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]Raclopride readily labels dopamine D₂ and D₃ receptors in brain tissue, but not D₄ receptors, due to its low affinity for D₄.[1]
In the human striatum, the density of D₂ receptors measured by [¹¹C]Raclopride binding was 1.7-1.8 times the density found using [¹¹C]methylspiperone, suggesting differences in binding to receptor monomers/dimers.[1]
Under therapeutic conditions, raclopride occupies between 60% and 75% of D₂ receptors in humans, as measured by [¹¹C]Raclopride PET imaging.[1]
Raclopride is classified as a typical neuroleptic (antipsychotic) that blocks D₂ receptors.[1]

Raclopride tartrate (0.1, 0.3, or 0.6 mg/kg; IP; 30 min; albino male mice; OF1 strain) dramatically shortens the amount of time that the mice spend engaging in aggressive behavior[2].

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Raclopride is a substituted benzamide with high selectivity as an antagonist of central dopaminergic D2 receptors and potential antipsychotic effects. In comparison with a classic DA receptor blocking agent like haloperidol, raclopride displays an atypical profile in preclinical tests for extrapyramidal side effects. Antiaggressive properties of raclopride on agonistic behavior have not yet been fully explored. In this work the effects of raclopride (0.1, 0.3, or 0.6 mg/kg) on aggressive and motor behaviors in male mice were studied. Aggression tests were performed 30 min after injections. Encounters were videotaped and behavior was evaluated, measuring the time spent in 11 broad categories of behavior. The results show a clear antiaggressive effect of raclopride, with very little motor impairment and some increase in exploratory behavior. This behavioral profile is very similar to the one observed with other atypical neuroleptics and differs somewhat from that found in the classic compounds.[2]

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Acute intraperitoneal administration of raclopride (0.1, 0.3, 0.6 mg/kg) produced a clear dose-dependent antiaggressive effect in isolated male mice, significantly reducing attack behavior compared to saline controls at all three doses (p < 0.02).[2]
Raclopride treatment did not cause significant motor impairment. Immobility times were minimal and did not increase significantly even at the highest dose (0.6 mg/kg).[2]
Nonsocial exploratory behavior showed a non-significant, dose-dependent increase following raclopride administration.[2]
The behavioral profile of raclopride (antiaggressive effect with minimal motor impairment) was similar to that of other atypical neuroleptics like sulpiride and clozapine, and different from classic neuroleptics like haloperidol which produce considerable motor impairment.[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

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)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)