| Drug Name: | Haloperidol (52-86-8) |
|---|---|
| PubChem ID: | 3559 |
| SMILES: | C1CN(CCC1(C2=CC=C(C=C2)Cl)O)CCCC(=O)C3=CC=C(C=C3)F |
| InchiKey: | LNEPOXFFQSENCJ-UHFFFAOYSA-N |
| Therapeutic Category: | Anti-Dyskinesia Agents, Antiemetics, Antipsychotic Agents, Autonomic Agents, Central Nervous System Agents, Central Nervous System Depressants, Dopamine Agents, Dopamine Antagonists, Gastrointestinal Agents, Neurotransmitter Agents, Peripheral Nervous System Agents, Psychotropic Drugs, Tranquilizing Agents |
| Molecular Weight (dalton) | : | 375.871 |
| LogP | : | 4.4256 |
| Ring Count | : | 2 |
| Hydrogen Bond Acceptor Count | : | 3 |
| Hydrogen Bond Donor Count | : | 1 |
| Total Polar Surface Area | : | 40.54 |
This panel provides information on interacting drugs and their ADRs along with references
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|---|---|---|
| Akathisia | D(2) dopamine receptor (P14416) | Antipsychotic response (D2@ D3@ D4)@antipsychotic-induced tardive dyskinesia (D3)@antipsychotic-induced acute akathisia (D3) [ ADR Type 2 ] | Pharmacogenetics and antipsychotic drugs |
| Akathisia | D(3) dopamine receptor (P35462) | Antipsychotic response (D2@ D3@ D4)@antipsychotic-induced tardive dyskinesia (D3)@antipsychotic-induced acute akathisia (D3) [ ADR Type 2 ] | Pharmacogenetics and antipsychotic drugs |
| Akathisia | D(4) dopamine receptor (P21917) | Antipsychotic response (D2@ D3@ D4)@antipsychotic-induced tardive dyskinesia (D3)@antipsychotic-induced acute akathisia (D3) [ ADR Type 2 ] | Pharmacogenetics and antipsychotic drugs |
| Detrimental Side Effects | Brain-derived neurotrophic factor (P23560) | Three days of haloperidol administration dramatically decreased BDNF immunostaining in the neurons @showing that blockade of dopaminergic receptors with haloperidol rapidly downregulates BDNF in reward and emotional centers of the brain@which leads to the efficacious or detrimental side effects of classical neuroleptic drugs [ ADR Type 5 ] | Changes in the pattern of brain-derived neurotrophic factor immunoreactivity in the rat brain after acute and subchronic haloperidol treatment |
| Detrimental Side Effects | dopaminergic receptors (P00014) | Three days of haloperidol administration dramatically decreased BDNF immunostaining in the neurons ,showing that blockade of dopaminergic receptors with haloperidol rapidly downregulates BDNF in reward and emotional centers of the brain,which leads to the efficacious or detrimental side effects of classical neuroleptic drugs. [ ADR Type 5 ] | Changes in the pattern of brain-derived neurotrophic factor immunoreactivity in the rat brain after acute and subchronic haloperidol treatment |
| Neuronal Apoptosis | Mitogen-activated protein kinase (P45983) | The c-Jun-NH(2)-terminal protein kinase and p38 mitogen-activated protein kinase were activated within 1 h and were sustained over the next 3 h following exposure of cortical neurons to haloperidol@which leads to Haloperidol-induced neuronal apoptosis [ ADR Type 2 ] | Haloperidol-induced neuronal apoptosis: role of p38 and c-Jun-NH(2)-terminal protein kinase |
| Neuronal Apoptosis | Mitogen-activated protein kinase 14 (Q16539) | The c-Jun-NH(2)-terminal protein kinase and p38 mitogen-activated protein kinase were activated within 1 h and were sustained over the next 3 h following exposure of cortical neurons to haloperidol@which leads to Haloperidol-induced neuronal apoptosis [ ADR Type 2 ] | Haloperidol-induced neuronal apoptosis: role of p38 and c-Jun-NH(2)-terminal protein kinase |
| Orofacial Dyskinesia | Catalase (P04040) | Coadministration of Ws extract significantly reduced the lipid peroxidation and significantly reversed the decrease in forebrain SOD and catalase levels,which strongly suggests that oxidative stress plays a significant role in HP-induced orofacial dyskinesia [ ADR Type 1 ] | Effect of Withania somnifera root extract on haloperidol-induced orofacial dyskinesia: possible mechanisms of action |
| Orofacial Dyskinesia | Superoxide dismutase (P00441) | Coadministration of Ws extract significantly reduced the lipid peroxidation and significantly reversed the decrease in forebrain SOD and catalase levels, which strongly suggests that oxidative stress plays a significant role in HP-induced orofacial dyskinesia [ ADR Type 1 ] | Effect of Withania somnifera root extract on haloperidol-induced orofacial dyskinesia: possible mechanisms of action |
| Parkinsonism | NADH-ubiquinone oxidoreductase chain 1 (P03886) | Haloperidol produces parkinsonism apparently through inhibition of NADH:ubiquinone oxidoreductase (complex I) of the mitochondrial electron transport chain. [ ADR Type 1 ] | Neuroleptic medications inhibit complex I of the electron transport chain |
| Seizures | G protein-activated inward rectifier potassium channel (P48549) | In oocytes co-injected with GIRK1 and GIRK2 mRNAs@ application of thioridazine immediately caused a reduction of inward currents through the basally active GIRK channels@underlies the side effect of seizures [ ADR Type 1 ] | Inhibition by various antipsychotic drugs of the G-protein-activated inwardly rectifying K(+) (GIRK) channels expressed in xenopus oocytes |
| Sinus Tachycardia | G protein-activated inward rectifier potassium channel (P48549) | In oocytes co-injected with GIRK1 and GIRK2 mRNAs@ application of thioridazine immediately caused a reduction of inward currents through the basally active GIRK channels@underlies the side effect of sinus tachycardia. [ ADR Type 1 ] | Inhibition by various antipsychotic drugs of the G-protein-activated inwardly rectifying K(+) (GIRK) channels expressed in xenopus oocytes |
| Tachycardia | G protein-activated inward rectifier potassium channel (P48549) | Antipsychotic drugs also inhibited the cardiac-type GIRK1/4 heteromultimeric channels@underlies the side effect of sinus tachycardia. [ ADR Type 1 ] | Inhibition by various antipsychotic drugs of the G-protein-activated inwardly rectifying K(+) (GIRK) channels expressed in xenopus oocytes |
| Tardive Dyskinesia | D(1A) dopamine receptor (P21728) | HP metabolites bind to the transporters for dopamine and serotonin@which is concerning a possible role of HP metabolites in the development of tardive dyskinesia. [ ADR Type 2 ] | Effects of haloperidol metabolites on neurotransmitter uptake and release: possible role in neurotoxicity and tardive dyskinesia |
| Tardive Dyskinesia | D(2) dopamine receptor (P14416) | Antipsychotic response (D2@ D3@ D4)@antipsychotic-induced tardive dyskinesia (D3)@antipsychotic-induced acute akathisia (D3) [ ADR Type 2 ] | Pharmacogenetics and antipsychotic drugs |
| Tardive Dyskinesia | D(3) dopamine receptor (P35462) | Antipsychotic response (D2@ D3@ D4)@antipsychotic-induced tardive dyskinesia (D3)@antipsychotic-induced acute akathisia (D3) [ ADR Type 2 ] | Pharmacogenetics and antipsychotic drugs |
| Tardive Dyskinesia | D(4) dopamine receptor (P21917) | Antipsychotic response (D2@ D3@ D4)@antipsychotic-induced tardive dyskinesia (D3)@antipsychotic-induced acute akathisia (D3) [ ADR Type 2 ] | Pharmacogenetics and antipsychotic drugs |
| Tardive Dyskinesia | Sodium-dependent serotonin transporter (P31645) | Haloperidol tetrahydropyridine (HPTP) inhibited the presynaptic uptake of dopamine and serotonin@ with greater affinity for the serotonin transporter@which is concerning a possible role of HP metabolites in the development of tardive dyskinesia [ ADR Type 1 ] | Effects of haloperidol metabolites on neurotransmitter uptake and release: possible role in neurotoxicity and tardive dyskinesia |
This panel provides drug-food interactions and their ADRs along with references
| Food | Toxicity | Reference |
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This panel provides information on metabolites and their ADRs along with references
| Metabolite | Toxicity | Place of Metabolism | Mechanism | Reference |
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This panel provides information on drug category