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Melperone
Skeletal formula of melperone
Space-filling model of the melperone molecule
Clinical data
Trade namesBuronil
AHFS/Drugs.comInternational Drug Names
Routes of
administration		Oral, intramuscular injection
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability87% (IM), 54% (Oral via syrup), 65% (Oral, tablet)[1]
Protein binding50%
MetabolismHepatic
Elimination half-life3–4 hours (oral)[1]
6 hours (IM)
ExcretionRenal (70% as metabolites, 5.5–10.4% as unchanged drug)[1][2]
Identifiers
  • 1-(4-fluorophenyl)-4-(4-methylpiperidin-1-yl)butan-1-one
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.107.027 Edit this at Wikidata
Chemical and physical data
FormulaC16H22FNO
Molar mass263.356 g·mol−1
3D model (JSmol)
  • Fc1ccc(cc1)C(=O)CCCN2CCC(CC2)C
  • InChI=1S/C16H22FNO/c1-13-8-11-18(12-9-13)10-2-3-16(19)14-4-6-15(17)7-5-14/h4-7,13H,2-3,8-12H2,1H3 checkY
  • Key:DKMFBWQBDIGMHM-UHFFFAOYSA-N checkY
  (verify)

Melperone (Bunil (PT), Buronil (AT, BE, CZ, DK, FI†, NL†, NO†, SE), Eunerpan (DE))[3] is an atypical antipsychotic of the butyrophenone chemical class, making it structurally related to the typical antipsychotic haloperidol. It first entered clinical use in 1960s.[4]

Marketing and indications

[edit]

It has been tried in treatment-resistant cases of schizophrenia with some (albeit limited) success.[4][5][6][7] It has also been reported effective in the treatment of L-DOPA and other forms of psychosis in Parkinson's disease[8] (although a multicentre, double-blind, placebo-controlled study conducted in 2012 failed to support these findings[9]). It is also known to possess anxiolytic properties.[10] It is marketed in the following countries:[3][11]

Adverse effects

[edit]

Melperone is reported to produce significantly less weight gain than clozapine and approximately as much weight gain as typical antipsychotics.[12] It is also purported to produce around as much prolactin secretion as clozapine (which is virtually nil).[13] It is also purported to produce sedative effects[14] and QT interval prolongation.[15] It is also known to produce less extrapyramidal side effects than the first-generation (typical) antipsychotic, thiothixene.[16] It can also produce (usually relatively mild) dry mouth.[17]

Other common adverse effects include[2][18][19]
Rare adverse effects include[2][18][19]
Unknown frequency adverse effects include[2][18][19]
  • Seizures (probably rare/uncommon)
  • Increased intraocular pressure
  • Intrahepatic cholestasis (probably rare)
  • Orthostatic hypotension (probably common)
  • Arrhythmias
  • Rash
  • Hyperprolactinemia (which can lead to e.g. galactorrhea, gynecomastia)
  • Weight gain
  • Increased appetite

Interactions

[edit]

Melperone is reported to be a CYP2D6 inhibitor.[20][21][22]

Pharmacology

[edit]

Melperone binds to the dopamine D2 receptor, just like all other clinically utilized antipsychotics, but it does so with a very low affinity and hence may be liable to rapidly dissociate from the D2 receptor hence potentially giving it the profile of an atypical antipsychotic.[23]

Receptor Ki [nM][24]
5-HT1A 2,200
5-HT1D 3,400
5-HT2A 230
5-HT2C 2,100
5-HT6 1,254
5-HT7 578
α1 180
α2 150
M1 >10,000
M2 2,400
M3 >10,000
M4 4,400
M5 >10,000
D2 194
D3 347
D4 555
H1 580

Synthesis

[edit]
Thieme Patents:[25][26] 86%:[27]

For the last step of the synthesis the sidechain 4-Chloro-4'-Fluorobutyrophenone [3874-54-2] (1) is attached to 4-Methylpiperidine (4-Pipecoline) [626-58-4] (2).

See also

[edit]

References

[edit]
[edit]
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Melperone

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Melperone is an atypical antipsychotic medication of the butyrophenone chemical class, characterized by its weak affinity for dopamine D2 receptors and low risk of extrapyramidal side effects, primarily used in Europe for the treatment of schizophrenia, agitation, confusion, and sleep disturbances in geriatric and psychiatric patients.[1] It has been employed clinically for over 30 years in the European Union, particularly in countries like Germany, where it is marketed under names such as Buronil for managing psychomotor agitation and behavioral disturbances associated with dementia.[1][2] Pharmacologically, melperone acts as an antagonist at both dopamine D2 and serotonin 5-HT2A receptors, contributing to its atypical profile with reduced incidence of motor side effects compared to typical antipsychotics like haloperidol, to which it is structurally related.[1] It exhibits rapid oral absorption with a bioavailability of 50-70%, a half-life of 3-4 hours, and hepatic metabolism followed by urinary elimination, allowing for short-term dosing in acute settings.[1] Early studies suggested its potential in treating psychosis associated with Parkinson's disease without exacerbating motor symptoms, but later clinical trials found it ineffective; sedation is a common adverse effect.[3][4] Developed in the mid-20th century as part of the butyrophenone series, melperone entered clinical use in Europe during the 1960s and has since been investigated for treatment-resistant schizophrenia, demonstrating efficacy in managing both positive and negative symptoms.[2][5] Despite its established role abroad, it remains investigational in the United States, with Phase II and III trials exploring its application in psychotic disorders, including a multicenter study that did not advance to approval.[1][6] Overdose risks include cardiac arrhythmias, underscoring the need for careful monitoring in therapeutic use.[1]

Introduction and History

Overview

Melperone is an atypical antipsychotic medication belonging to the butyrophenone chemical class, structurally related to the typical antipsychotic haloperidol, yet distinguished by its atypical properties, including a reduced risk of extrapyramidal side effects.[1][7] This classification stems from its balanced receptor profile, which contributes to a more favorable tolerability in clinical use compared to earlier butyrophenones.[8] Primarily employed in the management of psychoses, melperone is particularly indicated for elderly patients experiencing agitation, sleep disturbances, and behavioral issues associated with schizophrenia or other psychotic disorders.[1][2] It addresses symptoms such as confusion and psychomotor dysfunction in geriatric, psychiatric, and alcohol-dependent populations, offering a sedative option with anxiolytic benefits that supports its role in calming agitation without excessive motor impairment.[1][9]

Development and Clinical Introduction

Melperone was initially synthesized in the early 1960s by the Swedish pharmaceutical company Aktiebolag Ferrosan as part of ongoing research into butyrophenone derivatives, building on the success of haloperidol, which had been introduced as a potent typical antipsychotic in the late 1950s.[10] The compound, chemically known as 4'-fluoro-4-(4-methylpiperidin-1-yl)butyrophenone, was patented in 1963, with initial descriptions highlighting its potential antispasmodic and neuroleptic activities.[10] This development occurred amid a wave of interest in butyrophenone-class agents for psychiatric applications, aiming to refine therapeutic profiles beyond existing options. First clinical trials of melperone commenced in Europe during the mid-1960s, primarily evaluating its antipsychotic properties in patients with psychotic disorders.[11] These studies emphasized efficacy against core psychotic symptoms while observing a lower incidence of extrapyramidal motor side effects relative to contemporary typical antipsychotics like haloperidol.[11] Pharmacological investigations from this period, including distribution and toxicity assessments, supported progression to human testing, confirming melperone's tolerability at therapeutic doses.[12] Melperone entered clinical practice between 1965 and 1967, initially in Sweden and Germany, where it was marketed under the trade name Buronil in Sweden and Eunerpan in Germany by Ferrosan.[13] Early adoption focused on its role in managing acute psychotic states, with the drug positioned as a milder alternative within the butyrophenone family. Key early studies, including double-blind comparisons conducted in the late 1960s and early 1970s, demonstrated melperone's effectiveness in reducing symptoms of schizophrenia and agitation, often at doses of 100-300 mg daily. These findings contributed to its later recognition for atypical properties, distinguished by a favorable side-effect profile despite its structural relation to typical butyrophenones.[14] Regulatory approvals followed, granting prescription-only status across several European countries by the 1970s, though global expansion was constrained by the subsequent rise of second-generation antipsychotics.[1][14] As of 2025, melperone continues to be available by prescription in several European countries for its established indications.[1]

Medical Applications

Indications and Efficacy

Melperone is primarily indicated for the treatment of schizophrenia and other psychotic disorders, particularly in cases involving agitation, sleep disturbances, and behavioral disturbances in elderly patients, including those associated with dementia.[1][2] It has been established as an effective option for managing acute and chronic symptoms of schizophrenia in European clinical practice, with approvals focusing on its role in reducing hallucinations, delusions, and psychomotor agitation without significant motor side effects.[1] In geriatric populations, its sedative and anxiolytic effects make it suitable for addressing restlessness and confusion associated with psychoses, offering a lower risk of cognitive decline compared to typical antipsychotics.[1] Clinical evidence supports moderate efficacy in improving positive symptoms of schizophrenia, such as hallucinations and delusions, as demonstrated in randomized trials where melperone at 300 mg/day was comparable to thiothixene and superior to placebo in reducing overall psychopathology.[15][16] A case series of 17 patients with treatment-refractory schizophrenia reported that 41% continued melperone long-term, with responders showing 24–61% reductions in Brief Psychiatric Rating Scale (BPRS) scores, particularly in positive and negative symptoms, over 12–24 months.[11] Another 2011 case series in 21 refractory patients found limited overall response (only 14% continued treatment), but highlighted its utility in a subset intolerant to clozapine, with notable improvements in global functioning for those who benefited.[17] Across studies, melperone consistently exhibits a low incidence of extrapyramidal symptoms (EPS), attributed to its atypical profile, making it preferable for long-term use in symptom management.[15][11] Off-label applications include the management of confusion, psychomotor dysfunction, and L-DOPA-induced psychosis in Parkinson's disease patients, though evidence is limited. A 2012 randomized controlled trial concluded that melperone was ineffective for Parkinson's disease psychosis, showing no significant symptom reduction despite tolerability.[4] In comparative terms, melperone shares prolactin-sparing effects similar to clozapine, with both drugs showing minimal elevations in plasma prolactin levels compared to typical antipsychotics, though melperone may cause slightly higher increases in some female patients.[18] However, it appears less effective than second-generation atypicals like risperidone or olanzapine in broader schizophrenia trials, where response rates for refractory cases are lower than clozapine's 30–60%. Despite this, its favorable profile in elderly and treatment-resistant populations positions it as a targeted alternative where sedation and low EPS risk are prioritized.[11]

Dosage and Administration

Melperone is available in oral formulations including film-coated tablets of 10 mg, 25 mg, 50 mg, and 100 mg strengths, as well as an oral solution at 25 mg/5 mL.[1] In Europe, it is also supplied as an intramuscular injection for acute settings.[1] Oral administration is preferred for maintenance therapy and should be taken with food to reduce gastrointestinal upset, ideally in divided doses with the largest portion given in the evening to capitalize on its sedative properties.[19] For schizophrenia in adults, treatment typically begins with an initial oral dose of 25 mg at bedtime, titrated gradually based on tolerability to a maintenance range of 100–200 mg per day in divided doses.[19] In non-refractory cases, doses of 100–300 mg daily are standard, while refractory schizophrenia may require up to 600 mg per day under specialist oversight.[20] For acute agitation, an intramuscular dose of 50–100 mg may be administered initially, with repeats as needed up to a maximum of 200 mg per day.[21] In elderly patients, dosing should start at a lower level of 10–25 mg daily to minimize sedation risk, with cautious titration individualized to response.[2] Melperone is not recommended for children under 18 years due to limited safety data in pediatric populations.[1] For patients with hepatic impairment, dose reductions are advised given its primary hepatic metabolism and potential for non-linear pharmacokinetics at higher doses.[22] Long-term use is appropriate for chronic psychoses, with efficacy monitoring via clinical scales such as the Brief Psychiatric Rating Scale recommended at baseline, 6 weeks, 3 months, and subsequent reviews every 6 months.[19] Prescribing is generally initiated and supervised by psychiatrists, with regular assessment for ongoing need.[20]

Safety and Tolerability

Adverse Effects

Melperone is generally well-tolerated, particularly in patients with schizophrenia, due to its low incidence of extrapyramidal symptoms (EPS) compared to typical antipsychotics like haloperidol.[1][5] However, like other antipsychotics, it is associated with increased mortality in elderly patients with dementia-related psychosis.[23] Long-term studies spanning 1 to 15 years have reported no severe side effects definitively attributable to the drug.[24] Common adverse effects include sedation or drowsiness, dry mouth, dizziness, orthostatic hypotension, and constipation.[25][26] These anticholinergic and sedative properties are often more pronounced during initial treatment and contribute to its utility in agitation but may require dose adjustments.[19] Less common effects encompass mild weight gain (significantly less than with clozapine), fatigue, and blurred vision.[27][25] Weight changes with melperone are comparable to those seen with typical neuroleptics but remain modest overall.[27] Rare but serious adverse effects include QT interval prolongation (with potential risk of torsades de pointes) and neuroleptic malignant syndrome.[19][25] Melperone exhibits a unique tolerability profile with minimal EPS such as dystonia or parkinsonism relative to typical antipsychotics, and low prolactin elevation that reduces risks of sexual dysfunction.[1][5] Management strategies include dose reduction to alleviate sedation and routine ECG monitoring for QT prolongation risk in patients with predisposing factors like cardiac history.[19]

Contraindications and Drug Interactions

Melperone is contraindicated in patients with known hypersensitivity to the drug or other butyrophenones, as this can lead to severe allergic reactions.[28] It is also absolutely contraindicated in cases of severe central nervous system (CNS) depression, including comatose states or intoxication with CNS depressants such as alcohol or sedatives, due to the risk of exacerbated respiratory and cardiovascular suppression.[28] Additional contraindications include pheochromocytoma, a history of neuroleptic malignant syndrome, severe hepatic or renal impairment, angle-closure glaucoma, prostatic hypertrophy with urinary retention, paralytic ileus, myasthenia gravis, and Parkinson's disease.[28] Furthermore, melperone should not be used in patients with a history of QT interval prolongation, congenital long QT syndrome, or conditions predisposing to arrhythmias, such as hypokalemia, as it may further extend the QT interval and increase the risk of torsades de pointes.[28][19] Relative precautions are advised for patients with cardiovascular disease, where melperone's potential to cause orthostatic hypotension and QT prolongation necessitates careful monitoring to mitigate risks of syncope or cardiac events.[28] In individuals with epilepsy or conditions that lower the seizure threshold, melperone should be used cautiously, as antipsychotics in the butyrophenone class can potentially exacerbate seizure activity.[1] Hepatic impairment requires dose adjustment or avoidance in severe cases, given melperone's metabolism via hepatic cytochrome P450 enzymes, which may lead to accumulation and heightened toxicity.[28][29] Pharmacokinetic interactions arise primarily from melperone's inhibition of CYP2D6, which can elevate plasma levels of CYP2D6 substrates such as tricyclic antidepressants (e.g., nortriptyline), potentially increasing their toxicity like cardiotoxicity or anticholinergic effects.[30][31] Conversely, CYP3A4 inducers such as rifampin may accelerate melperone's metabolism, reducing its efficacy and requiring dose escalation.[1] Pharmacodynamic interactions include additive CNS depression and sedation when combined with benzodiazepines or alcohol, heightening risks of respiratory depression and impaired psychomotor function.[28][1] Melperone may potentiate QT prolongation when used with antiarrhythmics like amiodarone, increasing arrhythmia risk, and can enhance extrapyramidal symptoms (EPS) when co-administered with other antipsychotics, though concurrent use is generally avoided except during brief cross-titration periods.[28][19] Monitoring recommendations include baseline electrocardiogram (ECG) to assess QT interval and liver function tests, with periodic follow-up to detect changes, particularly in at-risk patients.[19][28] Melperone use during pregnancy should be avoided unless benefits clearly outweigh risks, with limited human data available; monitoring for neonatal effects is recommended if used near term.[28]

Pharmacology

Mechanism of Action

Melperone exerts its primary antipsychotic effects through low-affinity antagonism at dopamine D2 receptors, with a binding affinity (Ki) of 180 nM, which allows for blockade of hyperdopaminergic activity in the mesolimbic pathway to alleviate positive symptoms of schizophrenia while minimizing extrapyramidal side effects (EPS) due to its rapid dissociation kinetics from the receptor.[32] This loose binding profile enables transient occupancy, permitting physiological dopamine signaling in nigrostriatal pathways, in contrast to high-affinity typical antipsychotics that cause prolonged blockade and motor disturbances.[33] Secondary pharmacological actions include antagonism at serotonin 5-HT2A receptors (Ki = 120 nM), which contributes to its atypical antipsychotic profile by enhancing dopamine release in the prefrontal cortex and providing anxiolytic benefits through modulation of serotonergic tone.[32] Additionally, melperone blocks alpha-1 adrenergic receptors (Ki = 180 nM), leading to sedative effects and potential orthostatic hypotension via central and peripheral sympatholytic activity.[34] Moderate affinity for histamine H1 receptors (Ki = 580 nM) further promotes sedation, while binding to muscarinic acetylcholine receptors is minimal (Ki > 10,000 nM), resulting in negligible anticholinergic side effects.[34] Melperone shows low activity at dopamine D1 and D4 receptors, with affinities exceeding 100 nM, avoiding significant interference with cognitive or reward-related pathways mediated by these subtypes.[35] Animal microdialysis studies demonstrate that melperone increases dopamine release in the rat medial prefrontal cortex in a dose-dependent manner (3–10 mg/kg), an effect attributed to combined D2/5-HT2A antagonism that indirectly activates 5-HT1A receptors and disinhibits cortical dopaminergic neurons.[36] The atypical classification of melperone stems from its D2/5-HT2A receptor blockade ratio (Ki D2 / Ki 5-HT2A approximately 1.5), which spares the tuberoinfundibular pathway and results in minimal prolactin elevation compared to typical antipsychotics.[37] This profile supports its efficacy in schizophrenia with reduced endocrine disruptions.[38]

Pharmacokinetics

Melperone is rapidly absorbed following oral administration, with a bioavailability of 50-70% for syrup and tablet formulations. Peak plasma concentrations are attained within 1-2 hours orally and more rapidly with intramuscular injection.[1][39] The drug exhibits a volume of distribution of approximately 1.5 L/kg, reflecting tissue penetration. Melperone is bound to plasma proteins (85-90%) and effectively crosses the blood-brain barrier to exert its central effects.[40] Metabolism occurs primarily in the liver and produces minimal active metabolites. Melperone acts as a CYP2D6 inhibitor, which can affect co-administered drugs metabolized by this enzyme.[1][30] Elimination involves renal excretion predominantly as metabolites, with less than 1% of the parent drug recovered unchanged in urine. The elimination half-life is 3-4 hours following oral dosing and approximately 6 hours after intramuscular administration, allowing steady-state plasma levels to be reached within 1-2 days of regular dosing.[1][39] In special populations, such as the elderly or those with hepatic impairment, the half-life is prolonged due to diminished metabolic capacity, often requiring dose reductions to avoid accumulation and enhanced adverse effects.[41]

Chemistry

Chemical Structure and Properties

Melperone has the IUPAC name 1-(4-fluorophenyl)-4-(4-methylpiperidin-1-yl)butan-1-one and the alternative systematic name 4'-fluoro-4-(4-methylpiperidin-1-yl)butyrophenone. Its molecular formula is C₁₆H₂₂FNO, with a molecular weight of 263.35 g/mol. The core structure is that of a butyrophenone, featuring a 4-fluorophenyl ring attached to a carbonyl group at one end of a butanone chain and a 4-methylpiperidine moiety at the other end via a tertiary amine linkage. This arrangement contributes to its classification as an atypical antipsychotic within the butyrophenone family. The compound appears as a white to off-white crystalline powder. It melts at 78–82 °C and boils at 120–125 °C under reduced pressure (0.1 Torr). Melperone exhibits low aqueous solubility, approximately 0.049 mg/mL in water at physiological pH, rendering it sparingly soluble, while it is readily soluble in organic solvents such as ethanol (up to 20 mg/mL) and chloroform. Melperone is chemically stable under standard storage conditions, including refrigeration at -20 °C in a desiccated environment to prevent degradation. It is sensitive to light exposure, with recommendations to store it in the original packaging for protection. The piperidine nitrogen has a pKa of 8.9, indicating moderate basicity that influences its ionization and solubility profile in biological media. Structurally, melperone bears close resemblance to haloperidol, another butyrophenone antipsychotic, differing primarily in the halogen substituent on the phenyl ring (fluoro in melperone versus chloro in haloperidol); this substitution modulates lipophilicity, with melperone showing a calculated logP of 3.23 compared to haloperidol's higher value.

Synthesis

Melperone, chemically known as 1-(4-fluorophenyl)-4-(4-methylpiperidin-1-yl)butan-1-one, is primarily synthesized through a nucleophilic substitution reaction between 4-methylpiperidine and 4-chloro-1-(4-fluorophenyl)butan-1-one (γ-chloro-p-fluorobutyrophenone) in the presence of a base such as excess 4-methylpiperidine acting as an acid scavenger.[42] This key step typically occurs in a solvent like toluene at 100-110°C for 15 hours, with a catalytic amount of potassium iodide added to minimize side reactions and improve efficiency.[42] The reaction proceeds via an SN2 mechanism, where the nitrogen of 4-methylpiperidine displaces the chloride leaving group at the γ-position of the butyrophenone chain. The precursor, 4-chloro-1-(4-fluorophenyl)butan-1-one, is prepared in a prior step through Friedel-Crafts acylation of fluorobenzene with 4-chlorobutyryl chloride using anhydrous aluminum chloride as the Lewis acid catalyst.[43] This reaction is conducted in dichloromethane at 20°C for 4 hours, followed by quenching with ice water, extraction of the organic phase, drying over anhydrous sodium sulfate, and concentration under reduced pressure at 50°C, affording the precursor in 90% yield with 99% purity.[43] An alternative preparation of the precursor involves chlorination of 1-(4-fluorophenyl)butan-1-one at the γ-position, though the direct acylation route is more commonly employed due to its simplicity and high yield. Following the substitution, the crude melperone base is isolated by filtration and extraction, then converted to the hydrochloride salt by treatment with hydrochloric acid. Purification is achieved through distillation of the base under vacuum (110-125°C at <0.1 mmHg) followed by recrystallization of the salt from ethanol/ether, yielding 73% overall from the substitution step and a melting point of 209-211°C for the hydrochloride.[42] Typical laboratory yields for the full process range from 70-85%, with industrial-scale production optimized through refined conditions to achieve pharmaceutical-grade purity exceeding 99% via additional recrystallization or chromatography.[44] To enhance yields and reduce side reactions such as intramolecular cyclization of the ketone, a protected variant of the primary route is used in modern processes. The ketone group of 4-chloro-1-(4-fluorophenyl)butan-1-one is first protected as a dimethyl ketal by reaction with trimethoxymethane and methanol in the presence of sulfuric acid catalyst at 20-30°C, proceeding quantitatively.[44] The ketal then undergoes nucleophilic substitution with 4-methylpiperidine under basic conditions (e.g., sodium carbonate) and a phase-transfer catalyst like tetrabutylammonium hydrogensulfate in toluene at 90-105°C for 7-9 hours. Deprotection of the ketal occurs under acidic aqueous conditions, followed by crystallization of the base from hexane/heptane (overall yield >60%) and salt formation with HCl gas in ethyl acetate (>80% yield for the salting step).[44] An alternative, less common route to melperone involves a Grignard reaction on 4-fluorobenzonitrile with a 3-chloropropylmagnesium halide to form the chloroketone intermediate, followed by attachment of 4-methylpiperidine, though this method is rarely detailed in primary literature due to challenges in chain length control and lower selectivity compared to the acylation-substitution sequence. The original synthesis of melperone was developed in the 1960s by researchers at Ferrosan AB, with the first patents filed in 1963 describing the core alkylation approach; the key U.S. patent for the process was issued in 1974, and related patents expired in the 1980s.[42]

References

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  2. What is Melperone Hydrochloride used for? - Patsnap Synapse
  3. Melperone - an overview | ScienceDirect Topics
  4. https://www.sciencedirect.com/science/article/pii/S1353802010001112
  5. Melperone in the treatment of neuroleptic-resistant schizophrenia
  6. Melperone (an Anti-Psychotic) in Patients With Psychosis ...
  7. Melperone - an overview | ScienceDirect Topics
  8. The effect of melperone, an atypical antipsychotic drug, on cognitive ...
  9. Melperone in Low Doses in Anxious Neurotic Patients. A Double ...
  10. What is the mechanism of Melperone Hydrochloride?
  11. melperone | C16H22FNO - ChemSpider
  12. 3.5 Chemistry - Wiley Online Library
  13. Auditing Clinical Outcomes after Introducing Off-Licence Prescribing ...
  14. Melperone
  15. [Methylperon. (Buronil "Ferrosan"). A new butyrophenone neuroleptic]
  16. Contrasting Typical and Atypical Antipsychotic Drugs | Focus
  17. A comparison of two doses of melperone, an atypical antipsychotic ...
  18. Melperone in Treatment-Refractory Schizophrenia: A Case Series
  19. Melperone is ineffective in treating Parkinson's disease psychosis
  20. Melperone, an aytpical antipsychotic drug with clozapine-like effect ...
  21. Pharmacokinetics of parenteral and oral melperone in man - PubMed
  22. [PDF] Guidelines for the Use of Melperone
  23. [PDF] Guidelines for the Use of Melperone - KMPT formulary
  24. MELPERONE - JoDrugs
  25. Pharmacokinetics of parenteral and oral melperone in man
  26. Additional studies on side effects of melperone in long-term therapy ...
  27. Showing metabocard for Melperone (HMDB0254429)
  28. What are the side effects of Melperone Hydrochloride?
  29. Changes in weight and body mass index during treatment ... - PubMed
  30. Melperon-neuraxpharm : Uses, Side Effects, Interactions, Dosage ...
  31. Melperone Medication: Uses, Dosage, and Side Effects Explained
  32. Melperone is an inhibitor of the CYP2D6 catalyzed O-demethylation ...
  33. Melperone but Not Bisoprolol or Metoprolol Is a Clinically ... - PubMed
  34. Melperone hydrochloride | 1622-79-3 | Benchchem
  35. Rapid Release of Antipsychotic Drugs From Dopamine D2 Receptors
  36. Melperone hydrochloride | Antipsychotic Agent | MedChemExpress
  37. D4 dopamine receptor binding affinity does not distinguish between ...
  38. Atypical antipsychotic drugs, quetiapine, iloperidone, and ...
  39. The ratios of serotonin2 and dopamine2 affinities ... - PubMed - NIH
  40. The effect of melperone, an atypical antipsychotic drug, on cognitive ...
  41. melperone - Drug Central
  42. P-glycoprotein is a factor in the uptake of dextromethorphan, but not ...
  43. Current Status of Therapeutic Drug Monitoring in Mental Health ...
  44. https://patents.google.com/patent/US3816433A/en
  45. 4-Chloro-4'-fluorobutyrophenone synthesis - ChemicalBook
  46. IE20000051A1 - Melperone - Google Patents
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