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Chlorpromazine HCl

Alias:
Cat No.:V1249 Purity: ≥98%
Chlorpromazine HCl (Promacid; Chloractil; Klorpromex; Fenactil; Largactil; Propaphenin; Sonazine; Thorazine), the Hydrochloride salt form of chlorpromazine, is a potent dopamine and potassium channel inhibitor used as an antipsychotic medication for the treatment of psychotic disorders such as schizophrenia.
Chlorpromazine HCl
Chlorpromazine HCl Chemical Structure CAS No.: 69-09-0
Product category: Dopamine Receptor
This product is for research use only, not for human use. We do not sell to patients.
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1g
5g
10g
25g
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Other Forms of Chlorpromazine HCl:

  • Chlorpromazine
  • Chlorpromazine D6 hydrochloride
Official Supplier of:
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Top Publications Citing lnvivochem Products
Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Chlorpromazine HCl (Promacid; Chloractil; Klorpromex; Fenactil; Largactil; Propaphenin; Sonazine; Thorazine), the Hydrochloride salt form of chlorpromazine, is a potent dopamine and potassium channel inhibitor used as an antipsychotic medication for the treatment of psychotic disorders such as schizophrenia. It blocks the dopamine and potassium channels, exhibiting IC50 values of 6.1 and 16 μM for time-independent outward currents and inward-rectifying K+ currents, respectively. A classic antipsychotic drug with phenothiazine properties and anti-emetic properties is chlorpromazine hydrochloride (HCl). It prevents the brain from having too much dopamine by blocking postsynaptic dopamine receptors in limbic and cortical regions. This has an antipsychotic effect.

Biological Activity I Assay Protocols (From Reference)
Targets
D2 dopamine receptors (Ki = 363 nM ); 5-HT2A (Ki = 8.3 nM)
ln Vitro

In vitro activity: Chlorpromazine decreases GABAAR binding (kon) and increases GABAAR unbinding (koff) rates, which has an impact on miniature IPSCs (mIPSCs).[1] Voltage-dependent modulation of activated TRPA1 currents by chlorpromazine results in an increased open probability at negative potentials and a block at positive potentials.[2]

ln Vivo
Chlorpromazine independently increases the secretion of IL-10 and down-regulates the production of several T cell-derived lymphokines (IL-2, IFN-gamma, IL-4, TNF, and GM-CSF) in an in vivo model of acute superantigen-driven immune activation. An increased IL-10 mRNA accumulation coincides with the chlorpromazine-mediated amplification of the SEB-driven chlorpromazine secretion. [3]
Enzyme Assay
Recent studies have emphasized that nonequilibrium conditions of postsynaptic GABAA receptor (GABAAR) activation is a key factor in shaping the time course of IPSCs (Puia et al., 1994; Jones and Westbrook, 1995). Such nonequilibrium, resulting from extremely fast agonist time course, may affect the interaction between pharmacological agents and postsynaptic GABAARs. In the present study we found that chlorpromazine (CPZ), a widely used antipsychotic drug known to interfere with several ligand and voltage-gated channels, reduces the amplitude and accelerates the decay of miniature IPSCs (mIPSCs). A good qualitative reproduction of the effects of CPZ on mIPSCs was obtained when mIPSCs were mimicked by responses to ultrafast GABA applications to excised patches. Our experimental data and model simulations indicate that CPZ affects mIPSCs by decreasing the binding (kon) and by increasing the unbinding (koff) rates of GABAARs. Because of reduction of kon by CPZ, the binding reaction becomes rate-limiting, and agonist exposure of GABAARs during mIPSC is too short to activate the receptors to the same extent as in control conditions. The increase in unbinding rate is implicated as the mechanism underlying the acceleration of mIPSC decaying phase. The effect of CPZ on GABAAR binding rate, resulting in slower onset of GABA-evoked currents, provides a tool to estimate the speed of synaptic clearance of GABA. Moreover, the onset kinetics of recorded responses allowed the estimate the peak synaptic GABA concentration [1].
Cell Assay
Cell Line: U-87MG glioma cells
Concentration: 0, 10, 20, 40 μM
Incubation Time: 0, 24, 48 h
Result: Showed anti-proliferative activity in a dose- and time-dependent manner.
Animal Protocol
5- to 6-week-old athymic nude mice bearing intracranial U-87MG xenograft tumors[2]
20 mg/kg
Injected intraperitoneally; single daily for 7 days
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Readily absorbed from the GI tract. Bioavailability varies due to first-pass metabolism by the liver.
Kidneys, ~ 37% excreted in urine
20 L/kg
Chlorpromazine hydrochloride is rapidly absorbed from the GI tract and from parenteral sites of injection; however, following oral administration, the drug undergoes considerable metabolism during absorption (in the GI mucosa) and first pass through the liver. Although not clearly established in humans, chlorpromazine and its metabolites undergo enterohepatic circulation in animals.
Considerable interindividual variations in peak plasma concentrations have been reported with the same oral dose of chlorpromazine. The variability is thought to result from wide interindividual variation in bioavailability, apparently because of genetic differences in the rate of first-pass metabolism. As a result of first-pass metabolism, less chlorpromazine reaches systemic circulation as unchanged drug, and peak plasma chlorpromazine concentrations are much lower following oral administration than following im administration.
Following oral administration of chlorpromazine hydrochloride in a tablet formulation, the onset of pharmacologic action occurs within 30-60 minutes; the duration of action is 4-6 hours. The onset of pharmacologic action following oral administration of chlorpromazine hydrochloride in an extended-release formulation is approximately 30-60 minutes; the duration of action is 10-12 hours. The onset of pharmacologic action following rectal administration of chlorpromazine is generally slower than that following oral administration of chlorpromazine hydrochloride; rectally administered chlorpromazine has a duration of action of 3-4 hours.
Phenothiazines and their metabolites are distributed into most body tissues and fluids, with high concentrations being distributed into the brain, lungs, liver, kidneys, and spleen. /Phenothiazine General Statement/
For more Absorption, Distribution and Excretion (Complete) data for Chlorpromazine (17 total), please visit the HSDB record page.
Metabolism / Metabolites
Extensively metabolized in the liver and kidneys. It is extensively metabolized by cytochrome P450 isozymes CYP2D6 (major pathway), CYP1A2 and CYP3A4. Approximately 10 to 12 major metabolite have been identified. Hydroxylation at positions 3 and 7 of the phenothiazine nucleus and the N-dimethylaminopropyl side chain undergoes demethylation and is also metabolized to an N-oxide. In urine, 20% of chlopromazine and its metabolites are excreted unconjugated in the urine as unchanged drug, demonomethylchlorpromazine, dedimethylchlorpromazine, their sulfoxide metabolites, and chlorpromazine-N-oxide. The remaining 80% consists of conjugated metabolites, principally O-glucuronides and small amounts of ethereal sulfates of the mono- and dihydroxy-derivatives of chlorpromazine and their sulfoxide metabolites. The major metabolites are the monoglucuronide of N-dedimethylchlorpromazine and 7-hydroxychlorpromazine. Approximately 37% of the administered dose of chlorpromazine is excreted in urine.
Although the exact metabolic fate of chlorpromazine is not clearly established, the drug is extensively metabolized, principally in the liver and kidneys. About 10-12 metabolites which occur in humans in appreciable quantities have been identified. In addition to hydroxylation at positions 3 and 7 of the phenothiazine nucleus, the N-dimethylaminopropyl side chain of chlorpromazine undergoes demethylation and is also metabolized to an N-oxide. Two principal groups of metabolites have been found in urine. The unconjugated fraction, which represents approximately 20% of chlorpromazine and its metabolites excreted in urine, consists of unchanged drug, demonomethylchlorpromazine, dedimethylchlorpromazine, their sulfoxide metabolites, and chlorpromazine-N-oxide. The conjugated fraction, which represents approximately 80% of chlorpromazine and its metabolites excreted in urine, consists principally of O-glucuronides, with small amounts of ethereal sulfates of the mono- and dihydroxy-derivatives of chlorpromazine and their sulfoxide metabolites. The major metabolites found in urine are the monoglucuronide of N-dedimethylchlorpromazine and 7-hydroxychlorpromazine.
Most metabolites of phenothiazines are pharmacologically inactive; however, certain metabolites (eg, 7-hydroxychlorpromazine, mesoridazine) show moderate pharmacologic activity and may contribute to the action of the drugs. There is limited evidence to indicate that some phenothiazines (eg, chlorpromazine) may induce their own metabolism. /Phenothiazine General Statement/
Yields 2-chlorophenothiazine in man; promazine probably in dog and in man ... . Yields demethylchlorpromazine in man, rat, rabbit, mouse, dog, sheep, guinea pig ... . Yields chlorpromazine sulfoxide in man, rat, rabbit, dog ... . Yields chlorpromazine-n-oxide in man, rat, rabbit, dog, pig, sheep, guinea pig, mouse ... . Yields 3-hydroxychlorpromazine in man, rat, dog ... . Yields 7-hydroxychlorpromazine in man, rat, sheep, dog, rabbit, guinea pig ... . /From table/
As least 10 or 12 metabolites of chlorpromazine occur in human beings in appreciable quantities. Quantitatively, the most important of these are nor2-chlorpromazine (doubly methylated), chlorphenothiazine (removal of the entire side chain), methoxy and hydroxy products, and glucuronide conjugates of the hydroxylated compounds. In urine, 7-hydroxylated and dealkylated (nor2) metabolites and their conjugates predominate.
Chlorpromazine has known human metabolites that include 7-Hydroxychlorpromazine, Chlorpromazine S-oxide, Chlorpromazine, N-desmethyl, and Chlorpromazine N-glucuronide.
Extensively metabolized in the liver and kidneys. It is extensively metabolized by cytochrome P450 isozymes CYP2D6 (major pathway), CYP1A2 and CYP3A4. Approximately 10 to 12 major metabolite have been identified. Hydroxylation at positions 3 and 7 of the phenothiazine nucleus and the N-dimethylaminopropyl side chain undergoes demethylation and is also metabolized to an N-oxide. In urine, 20% of chlopromazine and its metabolites are excreted unconjugated in the urine as unchanged drug, demonomethylchlorpromazine, dedimethylchlorpromazine, their sulfoxide metabolites, and chlorpromazine-N-oxide. The remaining 80% consists of conjugated metabolites, principally O-glucuronides and small amounts of ethereal sulfates of the mono- and dihydroxy-derivatives of chlorpromazine and their sulfoxide metabolites. The major metabolites are the monoglucuronide of N-dedimethylchlorpromazine and 7-hydroxychlorpromazine. Approximately 37% of the administered dose of chlorpromazine is excreted in urine.
Route of Elimination: Kidneys, ~ 37% excreted in urine
Half Life: ~ 30 hours
Biological Half-Life
~ 30 hours
After 120 mg/sq m oral doses to human volunteers chlorpromazine displays a mean elimination half-life of approximately 18 hours (range, 6-119 hours).
Disappearance of chlorpromazine from plasma includes rapid distribution phase (half-life about 2 hours) and slower early elimination phase (half-life about 30 hours), but markedly variable values have been reported; the half-life of elimination from human brain is not known.
The pharmacokinetics of chlorpromazine in the newborn have not been reported. /Investigators/ studied the kinetics of removal of chlorpromazine from plasma in an infant whose mother was treated with high doses of chlorpromazine and lithium throughout the last trimester of pregnancy. The infant exhibited symptoms of severe neurologic depression that slowly abated over the first 9 days of life. The kinetics of plasma chlorpromazine removal were described with a two-compartment model, exhibiting a rapid half-life of 1.46 days and a slow half-life of 3.19 days. Both half-lives are considerably longer than the rapid and slow half-lives described in adults. Caution in exposing the fetus or newborn to chlorpromazine is warranted. Further information on the distribution and excretion of chlorpromazine by the newborn is needed.
Toxicity/Toxicokinetics
Toxicity Summary
IDENTIFICATION: Chlorpromazine is an antipsychotic medication. It is a synthetic dimethylamine derivative of phenothiazine. Chlorpromazine is a white to creamy-white (Base and hydrochloride). Powder or waxy solid (Base); crystallline powder (Hydrochloride). Chlorpromzaine is practically insoluble in water. Freely soluble in dilute mineral acids; practically insoluble in dilute alkali hydroxides. HUMAN EXPOSURE: Main risks and target organs: The principal pharmacological actions are psychotropic. It also exerts sedative and antiemetic activity. Chlorpromazine has actions at all levels of the central nervous system, primarily at subcortical levels, as well as on multiple organ systems. Chlorpromazine has strong antiadrenergic and weak peripheral anticholinergic activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic and antiserotonin activity. Summary of clinical effects: Central nervous depression may progress from drowsiness to coma, ultimately with areflexia. In early or mild intoxications, some patients suffer from restlessness, confusion and excitement. Tremor or muscular twitching, spasm, rigidity, convulsions, muscular hypotonia, difficulty in swallowing may be present. Extrapyramidal signs of overdose include dystonia, torticollis, oculogyric crises and opisthotonos. Either hypothermia or hyperthermia may be encountered. Difficulty in breathing, cyanosis, respiratory and/or vasomotor collapse, respiratory depression and distress, sudden apnea and even cyanosis may occur. Hypotension, tachycardia, cardiac arrhythmias, conduction defects, ventricular fibrillation or cardiac arrest may occur. Contraindications: Do not use in comatose states or in the presence of large amounts of central nervous system depressants (alcohol, barbiturates, anesthetics, narcotics, etc.) because chlorpromazine prolongs and intensifies the action of such CNS depressants. Chlorpromazine should be administered cautiously to persons with cardiovascular or liver disease. There is evidence that patients with a history of hepatic encephalopathy due to cirrhosis have increased sensitivity to the CNS effect of chlorpromazine (e.g. impaired cerebration and abnormal slowing of the EEG). Because of this CNS depressant effect, it should be used with caution in patients with chronic respiratory disorders such as severe asthma, emphysema and acute respiratory infections, particularly in children. Because it can suppress the cough reflex, aspiration of vomitus is possible. Subcutaneous injection is contraindicated. Routes of entry: Oral: Chlorpromazine is available in tablet or syrup forms for oral ingestion. Parenteral: It is present in injectable forms for use through the intramuscular or intravenous routes. Other: Rectal route with suppositories. Absorption by route of exposure: The absorption of orally administered chlorpromazine is dependent on the dosage form, the elixir giving the highest plasma concentration of drug. Peak plasma levels are reached at 2 to 3 hours. There is a wide inter-subject variability (ten times or more) in the plasma concentrations achieved. Plasma concentrations may be decreased significantly by food in the stomach and by the concomitant administration of anticholinergic antiparkinsonism drugs. Owing to the first-pass effect, plasma concentrations following oral administrations are much lower than those following intramuscular administrations. Distribution by route of exposure: Chlorpromazine is widely distributed in the body and crosses the blood-brain barrier to achieve higher concentrations in the brain than in the plasma. Chlorpromazine and its metabolites also cross the placental barrier and are excreted in milk. Chlorpromazine is highly bound to plasma proteins, varying from 91.8% to 97% over the range of clinical blood concentrations (0.01 to 1 mcg/mL). Binding is easily reversed. Biological half-life by route of exposure: Although the plasma half-life of chlorpromazine itself has been reported to be only a few hours, elimination of the metabolites may be very prolonged. Blood studies show a range of 2 to 3 days and for the urinary studies up to about 18 days. Chlorpromazine brings about changes that can persist much longer than these times after discontinuation of the drug. The exact relationship of persisting therapeutic effects to administered chlorpromazine is uncertain. There is the possibility that minute amounts of chlorpromazine and/or metabolites persist at active sites in slowly reversible or relatively irreversible ways. It also seems that some chlorpromazine is stored in adipose tissue and slowly mobilized after stopping chlorpromazine administration. Metabolism: Paths of metabolism of chlorpromazine include hydroxylation, and conjugation with glucuronic acid, N-oxidation, oxidation of a sulfur atom, and dealkylation. In man, after chronic use, the highest concentration of unconjugated chlorpromazine metabolites is found in the lung and liver. The 7-hydroxy chlorpromazine that is found in body tissues appears to be an active metabolite. Since there is some evidence that chlorpromazine can cause hepatic microsomal enzyme induction, it may accelerate its own metabolism; this may account for progressively decreasing plasma concentrations of free drug during maintenance of a fixed dosage schedule. One hundred and sixty-eight possible metabolites of chlorpromazine have been postulated and many of them actually isolated from human urine. In man, urinary excretion of chlorpromazine plus its sulfoxides varies from 1 to 20% of the daily dose administered. The average ratio of free chlorpromazine to the sulfoxide in the urine is about 1:16. There is much evidence that the sulfoxide undergoes additional metabolism, probably to sulfones. The various phenothiazine congeners of chlorpromazine undergo similar metabolic degradation. Demethylation is another method of detoxication by the liver. Elimination by route of exposure: Chlorpromazine is excreted in both urine and feces. Mode of action: Chlorpromazine has a wide range of activity arising from its depressant actions on the central nervous system and its alpha-adrenergic blocking and weak antimuscarinic activities. Chlorpromazine possesses sedative properties but patients usually develop tolerance rapidly to the sedation. Its action on the autonomic system produces vasodilation, hypotension, and tachycardia. Salivary and gastric secretions are reduced. The sulfoxides of the phenothiazines have been intensively studied and found to be significantly less potent than the parent compound. Teratogenicity: If given in high doses over a long period during pregnancy, chlorpromazine may cause damage to the retina of the fetus. Interactions: Chlorpromazine may block the antihypertensive effects of guanethidine. Patients being treated with phenothiazines should be advised that their susceptibility to alcohol may be increased. Chlorpromazine has been shown to increase the miotic and sedative effects of morphine. Chlorpromazine may enhance the respiratory depression produced particularly by CNS depressants. Mutual inhibition of liver enzymes concerned with the metabolism of both chlorpromazine and the other drug (e.g. a tricyclic antidepressant) might result in increased plasma-concentrations of either drug. Chlorpromazine is reported to interfere with a number of laboratory tests, such as pregnancy tests, thyroid function tests, the Coombs' test where a false positive result can be achieved, and adrenal medullary tests. It is also reported to interfere with estimations for serum 5-hydroxyindole-acetic acid, blood urea, urinary ketones and steroids, urinary porphobilinogen, and vitamin B12. Main adverse effects: Therapeutic doses of chlorpromazine, may cause palpitation, nasal stuffiness, dry mouth, and slight constipation. The patient may complain of being cold, drowsy, or weak. Orthostatic hypotension, which may result in syncope. A mild elevation of temperature may be seen during the first few days, particularly if the drug is given parenterally. On the other hand, hypothermia can occur and may be due both to the action on the heat regulating center and to direct peripheral vasodilation. Sensitivity and adaptation to environmental temperature change are impaired so that fatal hyperthermia and heat stroke are possible complications. Chlorpromazine has produced hematological disorders, including agranulocytosis, eosinophilia, leucopenia, hemolytic anemia, aplastic anemia, thrombocytopenic purpura and pancytopenia. Hyperglycemia, hypoglycemia and glycosuria have also been reported.
Chlorpromazine acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects).
Additionally, Chlorpromazine is a weak presynaptic inhibitor of Dopamine reuptake, which may lead to (mild) antidepressive and antiparkinsonian effects. This action could also account for psychomotor agitation and amplification of psychosis (very rarely noted in clinical use).
Interactions
... Dosage requirements for oral hypoglycemic agents may be increased in those receiving chlorpromazine ... .
QT interval-prolonging medications, including cisapride, erythromycin, and quinidine /may produce/ additive QT interval prolongation increasing the risk of developing cardiac arrhythmias when /concurrently administered with phenothiazines/. /Phenothiazines/
Concurrent use /of other photosensitizing medications/ with phenothiazines may cause additive photosensitizing effects. In addition, concurrent use of systemic methoxsalen, trixsalen, or tetracyclines with phenothiazines may potentiate intraocular photochemical damage to the choroid, retina, or lens. /Phenothiazines/
Prior administration of phenothiazines may decrease the pressor effect and shorten the duration of action of phenylephrine. /Phenothiazines/
For more Interactions (Complete) data for Chlorpromazine (37 total), please visit the HSDB record page.
Non-Human Toxicity Values
LD50 Rat oral 225 mg/kg
LD50 Rat oral 142 mg/kg
LD50 Rat ip 58 mg/kg
LD50 Rat sc 75 mg/kg
For more Non-Human Toxicity Values (Complete) data for Chlorpromazine (10 total), please visit the HSDB record page.
References

[1]. J Neurosci . 1999 Apr 1;19(7):2474-88.

[2]. J Biol Chem . 2007 Mar 9;282(10):7145-53.

[3]. J Immunol . 1995 Jan 15;154(2):861-70.

[4]. J Exp Med . 1991 Jun 1;173(6):1305-10.

[5]. Brain Res . 1986 Oct 22;385(2):219-26.

Additional Infomation
Therapeutic Uses
Antiemetics; Antipsychotic Agents, Phenothiazine; Dopamine Antagonists
/Chlorpromazine is indicated/ for the treatment of schizophrenia. /Included in US product label/
/Chlorpromazine is indicated/ to control nausea and vomiting. /Included in US product label/
/Chlorpromazine is indicated/ for relief of restlessness and apprehension before surgery. /Included in US product label/
For more Therapeutic Uses (Complete) data for Chlorpromazine (16 total), please visit the HSDB record page.
Drug Warnings
Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Analyses of seventeen placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality. The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear. Chlorpromazine Hydrochloride Injection, USP is not approved for the treatment of patients with dementia-related psychosis.
... Extrapyramidal reactions ... fairly common, usually 3 types ... Parkinsonian-like syndrome ... dystonia and dyskinesia, including torticollis, tics, and other involuntary muscle movements ... akathisia, shown by restlessness ... hyperreflexia, reported in newborn ... ./Phenothiazines/
The antiemetic action of chlorpromazine may mask the signs and symptoms of overdosage of other drugs and may obscure the diagnosis and treatment of other conditions such as intestinal obstruction, brain tumor and Reye's syndrome. When chlorpromazine is used with cancer chemotherapeutic drugs, vomiting as a sign of the toxicity of these agents may be obscured by the antiemetic effects of chlorpromazine.
Do not use /chlorpromazine/ in patients with known hypersensitivity to phenothiazines. Do not use in comatose states or in the presence of large amounts of central nervous system depressants (alcohol, barbiturates, narcotics, etc.).
For more Drug Warnings (Complete) data for Chlorpromazine (55 total), please visit the HSDB record page.
Pharmacodynamics
Chlorpromazine is a psychotropic agent indicated for the treatment of schizophrenia. It also exerts sedative and antiemetic activity. Chlorpromazine has actions at all levels of the central nervous system-primarily at subcortical levels-as well as on multiple organ systems. Chlorpromazine has strong antiadrenergic and weaker peripheral anticholinergic activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic and antiserotonin activity.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C17H20CL2N2S
Molecular Weight
355.33
Exact Mass
354.072
Elemental Analysis
C, 57.46; H, 5.67; Cl, 19.96; N, 7.88; S, 9.02
CAS #
69-09-0
Related CAS #
Chlorpromazine; 50-53-3; Chlorpromazine-d6 hydrochloride; 1228182-46-4
PubChem CID
2726
Appearance
White to off-white crystalline powder
Density
1.077 g/cm3 (15 C)
Boiling Point
450.1ºC at 760 mmHg
Melting Point
192-196°C
Index of Refraction
1.4436 (20ºC)
LogP
5.761
Hydrogen Bond Donor Count
0
Hydrogen Bond Acceptor Count
3
Rotatable Bond Count
4
Heavy Atom Count
21
Complexity
339
Defined Atom Stereocenter Count
0
SMILES
ClC1C([H])=C([H])C2=C(C=1[H])N(C1=C([H])C([H])=C([H])C([H])=C1S2)C([H])([H])C([H])([H])C([H])([H])N(C([H])([H])[H])C([H])([H])[H]
InChi Key
FBSMERQALIEGJT-UHFFFAOYSA-N
InChi Code
InChI=1S/C17H19ClN2S.ClH/c1-19(2)10-5-11-20-14-6-3-4-7-16(14)21-17-9-8-13(18)12-15(17)20;/h3-4,6-9,12H,5,10-11H2,1-2H3;1H
Chemical Name
3-(2-chlorophenothiazin-10-yl)-N,N-dimethylpropan-1-amine;hydrochloride
Synonyms

Promacid; Chloractil; Klorpromex; Fenactil; Hydrochloride; Chlorpromazine; Largactil; Propaphenin; Chloropromazine Hydrochloride; Sonazine; Thorazine

HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.  (2). This product is not stable in solution, please use freshly prepared working solution for optimal results.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: ~71 mg/mL (~199.8 mM)
Water: N/A
Ethanol: ~71 mg/mL (~199.8 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.04 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.08 mg/mL (5.85 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (5.85 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.8143 mL 14.0714 mL 28.1429 mL
5 mM 0.5629 mL 2.8143 mL 5.6286 mL
10 mM 0.2814 mL 1.4071 mL 2.8143 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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What volume of a given 10 mM stock solution is required to make 25 ml of a 25 μM solution?
Using the equation C1V1 = C2V2, where C1=10 mM, C2=25 μM, V2=25 ml and V1 is the unknown:
  • Enter 10 into the Concentration (Start) box and choose the correct unit (mM)
  • Enter 25 into the Concentration (End) box and select the correct unit (mM)
  • Enter 25 into the Volume (End) box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 62.5 μL (0.1 ml) appears in the Volume (Start) box
g/mol

Molecular Weight Calculator allows you to calculate the molar mass and elemental composition of a compound, as detailed below:

Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
Instructions to calculate molar mass (molecular weight) of a chemical compound:
  • To calculate molar mass of a chemical compound, please enter the chemical/molecular formula and click the “Calculate’ button.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
  • Molecular mass (or molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
  • Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
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Reconstitution Calculator allows you to calculate the volume of solvent required to reconstitute your vial.

  • Enter the mass of the reagent and the desired reconstitution concentration as well as the correct units
  • Click the “Calculate” button
  • The answer appears in the Volume (to add to vial) box
In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
Step 2: Enter in vivo formulation (This is only a calculator, not the exact formulation for a specific product. Please contact us first if there is no in vivo formulation in the solubility section.)
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

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