Remoxipride
Remoxipride Uses, Dosage, Side Effects, Food Interaction and all others data.
Remoxipride is an atypical antipsychotic agent that is specific for dopamine D2 receptors. It gained approval in the UK in 1989 but was withdrawn in 1993 after it was found to be associated with an increased incidence of aplastic anemia.
Remoxipride is a weak selective dopamine D2 receptor antagonist that was once used in the treatment of schizophrenia. It has a moderate therapeutic index and duration of action. Remoxipride was withdrawn due to deaths associated with aplastic anemia.
| Trade Name | Remoxipride |
| Generic | Remoxipride |
| Remoxipride Other Names | Remoxiprida, Remoxipride, Remoxipridum |
| Type | |
| Formula | C16H23BrN2O3 |
| Weight | Average: 371.269 Monoisotopic: 370.089205259 |
| Protein binding | Remoxipride is approximately 80% protein bound, mainly to α-1-acid glycoprotein. |
| Groups | Approved, Withdrawn |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Remoxipride is an discontinued atypical antipsychotic selective for dopamine D2 receptors.
Remoxipride is an atypical antipsychotic once used for the treatment of schizophrenia.
How Remoxipride works
Remoxipride is an atypical antipsychotic dopamine D2 antagonist. Chronic use upregulates the expression of D2 receptors, while downregulating the expression of D1 and D5 receptors in the prefrontal cortex. This activity may be related to the antipsychotic activity of remoxipride. Remoxipride displays weaker binding to D2 dopaminergic receptors that dopamine. This weaker binding is thought to account for the reduced incidence of Parkinsonism. Remoxipride also increases expression of the protein Fos in the nucleus accumbens but not the dorsolateral striatum, which may be responsible for a reduced incidence of extrapyramidal symptoms.
Toxicity
Remoxipride was withdrawn from the market after 8 cases of aplastic anemia were reported. Of those 8 cases, 2 were fatal.
Volume of Distribution
The volume of distribution of remoxipride in patients with normal creatinine clearance is 44.3 ± 8.3 L, in patients with moderate renal impairment is 37.4 ± 16.2 L, and in patients with severe renal impairment is 30.2 ± 9.4 L.
Elimination Route
Remoxipride is approximately 90% bioavailable. In patients with normal creatinine clearance, remoxipride reaches a Cmax of 5.5 ± 1.1 µmol/L, with a Tmax of 0.8 ± 0.2 h, and an AUC of 39 ± 9 µmol*h/L. In patients with moderate renal impairment, remoxipride reaches a Cmax of 7.7 ± 2.7 µmol/L, with a Tmax of 0.9 ± 0.4 h, and an AUC of 63 ± 34 µmol*h/L. In patients with severe renal impairment, remoxipride reaches a Cmax of 9.3 ± 2.3 µmol/L, with a Tmax of 1.4 ± 0.9 h, and an AUC of 123 ± 60 µmol*h/L.
Half Life
The half life of remoxipride in patients with normal creatinine clearance is 5.1 ± 1.6 h, in patients with moderate renal impairment is 6.1 ± 2.6 h, and in patients with severe renal impairment is 9.9 ± 3.8 h.
Clearance
The renal clearance of remoxipride in patients with normal creatinine clearance is 23.6 ± 7.0 mL/min, in patients with moderate renal impairment is 9.3 ± 3.8 mL/min, and in patients with severe renal impairment is 3.7 ± 2.9 mL/min. The systemic plasma clearance of remoxipride is 120 mL/min.
Elimination Route
A dose of remoxipride is 89% recovered in the urine and 7% in the feces. 10-40% of a dose of remoxipride is recovered in the urine as the unchanged parent drug.
Innovators Monograph
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