydroxy-3-(3-phenoxy)phenylquinoline-2-(H)-one (L-701,324) attenuated stress and DMCM-induced responses. These results indicate that glycine/NMDA receptor complex antagonists are comparable to benzodiazepine/GABA(A) receptor agonists in inhibiting stress and GABA(A) receptor inverse agonist activation of the midbrain cortical dopamine system. The findings explore the interactions between glycine/NMDA receptor antagonists, the midbrain cortical limbic dopamine system, and stress-related disorders. [3] The discovery that L-701,324 treatment promotes hippocampal neurogenesis is encouraging, suggesting that L-701,324 may be a pro-neurogenesis compound. Given the clear correlation between BDNF and neurogenesis, L-701,324 likely modulates neurogenesis by enhancing hippocampal BDNF expression. L-701,324 may also regulate some known pro-neurogenesis factors, such as sex-determining region Y-box 2 (SDR2) and pairing box protein 6 (P6), which requires further investigation. The neurobiological mechanisms of depression are quite complex. In addition to brain-derived neurotrophic factor (BDNF) dysfunction, monoamine neurotransmitter insufficiency, and hypothalamic-pituitary-adrenal (HPA) axis hyperfunction, recent studies have increasingly reported other depression-related targets, such as peroxisome proliferation-activating receptor α (PPARα), vascular endothelial growth factor (VEGF), salt-inducible kinase 2 (SIC2), and ΔFosB. Although experimental results involving K252a indicate that BDNF is involved in the antidepressant-like effects of L-701,324, we cannot rule out other protein targets besides BDNF. In summary, L-701,324 has an antidepressant-like effect in mice, and its mechanism of action is at least partly achieved by enhancing the hippocampal BDNF signaling pathway. [1]

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This study found that the glycine/NMDA receptor antagonist L-701,324 attenuated stress and benzodiazepine/GABAA receptor inverse agonist-induced changes in cortical dopamine metabolism, which is consistent with evidence that glutamate, especially the NMDA receptor complex, is involved in stress and anxiety responses. Therefore, behavioral studies have shown that antagonists of the NMDA receptor complex at glutamate, glycine, and ion channel sites exhibit anxiolytic activity in both conditioned and unconditioned reflex tests in rodents (Trullas et al., 1989; Corbett and Dunn, 1991; Dunn et al., 1992; Kehne et al., 1991; Faiman et al., 1994). The results of this study also support previous findings that antagonists of the glycine site of the NMDA receptor, which are insensitive to strychnine, interact with limbic dopamine neurons in the midbrain cortex, but only function when these neurons are activated. Therefore, studies have shown that R-(+)-HA-966 and L-701,324 not only lack the ability of non-competitive ion channel blockers phencyclidine and MK801 to increase dopamine metabolism and induce hyperactivity in the mesocortical limbic system, but also significantly attenuate these effects of PCP and MK801 (Bristow et al., 1993; Bristow et al., 1996a; Hutson et al., 1991; Hutson et al., 1995). Based on these and other studies, some research suggests that glycine/NMDA receptor antagonists exhibit atypical antipsychotic drug-like properties in rodents. Given the importance of the frontal cortex in the pathophysiology of schizophrenia, and the fact that stress may be a mitigating factor for relapse (Dohrenwend and Egri, 1981) and exacerbation of schizophrenia symptoms (Bebbington et al., 1993), the results of this study underscore the previous view that the glutamate system may play an important role in schizophrenia, and that such compounds may be a novel approach to treating schizophrenia. Whether such compounds have clinical efficacy in treating schizophrenia or anxiety-related disorders remains to be determined. [3]

C21H14CLNO3

363.7938

363.066

C, 69.33; H, 3.88; Cl, 9.75; N, 3.85; O, 13.19

142326-59-8

54682505

Typically exists as White to off-white solids at room temperature

1.4±0.1 g/cm3

584.7±50.0 °C at 760 mmHg

307.4±30.1 °C

0.0±1.7 mmHg at 25°C

1.680

5.5

62.32

2

3

3

26

558

0

ClC1C([H])=C([H])C2C(=C(C(N([H])C=2C=1[H])=O)C1C([H])=C([H])C([H])=C(C=1[H])OC1C([H])=C([H])C([H])=C([H])C=1[H])O[H]

FLVRDMUHUXVRET-UHFFFAOYSA-N

InChI=1S/C21H14ClNO3/c22-14-9-10-17-18(12-14)23-21(25)19(20(17)24)13-5-4-8-16(11-13)26-15-6-2-1-3-7-15/h1-12H,(H2,23,24,25)

7-chloro-4-hydroxy-3-(3-phenoxyphenyl)quinolin-2(1H)-one

L701,324; L701324; L 701324; L 701,324; 142326-59-8; L-701,324; L-701,324; 7-chloro-4-hydroxy-3-(3-phenoxyphenyl)quinolin-2(1H)-one; CHEMBL31741; 2(1H)-Quinolinone, 7-chloro-4-hydroxy-3-(3-phenoxyphenyl)-; 7-CHLORO-4-HYDROXY-3-(3-PHENOXYPHENYL)-1H-QUINOLIN-2-ONE; I9WY146163; L-701324; L-701,324.

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)

DMSO : ≥ 34 mg/mL (~93.46 mM)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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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。