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Haloperidol | CAS No: 52-86-8 | GMP-certified suppliers
A medication that treats schizophrenia, psychotic disorders, Tourette’s syndrome, and severe behavioral problems in children and adults after other therapies have failed.
Therapeutic categories
Primary indications
- Haloperidol is indicated for a number of conditions including for the treatment of schizophrenia, for the manifestations of psychotic disorders, for the control of tics and vocal utterances of Tourette’s Disorder in children and adults, for treatment of severe behavior problems in children of combative, explosive hyperexcitability (which cannot be accounted for by immediate provocation)
- Haloperidol is also indicated in the short-term treatment of hyperactive children who show excessive motor activity with accompanying conduct disorders consisting of some or all of the following symptoms: impulsivity, difficulty sustaining attention, aggressivity, mood lability, and poor frustration tolerance
- Haloperidol should be reserved for these two groups of children only after failure to respond to psychotherapy or medications other than antipsychotics
Product Snapshot
- Haloperidol is available as an oral tablet and injectable solution suitable for intramuscular and intravenous administration
- It is primarily used for the treatment of schizophrenia, psychotic disorders, Tourette’s Disorder, and severe behavioral problems in children
- Haloperidol is approved for use in key regulatory markets including the United States and Canada
Clinical Overview
Pharmacologically, haloperidol exerts its clinical effects through strong antagonism of dopamine D2 receptors, predominantly within the mesolimbic and mesocortical pathways of the brain. This blockade mitigates the hyperdopaminergic state hypothesized to underlie the positive symptoms of schizophrenia such as hallucinations, delusions, and psychomotor agitation. Tight binding to dopamine D2 receptors also accounts for its propensity to cause extrapyramidal symptoms (EPS), including drug-induced parkinsonism, akathisia, dystonia, and tardive dyskinesia. The drug additionally interacts with 5-HT2 and α1-adrenergic receptors, though with less affinity, and blocks dopamine receptors in the chemoreceptor trigger zone contributing to its antiemetic action.
Haloperidol exhibits variable metabolism potentially influenced by polymorphic CYP2D6 activity, though clinical relevance remains inconsistent. It undergoes hepatic metabolism and its elimination is affected by multiple cytochrome P450 enzymes. Notably, haloperidol carries risks of QT interval prolongation and cardiac arrhythmias such as Torsades de Pointes, especially with intravenous administration or higher-than-recommended doses. Neuroleptic malignant syndrome, characterized by hyperpyrexia, rigidity, altered mental state, and autonomic instability, is a rare but serious adverse effect.
Though largely supplanted in many settings by atypical antipsychotics due to a more favorable side effect profile, haloperidol remains a benchmark in clinical research and specific therapeutic contexts. When sourcing haloperidol API, attention to stringent quality control is essential to ensure compliance with pharmacopeial standards, particularly regarding impurity profiles and batch consistency due to the drug’s narrow therapeutic index and safety considerations. Supply chain verification for regulatory compliance and consistency in physicochemical properties is critical to support formulation development and assure patient safety.
Identification & chemistry
| Generic name | Haloperidol |
|---|---|
| Molecule type | Small molecule |
| CAS | 52-86-8 |
| UNII | J6292F8L3D |
| DrugBank ID | DB00502 |
Pharmacology
| Summary | Haloperidol is a first-generation antipsychotic primarily exerting its therapeutic effects through potent antagonism of dopamine D2 receptors within the mesolimbic and mesocortical pathways, thereby modulating hyperdopaminergic activity associated with psychotic symptoms. It also exhibits secondary effects on serotonin 5-HT2 and alpha-adrenergic receptors. Its pharmacodynamics involve dopamine receptor blockade that contributes to antipsychotic efficacy as well as a risk of extrapyramidal motor side effects due to dopaminergic pathway interactions. |
|---|---|
| Mechanism of action | While haloperidol has demonstrated pharmacologic activity at a number of receptors in the brain, it exerts its antipsychotic effect through its strong antagonism of the dopamine receptor (mainly D2), particularly within the mesolimbic and mesocortical systems of the brain. Schizophrenia is theorized to be caused by a hyperdopaminergic state within the limbic system of the brain. Dopamine-antagonizing medications such as haloperidol, therefore, are thought to improve psychotic symptoms by halting this over-production of dopamine. The optimal clinical efficacy of antipsychotics is associated with the blockade of approximately 60 % - 80 % of D2 receptors in the brain. While the exact mechanism is not entirely understood, haloperidol is known to inhibit the effects of dopamine and increase its turnover. Traditional antipsychotics, such as haloperidol, bind more tightly than dopamine itself to the dopamine D2 receptor, with dissociation constants that are lower than that for dopamine. It is believed that haloperidol competitively blocks post-synaptic dopamine (D2) receptors in the brain, eliminating dopamine neurotransmission and leading to the relief of delusions and hallucinations that are commonly associated with psychosis. It acts primarily on the D2-receptors and has some effect on 5-HT2 and α1-receptors, with negligible effects on dopamine D1-receptors. The drug also exerts some blockade of α-adrenergic receptors of the autonomic system. Antagonistic activity regulated through dopamine D2 receptors in the chemoreceptive trigger zone (CTZ) of the brain renders its antiemetic activity. Of the three D2-like receptors, only the D2 receptor is blocked by antipsychotic drugs in direct relation to their clinical antipsychotic abilities. Clinical brain-imaging findings show that haloperidol remains tightly bound to D2 dopamine receptors in humans undergoing 2 positron emission tomography (PET) scans with a 24h pause in between scans. A common adverse effect of this drug is the development of extrapyramidal symptoms (EPS), due to this tight binding of haloperidol to the dopamine D2 receptor. Due to the risk of unpleasant and sometimes lifelong extrapyramidal symptoms, newer antipsychotic medications than haloperidol have been discovered and formulated. Rapid dissociation of drugs from dopamine D2 receptors is a plausible explanation for the improved EPS profile of atypical antipsychotics such as [DB00734]. This is also consistent with the theory of a lower affinity for D2 receptors for these drugs. As mentioned above, haloperidol binds tightly to the dopamine receptor, potentiating the risk of extrapyramidal symptoms, and therefore should only been used when necessary. |
| Pharmacodynamics | Use of the first-generation antipsychotics (including haloperidol) is considered highly effective for the management of the "positive" symptoms of schizophrenia including hallucinations, hearing voices, aggression/hostility, disorganized speech, and psychomotor agitation. However, this class is limited by the development of movement disorders such as drug-induced parkinsonism, akathisia, dystonia, and tardive dyskinesia, and other side effects including sedation, weight gain, and prolactin changes. Compared to the lower-potency first-generation antipsychotics such as [DB00477], [DB01624], [DB00623], and [DB01403], haloperidol typically demonstrates the least amount of side effects within class, but demonstrates a stronger disposition for causing extrapyramidal symptoms (EPS).[A180613, A180616, A180625] Low‐potency medications have a lower affinity for dopamine receptors so that a higher dose is required to effectively treat symptoms of schizophrenia. In addition, they block many receptors other than the primary target (dopamine receptors), such as cholinergic or histaminergic receptors, resulting in a higher incidence of side effects such as sedation, weight gain, and hypotension. The balance between the wanted drug effects on psychotic symptoms and unwanted side effects are largely at play within dopaminergic brain pathways affected by haloperidol. Cortical dopamine-D2-pathways play an important role in regulating these effects and include the nigrostriatal pathway, which is responsible for causing extrapyramidal symptoms (EPS), the mesolimbic and mesocortical pathways, which are responsible for the improvement in positive schizophrenic symptoms, and the tuberoinfundibular dopamine pathway, which is responsible for hyperprolactinemia. A syndrome consisting of potentially irreversible, involuntary, dyskinetic movements may develop in patients. Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome. Cases of sudden death, QT-prolongation, and Torsades de Pointes have been reported in patients receiving haloperidol. Higher than recommended doses of any formulation and intravenous administration of haloperidol appear to be associated with a higher risk of QT-prolongation and Torsades de Pointes. Although cases have been reported even in the absence of predisposing factors, particular caution is advised in treating patients with other QT-prolonging conditions (including electrolyte imbalance [particularly hypokalemia and hypomagnesemia], drugs known to prolong QT, underlying cardiac abnormalities, hypothyroidism, and familial long QT-syndrome). A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with antipsychotic drugs. Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status (including catatonic signs) and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmias). Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis) and acute renal failure. |
Targets
| Target | Organism | Actions |
|---|---|---|
| 5-hydroxytryptamine receptor 2C | Humans | |
| Dopamine D2 receptor | Humans | antagonist |
| 5-hydroxytryptamine receptor 2A | Humans | other/unknown |
ADME / PK
| Absorption | Haloperidol is a highly lipophilic compound and is extensively metabolized in humans, which may cause a large interindividual variability in its pharmacokinetics. Studies have found a wide variance in pharmacokinetic values for orally administered haloperidol with 1.7-6.1 hours reported for time to peak plasma concentration (tmax), 14.5-36.7 hours reported for half-life (t1⁄2), and 43.73 μg/L•h [range 14.89-120.96 μg/L•h] reported for AUC. Haloperidol is well-absorbed from the gastrointestinal tract when ingested orally, however, the first-pass hepatic metabolism decreases its oral bioavailability to 40 - 75%. After intramuscular administration, the time to peak plasma concentration (tmax) is 20 minutes in healthy individuals or 33.8 minutes in patients with schizophrenia, with a mean half-life of 20.7 hours. Bioavailability following intramuscular administration is higher than that for oral administration. Administration of haloperidol decanoate (the depot form of haloperidol for long-term treatment) in sesame oil results in slow release of the drug for long-term effects. The plasma concentrations of haloperidol gradually rise, reaching its peak concentration at about 6 days after the injection, with an apparent half-life of about 21 days. Steady-state plasma concentrations are achieved after the third or fourth dose. |
|---|---|
| Half-life | Following oral administration, the half-life was found to be 14.5-36.7 hours. Following intramuscular injection, mean half-life was found to be 20.7 hours. |
| Protein binding | Studies have found that free fraction of haloperidol in human plasma is 7.5-11.6%. This was found to be comparable among healthy adults, young adults, elderly patients with schizophrenia, and even in patients with liver cirrhosis. |
| Metabolism | Haloperidol is extensively metabolised in the liver with only about 1% of the administered dose excreted unchanged in urine. In humans, haloperidol is biotransformed to various metabolites, including p-fluorobenzoylpropionic acid, 4-(4-chlorophenyl)-4-hydroxypiperidine, reduced haloperidol, pyridinium metabolites, and haloperidol glucuronide. In psychiatric patients treated regularly with haloperidol, the concentration of haloperidol glucuronide in plasma is the highest among the metabolites, followed, in rank order, by unchanged haloperidol, reduced haloperidol and reduced haloperidol glucuronide. The drug is thought to be metabolized primarily by oxidative N-dealkylation of the piperidine nitrogen to form fluorophenylcarbonic acids and piperidine metabolites (which appear to be inactive), and by reduction of the butyrophenone carbonyl to the carbinol, forming _hydroxyhaloperidol_. The enzymes involved in the biotransformation of haloperidol include cytochrome P450 (CYP) including CYP3A4 and CYP2D6, carbonyl reductase and uridine di-phosphoglucose glucuronosyltransferase enzymes. The greatest proportion of the intrinsic hepatic clearance of haloperidol is performed by glucuronidation and followed by the reduction of haloperidol to reduced haloperidol and by CYP-mediated oxidation. In studies of cytochrome-mediated disposition in vitro, CYP3A4 appears to be the major isoform of the enzyme responsible for the metabolism of haloperidol in humans. The intrinsic clearance of the back-oxidation of reduced haloperidol to the parent compound, oxidative N-dealkylation and pyridinium formation are of the same order of magnitude. This suggests that the same enzyme system is responsible for the above three metabolic reactions. In vivo human studies on haloperidol metabolism have shown that the glucuronidation of haloperidol accounts for 50 to 60% of haloperidol biotransformation and that approximately 23% of the biotransformation was accounted for by the reduction pathway. The remaining 20 to 30% ofthe biotransformation of haloperidol would be via N-dealkylation and pyridinium formation. |
| Route of elimination | In radiolabeling studies, approximately 30% of the radioactivity is excreted in the urine following a single oral administration of 14C-labelled haloperidol, while 18% is excreted in the urine as haloperidol glucuronide, demonstrating that haloperidol glucuronide is a major metabolite in the urine as well as in plasma in humans. |
| Volume of distribution | The apparent volume of distribution was found to range from 9.5-21.7 L/kg. This high volume of distribution is in accordance with its lipophilicity, which also suggests free movement through various tissues including the blood-brain barrier. |
| Clearance | Following intravenous administration, the plasma or serum clearance (CL) was found to be 0.39-0.708 L/h/kg (6.5 to 11.8 ml/min/kg). Following oral administration, clearance was found to be 141.65 L/h (range 41.34 to 335.80 L/h). Haloperidol clearance after extravascular administration ranges from 0.9-1.5 l/h/kg, however this rate is reduced in poor metabolizers of C_YP2D6_ enzyme. Reduced CYP2D6 enzyme activity may result in increased concentrations of haloperidol. The inter-subject variability (coefficient of variation, %) in haloperidol clearance was estimated to be 44% in a population pharmacokinetic analysis in patients with schizophrenia . Genetic polymorphism of CYP2D6 has been demonstrated to be an important source of inter-patient variability in the pharmacokinetics of haloperidol and may affect therapeutic response and incidence of adverse effects. |
Formulation & handling
- Haloperidol is a small molecule API formulated for both oral and parenteral (intramuscular and intravenous) administration.
- It exhibits low water solubility, requiring careful consideration in injectable solution formulation to ensure adequate bioavailability.
- Handling precautions should include awareness of potential CNS effects potentiated by alcohol consumption, relevant for patient safety counseling but not affecting API stability.
Regulatory status
| Lifecycle | The active pharmaceutical ingredient is currently marketed in Canada and the US, with patent protection expired or nearing expiration, indicating a mature market with potential for generic competition. |
|---|
| Markets | Canada, US |
|---|
Supply Chain
| Supply chain summary | Haloperidol has a broad manufacturing base with numerous originator and generic companies involved in production, including several major pharmaceutical firms. Its branded products are primarily marketed in North America, specifically in the US and Canada. Given the extensive participation of generic manufacturers and the availability of multiple generic presentations, patent expirations have allowed for robust generic competition in this market. |
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Safety
| Toxicity | Acute oral toxicity (LD50): 71 mg/kg in rats [MSDS]. |
|---|
- Handle with appropriate personal protective equipment to prevent ingestion, inhalation, or skin contact due to high acute oral toxicity (LD50: 71 mg/kg in rats)
- Avoid generation of dust and ensure adequate ventilation during processing to minimize exposure risk
- Store in a secure, labeled container to prevent accidental ingestion or cross-contamination in the manufacturing environment
Haloperidol is a type of Atypical antipsychotics
Atypical antipsychotics belong to the subcategory of pharmaceutical active pharmaceutical ingredients (APIs) used in the treatment of various mental disorders, particularly schizophrenia and bipolar disorder. These medications are designed to alleviate the symptoms of psychosis by targeting specific neuroreceptors in the brain.
Unlike traditional antipsychotics, atypical antipsychotics exhibit a different pharmacological profile, providing a more favorable side effect profile and improved efficacy. These medications primarily act on dopamine and serotonin receptors, regulating the neurotransmitter levels in the brain to restore the chemical balance.
The mechanism of action of atypical antipsychotics involves blocking dopamine receptors, particularly D2 receptors, as well as modulating serotonin receptors, notably 5-HT2A receptors. By inhibiting excessive dopamine transmission and enhancing serotonin activity, atypical antipsychotics help reduce hallucinations, delusions, and other psychotic symptoms.
Some commonly used atypical antipsychotics include risperidone, olanzapine, quetiapine, and aripiprazole. These APIs are typically formulated into oral tablets or capsules for convenient administration.
Despite their effectiveness, atypical antipsychotics may have potential side effects such as weight gain, metabolic abnormalities, sedation, and extrapyramidal symptoms. Therefore, close monitoring and individualized treatment plans are essential to ensure optimal therapeutic outcomes.
In conclusion, atypical antipsychotics are a crucial subcategory of APIs used in the treatment of mental disorders. Their distinct pharmacological profile and mechanism of action make them valuable in managing psychosis while minimizing adverse effects.
Haloperidol (Atypical antipsychotics), classified under Antipsychotics
Antipsychotics belong to the pharmaceutical API (Active Pharmaceutical Ingredient) category used to treat psychiatric disorders such as schizophrenia, bipolar disorder, and other related conditions. These medications play a crucial role in managing symptoms associated with psychosis, including hallucinations, delusions, and disorganized thinking.
Antipsychotics work by modulating the levels of neurotransmitters in the brain, particularly dopamine and serotonin. They can be categorized into two classes: first-generation (typical) antipsychotics and second-generation (atypical) antipsychotics. Typical antipsychotics primarily target dopamine receptors, while atypical antipsychotics also affect serotonin receptors.
The pharmaceutical API category of antipsychotics includes various well-known drugs, such as haloperidol, chlorpromazine, risperidone, quetiapine, and olanzapine. These APIs are often formulated into different dosage forms, including tablets, capsules, injections, and oral suspensions, to provide flexibility in administration and patient-specific needs.
Antipsychotics offer relief from psychotic symptoms by stabilizing the imbalanced neurotransmitter activity in the brain. However, they may also have certain side effects, such as sedation, weight gain, extrapyramidal symptoms, and metabolic disturbances. It is essential for healthcare professionals to carefully monitor patients receiving antipsychotic treatment to optimize therapeutic benefits while minimizing adverse effects.
In summary, antipsychotics are a vital category of pharmaceutical APIs used to manage psychiatric disorders by modulating neurotransmitter activity in the brain. Their effectiveness in treating psychosis has made them a cornerstone of mental health treatment, providing much-needed relief to individuals suffering from these conditions.
Haloperidol API manufacturers & distributors
Compare qualified Haloperidol API suppliers worldwide. We currently have 10 companies offering Haloperidol API, with manufacturing taking place in 4 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Duchefa Farma B.V. | Distributor | Netherlands | Italy | BSE/TSE, CoA, GMP, ISO9001, MSDS | 170 products |
| Gedeon Richter | Producer | Hungary | Hungary | CoA, GMP | 48 products |
| Humble Healthcaare | Producer | India | India | CoA | 30 products |
| Janssen Pharma | Producer | Belgium | Unknown | CEP, CoA, GMP, USDMF | 63 products |
| Piramal Healthcare | Producer | United Kingdom | India | CoA, GMP | 31 products |
| Rpg Life Sciences | Producer | India | India | CEP, CoA, WC | 13 products |
| SETV Global | Producer | India | India | CoA, FDA, GMP | 515 products |
| Sicor | Producer | Italy | Italy | CoA, GMP | 47 products |
| Tenatra Exports Private L... | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, MSDS | 263 products |
| Vamsi Labs | Producer | India | India | BSE/TSE, CEP, CoA, FDA, GMP, ISO9001, MSDS, USDMF, WC, WHO-GMP | 29 products |
When sending a request, specify which Haloperidol API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Haloperidol API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
