Controversially, some psychiatric patients may be given chlorpromazine by force, even if they do not suffer any of the typical conditions the drug is prescribed for.[12]
A 2014 systematic review carried out by Cochrane included 55 trials that compared the effectiveness of chlorpromazine versus placebo for the treatment of schizophrenia. Compared to the placebo group, patients under chlorpromazine experienced less relapse during 6 months to 2 years follow-up. No difference was found between the two groups beyond two years of follow-up. Patients under chlorpromazine showed a global improvement in symptoms and functioning. The systematic review also highlighted the fact that the side effects of the drug were 'severe and debilitating', including sedation, considerable weight gain, a lowering of blood pressure, and an increased risk ofacute movement disorders. They also noted that the quality of evidence of the 55 included trials was very low and that 315 trials could not be included in the systematic review due to their poor quality. They called for further research on the subject, as chlorpromazine is a cheap benchmark drug and one of the most used treatments for schizophrenia worldwide.[14]
Chlorpromazine has also been used inporphyria and as part oftetanus treatment. It is still recommended for short-term management of severe anxiety and psychotic aggression. Resistant and severehiccups, severenausea/emesis, andpreanesthetic conditioning are other uses.[15][16] Symptoms ofdelirium in hospitalizedAIDS patients have been effectively treated with low doses of chlorpromazine.[17]
Chlorpromazine is occasionally used off-label for treatment of severemigraine.[18][19] It is often, particularly aspalliation, used in small doses to reduce nausea byopioid-treated cancer patients and to intensify and prolong the analgesia of the opioids as well.[18][20] Efficacy has been shown in treatment of symptomatichypertensive emergency.
In Germany, chlorpromazine still carries label indications forinsomnia, severepruritus, and preanesthesia.[21]
Chlorpromazine has been used as ahallucinogen antidote or "trip killer" to block the effects ofserotonergic psychedelics likepsilocybin,lysergic acid diethylamide (LSD), andmescaline.[22][23][24][25] However, it was said to not be completely effective and could exacerbate symptoms under certain situations.[22] The results of clinical studies of chlorpromazine for this use have been inconsistent, with reduced effects, no change in effects, and even enhanced effects all reported.[23]Intravenous chlorpromazine is described as completely abolishing the autonomic and psychoactive effects of LSD, whereasoral chlorpromazine is said to be much less effective.[26]
Chlorpromazine and other phenothiazines have been demonstrated to possess antimicrobial properties, but are not currently used for this purpose except for a very small number of cases. For example, Mikiet al. 1992 trialed daily doses of chlorpromazine, reversingchloroquine resistance inPlasmodium chabaudi isolates inmice.[27] Weekset al., 2018 find that it also possesses a wide spectrumanthelmintic effect.[28]
Previoushypersensitivity (including jaundice, agranulocytosis, etc.) to phenothiazines, especially chlorpromazine, or any of the excipients in the formulation being used.
There appears to be a dose-dependent risk for seizures with chlorpromazine treatment.[32]Tardive dyskinesia (involuntary, repetitive body movements) andakathisia (a feeling of inner restlessness and inability to stay still) are less commonly seen with chlorpromazine than they are with high potency typical antipsychotics such ashaloperidol[33] ortrifluoperazine, and some evidence suggests that, with conservative dosing, the incidence of such effects for chlorpromazine may be comparable to that of newer agents such asrisperidone orolanzapine.[34]
Chlorpromazine may deposit in ocular tissues when taken in high dosages for long periods of time.
5 times more likely to have considerable weight gain, around 40% with chlorpromazine gaining weight
RR 4.9 CI 2.3 to 10.4
Very low(estimate of effect uncertain)
Sedation
3 times more likely to cause sedation, around 30% with chlorpromazine
RR 2.8 CI 2.3 to 3.5
Acute movement disorder
3.5 times more likely to cause easily reversible but unpleasant severe stiffening of muscles, around 6% with chlorpromazine
RR 3.5 CI 1.5 to 8.0
Parkinsonism
2 times more likely to cause parkinsonism (symptoms such as tremor, hesitancy of movement, decreased facial expression), around 17% with chlorpromazine
RR 2.1 CI 1.6 to 2.8
Decreased blood pressure with dizziness
3 times more likely to cause decreased blood pressure and dizziness, around 15% with chlorpromazine
TheBritish National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse.[35] Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite.[36] Other symptoms may include restlessness, increased sweating, and trouble sleeping.[36] Less commonly, there may be a feeling of the world spinning, numbness, or muscle pains.[36] Symptoms generally resolve after a short period of time.[36]
There is tentative evidence that discontinuation of antipsychotics can result in psychosis.[37] It may also result in reoccurrence of the condition that is being treated.[38] Rarely, tardive dyskinesia can occur when the medication is stopped.[36]
Consuming food prior to taking chlorpromazine orally limits its absorption; likewise, cotreatment withbenztropine can also reduce chlorpromazine absorption.[4]Alcohol can also reduce chlorpromazine absorption.[4] Antacids slow chlorpromazine absorption.[4]Lithium and chronic treatment withbarbiturates can increase chlorpromazine clearance significantly.[4]Tricyclic antidepressants (TCAs) can decrease chlorpromazine clearance and hence increase chlorpromazine exposure.[4] Cotreatment withCYP1A2 inhibitors likeciprofloxacin,fluvoxamine orvemurafenib can reduce chlorpromazine clearance and hence increase exposure and potentially also adverse effects.[4] Chlorpromazine can also potentiate the CNS depressant effects of drugs likebarbiturates,benzodiazepines,opioids, lithium and anesthetics and hence increase the potential for adverse effects such asrespiratory depression andsedation.[4]
Chlorprozamine is also a moderate inhibitor ofCYP2D6 and a substrate forCYP2D6 and hence can inhibit its own metabolism.[15] It can also inhibit the clearance ofCYP2D6 substrates such asdextromethorphan, potentiating their effects.[15] Other drugs likecodeine andtamoxifen, which requireCYP2D6-mediated activation into their respective active metabolites, may have their therapeutic effects attenuated.[15] Likewise,CYP2D6 inhibitors such asparoxetine orfluoxetine can reduce chlorpromazine clearance, increasing serum levels of chlorpromazine and potentially its adverse effects.[4] Chlorpromazine also reducesphenytoin levels and increasesvalproic acid levels.[4] It also reducespropranolol clearance and antagonizes the therapeutic effects ofantidiabetic agents,levodopa (aParkinson's medication. This is likely because chlorpromazine antagonizes the D2 receptor which is one of the receptors dopamine, a levodopa metabolite, activates),amphetamines andanticoagulants.[4] It may also interact with anticholinergic drugs such asorphenadrine to producehypoglycaemia (low blood sugar).[4]
Chlorpromazine may also interact withepinephrine (adrenaline) to produce a paradoxical fall in blood pressure.[4]Monoamine oxidase inhibitors (MAOIs) andthiazide diuretics may also accentuate the orthostatic hypotension experienced by those receiving chlorpromazine treatment.[4] Quinidine may interact with chlorpromazine to increasemyocardial depression.[4] Likewise, it may also antagonize the effects ofclonidine andguanethidine.[4] It also may reduce the seizure threshold and hence a corresponding titration of anticonvulsant treatments should be considered.[4]Prochlorperazine anddesferrioxamine may also interact with chlorpromazine to produce transient metabolicencephalopathy.[4]
Chlorpromazine is classified as a low-potencytypical antipsychotic. Low-potency antipsychotics have moreanticholinergic side effects, such as dry mouth, sedation, and constipation, and lower rates ofextrapyramidal side effects, while high-potency antipsychotics (such ashaloperidol) have the reverse profile.[15]
Chlorpromazine is a very effective antagonist ofD2dopamine receptors and similar receptors, such asD3 andD5. Unlike most other drugs of this genre, it also has a high affinity forD1 receptors. Blocking these receptors causes diminished neurotransmitter binding in the forebrain, resulting in many different effects.Dopamine, unable to bind with a receptor, causes a feedback loop that causes dopaminergic neurons to release more dopamine. Therefore, upon first taking the drug, patients will experience an increase in dopaminergic neural activity. Eventually, dopamine production in the neurons will drop substantially and dopamine will be removed from thesynaptic cleft. At this point, neural activity decreases greatly; the continual blockade of receptors only compounds this effect.[15]
Chlorpromazine acts as anantagonist (blocking agent) on different postsynaptic and presynaptic receptors:
Dopamine receptors (subtypes D1, D2, D3 and D4), which account for its different antipsychotic properties on productive and unproductive symptoms, in the mesolimbic dopamine system accounts for the antipsychotic effect whereas the blockade in the nigrostriatal system produces the extrapyramidal effects
Serotonin receptors (5-HT2, 5-HT6 and 5-HT7), with anxiolytic, antidepressant and antiaggressive properties as well as an attenuation ofextrapyramidal side effects, but also leading to weight gain and ejaculation difficulties.
α1- and α2-adrenergic receptors (accounting for sympatholytic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism – controversial. Also associated with weight gain as a result of blockage of the adrenergic alpha 1 receptor as well as withintraoperative floppy iris syndrome due to its effect on the iris dilator muscle.[47]
The presumed effectiveness of the antipsychotic drugs relied on their ability to block dopamine receptors. This assumption arose from the dopamine hypothesis that maintains that both schizophrenia and bipolar disorder are a result of excessive dopamine activity. Furthermore, psychomotor stimulants like cocaine that increase dopamine levels can cause psychotic symptoms if taken in excess.[48]
Chlorpromazine and other typicalantipsychotics are primarily blockers ofD2 receptors. An almost perfect correlation exists between the therapeutic dose of a typical antipsychotic and the drug's affinity for the D2 receptor. Therefore, a larger dose is required if the drug's affinity for the D2 receptor is relatively weak. A correlation exists between average clinical potency and affinity of the antipsychotics fordopamine receptors.[49]Chlorpromazine tends to have a greater effect atserotonin receptors than atD2 receptors, which is notably the opposite effect of the other typical antipsychotics. Therefore, chlorpromazine's effects on dopamine and serotonin receptors are more similar to the atypical antipsychotics than to the typical antipsychotics.[49]
Chlorpromazine and other antipsychotics withsedative properties such aspromazine andthioridazine are among the most potent agents atα-adrenergic receptors. Furthermore, they are also among the most potent antipsychotics athistamineH1 receptors. This finding is in agreement with the pharmaceutical development of chlorpromazine and other antipsychotics as anti-histamine agents. Furthermore, the brain has a higher density of histamine H1 receptors than any body organ examined which may account for why chlorpromazine and otherphenothiazine antipsychotics are as potent at these sites as the most potent classicalantihistamines.[50]
In addition to influencing the neurotransmitters dopamine, serotonin,epinephrine,norepinephrine, andacetylcholine it has been reported that antipsychotic drugs could achieve glutamatergic effects. This mechanism involves the direct effects of antipsychotic drugs onglutamate receptors. By using the technique of functional neurochemical assay chlorpromazine and phenothiazine derivatives have been shown to have inhibitory effects onNMDA receptors that appeared to be mediated by action at the Zn site. It was found that there is an increase of NMDA activity at low concentrations and suppression at high concentrations of the drug. No significant difference inglycine activity from the effects of chlorpromazine was reported. Further work will be necessary to determine if the influence in NMDA receptors by antipsychotic drugs contributes to their effectiveness.[51]
Pharmacokinetic parameters of chlorpromazine[4][15][54]
Bioavailability
tmax
CSS
Protein bound
Vd
t1/2
Details of metabolism
Excretion
Notes
10–80%
1–4 hours (Oral); 6–24 hours (IM)
100–300 ng/mL
90–99%
10–35 L/kg (mean: 22 L/kg)
30±7 hours
CYP2D6,CYP1A2—mediated into over 10 major metabolites.[15] The major routes of metabolism include hydroxylation, N-oxidation, sulfoxidation, demethylation, deamination and conjugation. There is little evidence supporting the development of metabolic tolerance or an increase in the metabolism of chlorpromazine due to microsomal liver enzymes following multiple doses of the drug.[55]
Urine (43–65% after 24 hours)
Its high degree oflipophilicity (fat solubility) allows it to be detected in the urine for up to 18 months.[4][56] Less than 1% of the unchanged drug is excreted via the kidneys in the urine, in which 20–70% is excreted as conjugated or unconjugated metabolites, whereas 5–6% is excreted in feces.[56]
Advertisement for Thorazine (chlorpromazine) from the early 1960s[57]
In 1933, the French pharmaceutical companyLaboratoires Rhône-Poulenc began to search for newantihistamines. In 1947, it synthesizedpromethazine, aphenothiazine derivative, which was found to have more pronounced sedative and antihistaminic effects than earlier drugs.[58]: 77 A year later, the French surgeon Pierre Huguenard used promethazine together withpethidine as part of a cocktail to induce relaxation and indifference in surgical patients. Another surgeon,Henri Laborit, believed the compound stabilized the central nervous system by causing "artificial hibernation" and described this state as "sedation withoutnarcosis". He suggested to Rhône-Poulenc that they develop a compound with better-stabilizing properties.[59] In December 1950, the chemist Paul Charpentier produced a series of compounds that included RP4560 or chlorpromazine.[6]
Chlorpromazine was distributed for testing to physicians between April and August 1951. Laborit trialled the medicine at theVal-de-Grâce military hospital in Paris, using it as an anaesthetic booster in intravenous doses of 50 to 100 mg in surgery patients and confirming it as the best drug to date in calming and reducing shock, with patients reporting improved well being afterward. He also noted itshypothermic effect and suggested it may induce artificial hibernation. Laborit thought this would allow the body to better tolerate major surgery by reducing shock, a novel idea at the time.[6]
Following on, Laborit considered whether chlorpromazine may have a role in managing patients with severeburns,Raynaud's phenomenon, or psychiatric disorders. At the Villejuif Mental Hospital in November 1951, he and Montassut administered anintravenous dose to psychiatrist Cornelia Quarti, who was acting as a volunteer. Quarti noted the indifference but fainted upon getting up to go to the toilet, and so further testing was discontinued. (Orthostatic hypotension is a known side effect of chlorpromazine). Despite this, Laborit continued to push for testing in psychiatric patients during early 1952. Psychiatrists were reluctant initially, but on 19 January 1952, it was administered (alongside pethidine,pentothal and ECT) to Jacques Lh., a 24-year-old manic patient, who responded dramatically; he was discharged after three weeks, having received 855 mg of the drug in total.[6]
Pierre Deniker had heard about Laborit's work from his brother-in-law, who was a surgeon, and ordered chlorpromazine for a clinical trial at theSainte-Anne Hospital Center in Paris where he was chief of the men's service.[6] Together with the hospital directorJean Delay, they published their first clinical trial in 1952, in which they treated thirty-eightpsychotic patients with daily injections of chlorpromazine without the use of other sedating agents.[60] The response was dramatic; treatment with chlorpromazine went beyond simple sedation, with patients showing improvements in thinking andemotional behaviour.[61] They also found that doses higher than those used by Laborit were required, giving patients 75–100 mg daily. Known colloquially as "Laborit's drug", chlorpromazine was released onto the market in 1953 by Rhône-Poulenc and given the trade nameLargactil, derived fromlarge "broad" andacti* "activity".[6]
Deniker then visited America, where the publication of their work alerted the American psychiatric community that the new treatment might represent a real breakthrough. Heinz Lehmann of theVerdun Protestant Hospital in Montreal trialled it in seventy patients and also noted its striking effects, with patients' symptoms resolving after many years of unrelenting psychosis.[62] By 1954, chlorpromazine was being used in the United States to treatschizophrenia,mania,psychomotor excitement, and otherpsychotic disorders.[15][63][64]Rhône-Poulenc licensed chlorpromazine to Smith Kline & French (today'sGlaxoSmithKline) in 1953. In 1955 it was approved in the United States for the treatment of emesis (vomiting). The effect of this drug in emptyingpsychiatric hospitals has been compared to that ofpenicillin oninfectious diseases.[60]
The popularity of the drug fell in the late 1960s as newer drugs came on the scene. From chlorpromazine several other similar antipsychotics were developed, leading to the discovery ofantidepressants.[65]
The veterinary use of chlorpromazine has generally been superseded by the use ofacepromazine.[72]
Chlorpromazine may be used as anantiemetic in dogs and cats, or, less often, as a sedative before anesthesia.[73] In horses, it often causesataxia andlethargy and is therefore seldom used.[72][73]
^abcdefLópez-Muñoz F, Alamo C, Cuenca E, Shen WW, Clervoy P, Rubio G (2005). "History of the discovery and clinical introduction of chlorpromazine".Annals of Clinical Psychiatry.17 (3):113–135.doi:10.1080/10401230591002002.PMID16433053.
^World Health Organization (2019).World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization.hdl:10665/325771. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
^World Health Organization (2021).World Health Organization model list of essential medicines: 22nd list (2021). Geneva: World Health Organization.hdl:10665/345533. WHO/MHP/HPS/EML/2021.02.
^López-Muñoz F, Alamo C, Cuenca E, Shen WW, Clervoy P, Rubio G (2005). "History of the discovery and clinical introduction of chlorpromazine".Annals of Clinical Psychiatry.17 (3):113–135.doi:10.1080/10401230591002002.PMID16433053.
^Leucht S, Cipriani A, Spineli L, Mavridis D, Orey D, Richter F, et al. (September 2013). "Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis".Lancet.382 (9896):951–962.doi:10.1016/S0140-6736(13)60733-3.PMID23810019.S2CID32085212.
^Breitbart W, Marotta R, Platt MM, Weisman H, Derevenco M, Grau C, et al. (February 1996). "A double-blind trial of haloperidol, chlorpromazine, and lorazepam in the treatment of delirium in hospitalized AIDS patients".The American Journal of Psychiatry.153 (2):231–237.doi:10.1176/ajp.153.2.231.PMID8561204.
^ab"Chlorpromazine".Martindale: The Complete Drug Reference. London: Pharmaceutical Press. 30 January 2013. Retrieved8 December 2013.
^Richter PA, Burk MP (July–August 1992). "The potentiation of narcotic analgesics with phenothiazines".The Journal of Foot Surgery.31 (4):378–380.PMID1357024.
^abBrimblecombe RW, Pinder RM (1975). "Indolealkylamines and Related Compounds".Hallucinogenic Agents. Bristol: Wright-Scientechnica. pp. 98–144.ISBN978-0-85608-011-1.OCLC2176880.OL4850660M.Chlorpromazine is the recommended treatment for those 'bad trips' (Consroe, 1973), although it is not a complete antagonist and can exacerbate the symptoms of other drugs which may be present in illicit samples of LSD or be mistaken for LSD. Usually, the dose is 25-50 mg. intramuscularly, repeated every 30 minutes until the situation is under control.
^Suran M (February 2024). "Study Finds Hundreds of Reddit Posts on "Trip-Killers" for Psychedelic Drugs".JAMA.331 (8):632–634.doi:10.1001/jama.2023.28257.PMID38294772.
Henry M, Alibert S, Rogier C, Barbe J, Pradines B (1 April 2008). "Inhibition of efflux of quinolines as new therapeutic strategy in malaria".Current Topics in Medicinal Chemistry.8 (7).Bentham:563–578.doi:10.2174/156802608783955593.PMID18473883.S2CID13127221.
Miki A, Tanabe K, Nakayama T, Kiryon C, Ohsawa K (March 1992). "Plasmodium chabaudi: association of reversal of chloroquine resistance with increased accumulation of chloroquine in resistant parasites".Experimental Parasitology.74 (2).AP:134–142.doi:10.1016/0014-4894(92)90040-h.PMID1740175.S2CID37364349.
^Leucht S, Wahlbeck K, Hamann J, Kissling W (May 2003). "New generation antipsychotics versus low-potency conventional antipsychotics: a systematic review and meta-analysis".Lancet.361 (9369):1581–1589.doi:10.1016/S0140-6736(03)13306-5.PMID12747876.S2CID40851775.
^Joint Formulary Committee B, ed. (March 2009). "4.2.1".British National Formulary (57 ed.). United Kingdom: Royal Pharmaceutical Society of Great Britain. p. 192.ISBN978-0-85369-845-6.Withdrawal of antipsychotic drugs after long-term therapy should always be gradual and closely monitored to avoid the risk of acute withdrawal syndromes or rapid relapse.
^Moncrieff J (July 2006). "Does antipsychotic withdrawal provoke psychosis? Review of the literature on rapid onset psychosis (supersensitivity psychosis) and withdrawal-related relapse".Acta Psychiatrica Scandinavica.114 (1):3–13.doi:10.1111/j.1600-0447.2006.00787.x.PMID16774655.S2CID6267180.
^Thomas K (2024).Toxicology and Pharmacological Interactions of Classic Psychedelics. Current Topics in Behavioral Neurosciences. Berlin, Heidelberg: Springer Berlin Heidelberg.doi:10.1007/7854_2024_508.PMID39042251. Retrieved14 May 2025.Chlorpromazine, an antipsychotic with relatively strong binding affinity for 5-HT2A (Ki = 2 nM), pretreatment dosed at 25–100 mg dosed 30 min prior to LSD 15–60 μg also reduced the intensity of psychedelic subjective effects (Isbell 1957; Murphree 1962; Maheux et al. 2005).
^Maheux J, Ethier I, Rouillard C, Lévesque D (April 2005). "Induction patterns of transcription factors of the nur family (nurr1, nur77, and nor-1) by typical and atypical antipsychotics in the mouse brain: implication for their mechanism of action".The Journal of Pharmacology and Experimental Therapeutics.313 (1):460–473.doi:10.1124/jpet.104.080184.hdl:20.500.11794/17025.PMID15615863.S2CID1436507.
^abcdeSilvestre JS, Prous J (June 2005). "Research on adverse drug events. I. Muscarinic M3 receptor binding affinity could predict the risk of antipsychotics to induce type 2 diabetes".Methods and Findings in Experimental and Clinical Pharmacology.27 (5):289–304.doi:10.1358/mf.2005.27.5.908643.PMID16082416.
^abcvon Coburg Y, Kottke T, Weizel L, Ligneau X, Stark H (January 2009). "Potential utility of histamine H3 receptor antagonist pharmacophore in antipsychotics".Bioorganic & Medicinal Chemistry Letters.19 (2):538–542.doi:10.1016/j.bmcl.2008.09.012.PMID19091563.
^Tsai LM (2021).Lens and cataract. San Francisco: American Academy of Ophthalmology. p. 162.ISBN978-1-68104-449-1.
^abMcKim WA (2007).Drugs and behavior: an introduction to behavioral pharmacology (6th ed.). Upper Saddle River, New Jersey: Prentice Hall. p. 416.ISBN978-0-13-219788-5.
^Peroutka SJ, Synder SH (December 1980). "Relationship of neuroleptic drug effects at brain dopamine, serotonin, alpha-adrenergic, and histamine receptors to clinical potency".The American Journal of Psychiatry.137 (12):1518–1522.doi:10.1176/ajp.137.12.1518.PMID6108081.
^Dahl SG, Strandjord RE (April 1977). "Pharmacokinetics of chlorpromazine after single and chronic dosage".Clinical Pharmacology and Therapeutics.21 (4):437–448.doi:10.1002/cpt1977214437.PMID849674.S2CID6645825.
^abYeung PK, Hubbard JW, Korchinski ED, Midha KK (1993). "Pharmacokinetics of chlorpromazine and key metabolites".European Journal of Clinical Pharmacology.45 (6):563–569.doi:10.1007/BF00315316.PMID8157044.S2CID6410850.
^"Thorazine advertisement". Smith Kline & French. c. 1963.When the patient lashes out against 'them' – Thorazine (brand of chlorpromazine) quickly puts an end to his violent outburst. 'Thorazine' is especially effective when the psychotic episode is triggered by delusions or hallucinations. At the outset of treatment, Thorazine's combination of antipsychotic and sedative effects provides both emotional and physical calming. Assaultive or destructive behavior is rapidly controlled. As therapy continues, the initial sedative effect gradually disappears. However, the antipsychotic effect continues, helping to dispel or modify delusions, hallucinations, and confusion while keeping the patient calm and approachable. Smith Kline and French Laboratories
^Afeltra J, Verweij PE (July 2003). "Antifungal activity of nonantifungal drugs".European Journal of Clinical Microbiology & Infectious Diseases.22 (7). Springer Nature:397–407.doi:10.1007/s10096-003-0947-x.PMID12884072.S2CID10489462.
^Baksheeva VE, La Rocca R, Allegro D, Derviaux C, Pasquier E, Roche P, et al. (2025). "NanoDSF Screening for Anti-tubulin Agents Uncovers New Structure–Activity Insights".Journal of Medicinal Chemistry.68 (16):17485–17498.doi:10.1021/acs.jmedchem.5c01008.PMID40815226.
^abPlumb DC (2015).Plumb's Veterinary Drug Handbook (8th ed.). John Wiley & Sons.ISBN978-1-118-91192-1.
^abPosner LA, Burns P (2009). "Chapter 13: Sedative agents: tranquilizers, alpha-2 agonists, and related agents". In Riviere JE, Papich MG, Adams RH (eds.).Veterinary pharmacology and therapeutics (9 ed.). Ames, Iowa: Wiley-Blackwell. pp. 337–80.ISBN978-0-8138-2061-3.
^"Chlorpromazine: summary report"(PDF).European Medicines Agency. Committee for Veterinary Medicinal Products. June 1996.Archived(PDF) from the original on 18 January 2017. Retrieved17 January 2017.
