D₂ Receptor ( Ki = 1.8 nM ); D₃ Receptor ( Ki = 3.5 nM ); D₄ Receptor ( Ki = 2400 nM )); D₁ Receptor ( Ki = 18000 nM )
Dopamine D₂ receptor: Raclopride binds with a dissociation constant (Ki) of 1.8 nM (Table 2).[1]
Dopamine D₃ receptor: Raclopride binds with a dissociation constant (Ki) of 3.5 nM (Table 2).[1]
Dopamine D₄ receptor: Raclopride has very low affinity, with a dissociation constant (Ki) of 2400 nM (Table 2).[1]

[³H]雷氯必利可以轻易标记脑组织中的多巴胺D₂和D₃受体，但由于其对D₄受体亲和力低，不能标记D₄受体。[1]
在人纹状体中，通过[¹¹C]雷氯必利结合测得的D₂受体密度，是使用[¹¹C]甲基螺环哌隆测得的密度的1.7-1.8倍，这表明其与受体单体/二聚体的结合存在差异。[1]
在治疗条件下，通过[¹¹C]雷氯必利PET成像测量，雷氯必利占据了人类60%至75%的D₂受体。[1]
雷氯必利被归类为典型的神经阻滞剂（抗精神病药），可阻断D₂受体。[1]

酒石酸雷氯必利（0.1、0.3 或 0.6 mg/kg；腹腔注射；30 分钟；OF1 品系的白化雄性小鼠）显着减少分配给攻击行为的时间[2]。

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Raclopride是一种替代苯甲酰胺，作为中枢多巴胺能D2受体的拮抗剂，具有高选择性和潜在的抗精神病作用。与经典的DA受体阻滞剂如氟哌啶醇相比，雷氯pride在锥体外系副作用的临床前试验中表现出非典型特征。raclopride对拮抗行为的抗攻击特性尚未得到充分的研究。本实验研究了0.1、0.3、0.6 mg/kg盐酸雷氯pride对雄性小鼠攻击行为和运动行为的影响。注射后30分钟进行攻击试验。会面被录下来，行为被评估，用11大类行为来衡量所花的时间。结果显示，雷氯pride有明显的抗攻击作用，几乎没有运动障碍，但探索性行为有所增加。这种行为特征与观察到的其他非典型抗精神病药非常相似，与经典化合物中的发现有所不同。[2]

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急性腹腔注射雷氯必利（0.1、0.3、0.6 mg/kg）在隔离饲养的雄性小鼠中产生了明确的剂量依赖性抗攻击作用，所有三个剂量均显著减少了攻击行为（与生理盐水对照组相比，p < 0.02）。[2]
雷氯必利处理未引起显著的运动功能损害。即使在最高剂量（0.6 mg/kg）下，不动时间也极少且未显著增加。[2]
给予雷氯必利后，非社会性探索行为表现出不显著的、剂量依赖性的增加。[2]
雷氯必利的行为特征（抗攻击作用且运动损害最小）与其他非典型神经阻滞剂（如舒必利和氯氮平）相似，而与产生明显运动损害的经典神经阻滞剂（如氟哌啶醇）不同。[2]

Animals: 90 male OF1 strain albino mice were used. Half were individually housed for 30 days to induce isolation-induced aggression. The other half were group-housed and rendered temporarily anosmic by intranasal lavage with 4% zinc sulfate solution to serve as non-aggressive "standard opponents".[2]
Drug formulation and administration: Raclopride tartrate was dissolved in physiological saline. Mice were injected intraperitoneally (IP) with doses of 0.1, 0.3, or 0.6 mg/kg in a volume of 0.01 ml/g body weight. Control animals received physiological saline only.[2]
Experimental procedure: Aggression tests were conducted 30 minutes after injection. An experimental mouse (treated) and a standard opponent (anosmic) were placed in a neutral glass cage (60x33x30 cm) for a 10-minute encounter, preceded by a 1-minute adaptation period separated by a barrier. Encounters were videotaped under white light during the dark phase of the light/dark cycle.[2]
Behavioral analysis: Videotapes were analyzed by a blinded observer using a custom program. The time spent in 11 broad behavioral categories was recorded for the experimental/control mice only.[2]

Raclopride can easily cross the blood-brain barrier and reach high concentrations in the brain shortly after injection. [2]

Raldapride can induce rigidity in animals, a common side effect of typical D₂ receptor antagonists. [1]
Litanserin (a 5-HT₂ receptor antagonist) does not antagonize raldapride-induced rigidity, suggesting that rigidity is primarily mediated by D₂ receptor blockade. [1]

[1]. Dopamine receptor pharmacology. Trends Pharmacol Sci. 1994;15(7):264-270.

[2]. Behavioral profile of raclopride in agonistic encounters between male mice. Pharmacol Biochem Behav. 1994;47(3):753-756.

3,5-Dichloro-N-[[(2S)-1-ethyl-2-pyrrolyl]methyl]-2-hydroxy-6-methoxybenzamide belongs to the salicylamide class of compounds. Raclopride has been used in research trials for Parkinson's disease. It is a substituted benzamide with antipsychotic properties. It is a dopamine D2 receptor (see “Receptor, Dopamine D2”) antagonist. Dopamine receptors are major targets for the treatment of schizophrenia, Parkinson's disease, and Huntington's disease, as discussed in this review by Philip Seeman and Hubert Van Tol. Drugs that selectively target specific subtypes of dopamine receptors can improve treatment efficacy. The degree to which most antipsychotic drugs block D2 receptors is directly related to clinical efficacy, except for clozapine, which tends to target D4 receptors. D1 and D2 receptors can mutually enhance each other, possibly through G protein subunits. In schizophrenia, the density of D2 and D3 receptors increases by 10%, while the density of D4 receptors increases by 600%. Therefore, the D4 receptor may become a target for future antipsychotic drugs. Although antipsychotic drugs initially helped in the discovery of dopamine receptors, the five currently cloned dopamine receptors are facilitating the discovery of selective antipsychotics and anti-Parkinson's disease drugs. Antipsychotics: These drugs can control manic psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and have a sedative effect. They are used to treat schizophrenia, Alzheimer's disease, postoperative transient psychosis, or myocardial infarction, among other conditions. These drugs are often referred to as neuroleptics, implying that they may produce neurological side effects, but not all antipsychotics produce such side effects. Many of these drugs may also be effective for nausea, vomiting, and itching. (See all compounds classified as antipsychotics.) Dopamine antagonists: These drugs bind to dopamine receptors but do not activate the receptors, thereby blocking the action of dopamine or exogenous agonists. Many medications used to treat psychotic disorders (antipsychotics) are dopamine antagonists, although their therapeutic effects may be attributed to long-term regulation of the brain rather than the acute effects of blocking dopamine receptors. Dopamine antagonists are also used for other clinical purposes, including as antiemetics, for the treatment of Tourette syndrome, and for the treatment of hiccups. Dopamine receptor blockade is associated with neuroleptic malignancy.

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Raldipride is a benzamide antipsychotic and a selective dopamine D₂/D₃ receptor antagonist. [1]
It is available as a radioligand ([³H]raldipride and [¹¹C]raldipride) for labeling and quantifying D₂ and D₃ receptors in vitro and in vivo (PET imaging). [1]
The difference in binding density between [³H]nemonapride (labeled D₂, D₃, and D₄) and [³H]ralapride (labeled D₂ and D₃) can be used to estimate the density of D₄ receptors in tissues. [1]
Most typical antipsychotic drugs, including ralapride, act primarily on D₂ and D₃ receptors, unlike clozapine, which targets D₄ receptors. [1]

C19H26CL2N2O9

497.32374

496.102

C, 45.89; H, 5.27; Cl, 14.26; N, 5.63; O, 28.95

98185-20-7

Raclopride; 84225-95-6

16219926

Solid powder

1.127

176.86

6

10

8

32

520

3

CC[NH+]1CCC[C@H]1CNC(=O)c2c(c(cc(c2OC)Cl)Cl)O.[C@@H]([C@H](C(=O)[O-])O)(C(=O)O)O

QULBVRZTKPQGCR-NDAAPVSOSA-N

InChI=1S/C15H20Cl2N2O3.C4H6O6/c1-3-19-6-4-5-9(19)8-18-15(21)12-13(20)10(16)7-11(17)14(12)22-2;5-1(3(7)8)2(6)4(9)10/h7,9,20H,3-6,8H2,1-2H3,(H,18,21);1-2,5-6H,(H,7,8)(H,9,10)/t9-;1-,2-/m01/s1

3,5-dichloro-N-[[(2S)-1-ethylpyrrolidin-2-yl]methyl]-2-hydroxy-6-methoxybenzamide;(2R,3R)-2,3-dihydroxybutanedioic acid

Raclopride; FLA-870; FLA870; Raclopride tartrate; 98185-20-7; EXZ5FGZ55J; Raclopride (tartrate); UNII-EXZ5FGZ55J; 98185-20-7 (tartrate); (S)-3,5-dichloro-N-((1-ethylpyrrolidin-2-yl)methyl)-2-hydroxy-6-methoxybenzamide (2R,3R)-2,3-dihydroxysuccinate; (S)-(-)-3,5-Dichloro-N-((1-ethyl-2-pyrrolidinyl)methyl)-6-methoxysalicylamide L-(+)-tartrate; FLA 870; Raclopride tartrate

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: ~100 mg/mL (~288 mM)
H2O: ~0.1 mg/mL (~0.3 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。