Amisulpride

Research use only, not for human use.

Amisulpride(DAN 2163) is an antipsychotic drug, which is a selective dopamine antagonist.

Amisulpride(DAN 2163) is an antipsychotic drug, which is a selective dopamine antagonist (Ki=2.8 nM D2 receptor; Ki=3.2 nM D3 receptor).(In Vitro):Amisulpride is an atypical dopamine D2/D3 receptor antagonist with Kis of 2.8 and 3.2 nM for human dopamine D2 and D3, respectively. Amisulpride (100 nM) inhibits quinpirole-elicited [3H]thymidine incorporation with an IC50 value of 22±3 nM (n=3). Amisulpride slightly but significantly increases [3H]dopamine release from slices of the rat striatum (S2/S1=0.88±0.04 under control conditions, n=6; 1.04±0.08 in the presence of 100 nM Amisulpride,n=4; P<0.05) and opposes the inhibitory effects of 7-OH-DPAT in both brain areas.(In Vivo):Only the highest dose of Amisulpride (100 mg/kg) significantly reduces dopamine levels in the striatum or limbic system. Amisulpride significantly increases the synthesis of dopamine in the rat striatum and limbic system at doses of 20 and 100 mg/kg. Amisulpride (0.5 to 75 mg/kg) fails to provoke an additional increase in dopa accumulation in the striatum but slightly accelerates, at 75 mg/kg, dopamine synthesis in the limbic system. In comparison with vehicle-treated controls, Amisulpride (10 mg/kg) increases extracellular dopamine levels. The administration of Amisulpride (0.5 to 15 mg/kg s.c.) provokes a time- and dose-dependent increase in the stimulation-evoked dopamine release. Amisulpride decreases striatal ACh levels significantly at 30 and 100 mg/kg (87.5% and 56.3% of control levels, respectively). In both acute study, Amisulpride (70 mg/kg, p.o.) significantly increases the duration of swimming behavior [F(3,28)=45.90, p<0.01].

Amisulpride is an atypical dopamine D2/D3 receptor antagonist with Kis of 2.8 and 3.2 nM for human dopamine D2 and D3, respectively. Amisulpride (100 nM) inhibits quinpirole-elicited [3H]thymidine incorporation with an IC50 value of 22±3 nM (n=3). Amisulpride slightly but significantly increases [3H]dopamine release from slices of the rat striatum (S2/S1=0.88±0.04 under control conditions, n=6; 1.04±0.08 in the presence of 100 nM Amisulpride,n=4; P<0.05) and opposes the inhibitory effects of 7-OH-DPAT in both brain areas.

Only the highest dose of Amisulpride (100 mg/kg) significantly reduces dopamine levels in the striatum or limbic system. Amisulpride significantly increases the synthesis of dopamine in the rat striatum and limbic system at doses of 20 and 100 mg/kg. Amisulpride (0.5 to 75 mg/kg) fails to provoke an additional increase in dopa accumulation in the striatum but slightly accelerates, at 75 mg/kg, dopamine synthesis in the limbic system. In comparison with vehicle-treated controls, Amisulpride (10 mg/kg) increases extracellular dopamine levels. The administration of Amisulpride (0.5 to 15 mg/kg s.c.) provokes a time- and dose-dependent increase in the stimulation-evoked dopamine release. Amisulpride decreases striatal ACh levels significantly at 30 and 100 mg/kg (87.5% and 56.3% of control levels, respectively). In both acute study, Amisulpride (70 mg/kg, p.o.) significantly increases the duration of swimming behavior [F(3,28)=45.90, p<0.01].

DAN 2163 | Solian

Endocrinology/Hormones

5-HT Receptor

5-HT| Dopamine

Cancer

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71675-85-9

369.49

C17H27N3O4S

>98% (HPLC)

Ethanol: 74 mg/mL (200.28 mM); DMSO: 74 mg/mL (200.28 mM)

CCN1CCCC1CNC(=O)C1=CC(=C(N)C=C1OC)S(=O)(=O)CC

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(-20℃)

With Ice Pack

≥ 2 years