D2 dopamine receptors; 5-HT2A[1][6].

Chlorpromazine hlorpromazine (0, 10, 20, 40 μM; 0, 24, 48 h) suppresses U-87MG glioma cell proliferation in a time- and dose-dependent manner[2]. The levels of cyclin A and cyclin B1 in U-87MG glioma cells are decreased by chlorpromazine (20 μM; 0, 12, 24, 48 h) 12 hours later[2]. Cell cycle progression is inhibited by 20 μM of chlorpromazine[2]. In sEV-treated bone marrow cells, chlorpromazine (10 μM; 1 h) greatly lowers MDSCs and significantly suppresses the internalization of sEV (MDSCs can significantly suppress the immune cell response, producing immunosuppression in cancer cells)[3]. The hNav1.7 current is blocked by chlorpromazine (3, 10, 20, 40, and 60 µM) in a concentration-dependent way[4]. HERG potassium channels are blocked by chlorpromazine, which has an IC50 value of 21.6 µM and a Hill coefficient of 1.11[5].

Chlorpromazine (20 mg/kg; ip; single daily for 7 days) inhibits xenograft tumor growth in nude mouse[2].

Cell Proliferation Assay[2]
Cell Types: U-87MG glioma cells
Tested Concentrations: 0, 10, 20, 40 μM
Incubation Duration: 0, 24, 48 h
Experimental Results: demonstrated anti-proliferative activity in a dose - and time-dependent manner.

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Immunofluorescence[3]
Cell Types: Bone marrow cells (sEV-treated)
Tested Concentrations: 10 µM
Incubation Duration: 1 h
Experimental Results: decreased MDSCs and suppressed the sEV internalization.

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Western Blot Analysis[2]
Cell Types: U-87MG glioma cells
Tested Concentrations: 20 μM
Incubation Duration: 0, 12, 24, 48 h
Experimental Results: diminished the levels of cyclin A and cyclin B1 12 h later, whereas levels of cyclin D1, proliferating cell nuclear antigen and GAPDH remained unchanged.

Animal/Disease Models: 5- to 6 weeks old athymic nude mice bearing intracranial U-87MG xenograft tumors[2].
Doses: 20 mg/kg
Route of Administration: Injected intraperitoneally (ip); single daily for 7 days
Experimental Results: Inhibited tumor growth on day 17.

Absorption, Distribution and Excretion
Chlorpromazine hydrochloride is readily absorbed from the gastrointestinal tract. Bioavailability varies due to first-pass metabolism in the liver. It is excreted by the kidneys, with approximately 37% excreted in the urine. 20 L/kg Chlorpromazine hydrochloride is rapidly absorbed from the gastrointestinal tract and injection site; however, after oral administration, the drug undergoes significant metabolism during absorption (in the gastrointestinal mucosa) and during first-pass metabolism in the liver. Although not fully understood in humans, chlorpromazine and its metabolites undergo enterohepatic circulation in animals. Significant individual differences in peak plasma concentrations have been reported even with the same oral dose of chlorpromazine. This difference is believed to be due to individual variations in bioavailability, which is clearly due to genetic differences in first-pass metabolic rates. Due to first-pass metabolism, a smaller amount of the original drug enters systemic circulation after oral administration of chlorpromazine, resulting in significantly lower peak plasma concentrations after oral administration compared to intramuscular administration. After oral administration of chlorpromazine hydrochloride tablets, the drug takes effect within 30–60 minutes, with a duration of action of 4–6 hours. After oral administration of chlorpromazine hydrochloride in sustained-release form, the onset of action is approximately 30-60 minutes, and the duration of action is 10-12 hours. After rectal administration, the onset of action of chlorpromazine is generally slower than that of oral chlorpromazine hydrochloride. The duration of action of rectal chlorpromazine is 3-4 hours. Phenothiazine drugs and their metabolites are distributed in most body tissues and fluids, with higher concentrations in the brain, lungs, liver, kidneys, and spleen. /Overview of Phenothiazine Drugs/ For more complete data on the absorption, distribution, and excretion of chlorpromazine (17 metabolites), please visit the HSDB record page. Metabolism/Metabolites It is extensively metabolized in the liver and kidneys. It is primarily metabolized via the cytochrome P450 isoenzyme CYP2D6 (major pathway), CYP1A2, and CYP3A4. Approximately 10 to 12 major metabolites have been identified. Hydroxylation at the 3 and 7 positions of the phenothiazine ring and demethylation of the N-dimethylaminopropyl side chain lead to metabolism into N-oxide. In urine, 20% of chlorpromazine and its metabolites are excreted unbound, including the parent drug, normethylchlorpromazine, nordimethylchlorpromazine, their sulfoxide metabolites, and chlorpromazine-N-oxide. The remaining 80% are conjugated metabolites, primarily O-glucuronides of monohydroxy and dihydroxy derivatives of chlorpromazine and its sulfoxide metabolites, and small amounts of ether sulfates. The major metabolites are monoglucuronides of N-desdimethylchlorpromazine and 7-hydroxychlorpromazine. Approximately 37% of the administered dose of chlorpromazine is excreted in the urine. Although the exact metabolic pathway of chlorpromazine is not fully understood, the drug is extensively metabolized primarily in the liver and kidneys. Approximately 10-12 metabolites present in significant amounts in the human body have been identified. In addition to hydroxylation at the 3 and 7 positions of the phenothiazine ring, the N-dimethylaminopropyl side chain of chlorpromazine undergoes demethylation and is metabolized to N-oxide. Two main classes of metabolites have been found in urine. The unconjugated moiety accounts for approximately 20% of chlorpromazine and its metabolites in urine, including the active ingredient, normethylchlorpromazine, nordimethylchlorpromazine, their sulfoxide metabolites, and chlorpromazine-N-oxide. The conjugated moiety accounts for approximately 80% of chlorpromazine and its metabolites in urine, mainly composed of O-glucuronide, with smaller amounts of ether sulfates of chlorpromazine monohydroxy and dihydroxy derivatives and their sulfoxide metabolites. The main metabolites found in urine are monoglucuronides of N-desdimethylchlorpromazine and 7-hydroxychlorpromazine. Most phenothiazine metabolites are pharmacologically inactive; however, some metabolites (e.g., 7-hydroxychlorpromazine, mesoridine) have moderate pharmacological activity and may contribute to the drug's action. Limited evidence suggests that some phenothiazine drugs (e.g., chlorpromazine) may induce auto-metabolism. /Overview of Phenothiazine Drugs/
In humans, 2-chlorophenothiazine is produced; chlorpromazine may be present in dogs and humans…. In humans, rats, rabbits, mice, dogs, sheep, and guinea pigs, demethylchlorpromazine is produced…. In humans, rats, rabbits, and dogs, chlorpromazine sulfoxide is produced…. In humans, rats, rabbits, dogs, pigs, sheep, guinea pigs, and mice, chlorpromazine-N-oxide is produced…. In humans, rats, and dogs, 3-hydroxychlorpromazine is produced…. In humans, rats, sheep, dogs, rabbits, and guinea pigs, 7-hydroxychlorpromazine is produced…. /Excerpt from Table/
At least 10 or 12 chlorpromazine metabolites are present in large quantities in humans. In terms of quantity, the most important metabolites are demethyl-2-chloropromazine (dimethylation), chlorophenothiazine (removal of the entire side chain), methoxy and hydroxyl products, and glucuronide conjugates of hydroxylated compounds. In urine, 7-hydroxylated and dealkylated (normethyl 2) metabolites and their conjugates are predominant. Known metabolites of chlorpromazine include 7-hydroxychlorpromazine, chlorpromazine S-oxide, N-desmethylchlorpromazine, and chlorpromazine N-glucuronide. Chlorpromazine is extensively metabolized in the liver and kidneys. It is primarily metabolized via cytochrome P450 isoenzymes CYP2D6 (the major pathway), CYP1A2, and CYP3A4. Approximately 10 to 12 major metabolites have been identified. Hydroxylation at the 3 and 7 positions of the phenothiazine ring and demethylation of the N-dimethylaminopropyl side chain lead to N-oxide. In urine, 20% of chlorpromazine and its metabolites are excreted unconjugated, including the original drug, normethylchlorpromazine, nordimethylchlorpromazine, their sulfoxide metabolites, and chlorpromazine-N-oxide. The remaining 80% are conjugated metabolites, primarily O-glucuronides of monohydroxy and dihydroxy derivatives of chlorpromazine and its sulfoxide metabolites, and small amounts of ether sulfates. The major metabolites are monoglucuronides of N-dedimethylchlorpromazine and 7-hydroxychlorpromazine. Approximately 37% of the administered dose is excreted in the urine.
Excretion route: Renal, approximately 37% excreted in urine.
Half-life: Approximately 30 hours.
Biological half-life: Approximately 30 hours.
In human volunteers, the mean elimination half-life after oral administration of 120 mg/m² chlorpromazine is approximately 18 hours (range: 6–119 hours).
Disappearance of chlorpromazine from plasma includes a rapid distribution phase (half-life approximately 2 hours) and a slower early elimination phase (half-life approximately 30 hours), but reported values vary considerably; the elimination half-life of chlorpromazine in the human brain is unknown.
Pharmacokinetics of chlorpromazine in neonates have not been reported. Researchers investigated the plasma clearance kinetics of chlorpromazine in an infant whose mother received high-dose chlorpromazine and lithium treatment during late pregnancy. The infant presented with severe neurological depression after birth, which gradually subsided within the first nine days. A two-compartment model was used to characterize the plasma clearance kinetics of chlorpromazine, revealing a rapid half-life of 1.46 days and a slow half-life of 3.19 days. Both half-lives are significantly longer than the rapid and slow half-lives of chlorpromazine in adults. Therefore, caution should be exercised when dealing with fetal or neonatal exposure to chlorpromazine. Further research is needed on the distribution and excretion of chlorpromazine in newborns.

Toxicity Summary
Identification: Chlorpromazine is an antipsychotic drug. It is a synthetic dimethylamine derivative of phenothiazine. Chlorpromazine is a white to off-white powder (base and hydrochloride). The base is a powder or waxy solid; the hydrochloride is a crystalline powder. Chlorpromazine is practically insoluble in water. It is readily soluble in dilute mineral acids; practically insoluble in dilute alkali hydroxides. Human Exposure: Main Risks and Target Organs: The primary pharmacological action is psychoactive. It also has sedative and antiemetic effects. Chlorpromazine acts on all levels of the central nervous system, primarily the subcortical level, and multiple organ systems. Chlorpromazine has potent antiadrenergic activity and weak peripheral anticholinergic activity; its ganglion blocking effect is relatively weak. It also has mild antihistamine and antiserotonin activity. Clinical Manifestations Overview: Central nervous system depression can progress from drowsiness to coma, eventually leading to loss of reflexes. In early or mild poisoning, some patients may experience agitation, confusion, and excitement. Tremors or muscle twitching, spasms, rigidity, seizures, hypotonia, and dysphagia may occur. Extrapyramidal overdose symptoms include dystonia, torticollis, oculomotor crisis, and opisthotonus. Hypothermia or hyperthermia may occur. Respiratory distress, cyanosis, respiratory and/or vasomotor failure, respiratory depression and respiratory distress, sudden apnea, and even cyanosis may occur. Hypotension, tachycardia, arrhythmias, conduction block, ventricular fibrillation, or cardiac arrest may occur. Contraindications: Chlorpromazine is contraindicated in the presence of coma or large doses of central nervous system depressants (alcohol, barbiturates, anesthetics, etc.), as it can prolong and enhance the effects of such central nervous system depressants. Patients with cardiovascular disease or liver disease should use chlorpromazine with caution. There is evidence that patients with a history of hepatic encephalopathy due to cirrhosis are more sensitive to the central nervous system effects of chlorpromazine (e.g., impaired brain function and abnormally slowed EEG). Because chlorpromazine has a central nervous system depressant effect, it should be used with caution in patients with chronic respiratory diseases, especially children, such as severe asthma, emphysema, and acute respiratory infections. Aspiration of vomit may occur because chlorpromazine can suppress the cough reflex. Subcutaneous injection is contraindicated. Routes of administration: Oral: Chlorpromazine is available in tablet and syrup forms for oral administration. Injection: Injectable forms are available for intramuscular or intravenous administration. Other: Rectal administration, suppositories. Absorption: The absorption of oral chlorpromazine depends on the dosage form; oral solutions achieve the highest plasma concentrations. Peak plasma concentrations are reached in 2 to 3 hours. Individual plasma concentrations vary considerably (up to tenfold or more). Gastric food and concurrent administration of anticholinergic anti-Parkinson's drugs can significantly reduce plasma concentrations. Due to the first-pass effect, plasma concentrations after oral administration are much lower than those after intramuscular administration. Distribution: Chlorpromazine is widely distributed throughout the body and can cross the blood-brain barrier, with higher concentrations in brain tissue than in plasma. Chlorpromazine and its metabolites can cross the placental barrier and are secreted in breast milk. Chlorpromazine is highly bound to plasma proteins, with binding rates ranging from 91.8% to 97% within the clinical plasma concentration range (0.01 to 1 μg/mL). This binding is readily reversed. Biological half-life (by route of exposure): While the plasma half-life of chlorpromazine itself has been reported to be only a few hours, the elimination of its metabolites can be very prolonged. Blood studies show half-lives of 2 to 3 days, while urine studies show half-lives of up to approximately 18 days. Changes caused by chlorpromazine can persist for a longer period after discontinuation. The exact relationship between sustained therapeutic effects and the chlorpromazine used is unclear. It is possible that trace amounts of chlorpromazine and/or its metabolites may remain at the active site in a slow, reversible, or relatively irreversible manner. Chlorpromazine appears to be partially stored in adipose tissue and slowly released after discontinuation. Metabolism: The metabolic pathways of chlorpromazine include hydroxylation, glucuronic acid conjugation, N-oxidation, sulfur atom oxidation, and dealkylation. In humans, the highest concentrations of unconjugated chlorpromazine metabolites are found in the lungs and liver after prolonged use of chlorpromazine. 7-Hydroxychlorpromazine, found in tissues, appears to be an active metabolite. Given evidence that chlorpromazine can induce the activity of hepatic microsomal enzymes, it may accelerate its own metabolism; this could explain the gradual decrease in free drug plasma concentrations during maintenance of a fixed-dose regimen. Currently, 168 possible chlorpromazine metabolites have been identified, many of which have been isolated from human urine. In humans, chlorpromazine and its sulfoxides are excreted in urine at rates ranging from 1% to 20% of the daily dose. The average ratio of free chlorpromazine to sulfoxides in urine is approximately 1:16. Extensive evidence suggests that sulfoxides are further metabolized, potentially converting into sulfones. Various phenothiazine homologues of chlorpromazine undergo similar metabolic degradation. Hepatic demethylation is another detoxification pathway. Excretion pathways: Chlorpromazine is primarily excreted via urine and feces. Mechanism of action: Chlorpromazine has broad activity due to its central nervous system depressant effects, alpha-adrenergic blocking effects, and weak anticholinergic effects. Chlorpromazine has a sedative effect, but patients usually develop tolerance to it quickly. Its effects on the autonomic nervous system can cause vasodilation, hypotension, and tachycardia. It also reduces salivation and gastric juice secretion. Phenothiazine sulfoxides have been extensively studied and found to be significantly less potent than the parent compound. Teratogenicity: Long-term use of high doses of chlorpromazine during pregnancy may damage the fetal retina. Drug interactions: Chlorpromazine may block the hypotensive effect of guanethidine. Patients taking phenothiazine drugs should be informed that their sensitivity to alcohol may be increased. Chlorpromazine has been shown to enhance the miotic and sedative effects of morphine. Chlorpromazine may enhance respiratory depression, especially respiratory depression caused by central nervous system depressants. Mutual inhibition of hepatic enzymes involved in the metabolism of chlorpromazine and another drug (such as tricyclic antidepressants) may lead to increased plasma concentrations of one of the drugs. Chlorpromazine has been reported to interfere with various laboratory tests, such as pregnancy tests, thyroid function tests, Coombs tests (potentially producing false positives), and adrenal medullary examinations. Furthermore, it can interfere with the measurement of serum 5-hydroxyindoleacetic acid, blood urea, urinary ketones and steroids, urinary bilirubinogen, and vitamin B12. Major adverse reactions: Therapeutic doses of chlorpromazine may cause palpitations, nasal congestion, dry mouth, and mild constipation. Patients may complain of chills, drowsiness, or fatigue. Orthostatic hypotension may lead to syncope. Mild fever may occur in the first few days of use, especially with parenteral administration. Conversely, hypothermia may also occur, possibly due to the drug's effect on the thermoregulatory center and direct peripheral vasodilation. Impaired sensitivity and adaptability to changes in ambient temperature may lead to complications such as fatal hyperthermia and heatstroke. Chlorpromazine can cause a variety of hematologic disorders, including agranulocytosis, eosinophilia, leukopenia, hemolytic anemia, aplastic anemia, thrombocytopenic purpura, and pancytopenia. Hyperglycemia, hypoglycemia, and glycosuria have also been reported. Chlorpromazine acts as an antagonist (blocker) on different postsynaptic receptors—dopaminergic receptors (D1, D2, D3, and D4 subtypes—with different antipsychotic properties for productive and nonproductive symptoms), serotonergic receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressant, and anti-aggressive effects, and can reduce the side effects of extrapyramidal drugs, but can also cause weight gain, hypotension, sedation, and ejaculatory dysfunction), histaminergic receptors (H1 receptors, with sedative, antiemetic, dizziness, hypotension, and weight gain effects), and α1/α2 receptors (with antisympathetic effects, can lower blood pressure, cause reflex tachycardia, and dizziness). Side effects of chlorpromazine include sedation, excessive salivation, urinary incontinence, and sexual dysfunction (but it may also alleviate pseudo-Parkinsonian syndrome—this is controversial). In addition, chlorpromazine acts on muscarinic (cholinergic) M1/M2 receptors (causing anticholinergic symptoms such as dry mouth, blurred vision, constipation, difficulty/inability to urinate, sinus tachycardia, ECG changes, and memory loss, but its anticholinergic effect may reduce extrapyramidal side effects). Furthermore, chlorpromazine is a weak presynaptic dopamine reuptake inhibitor, which may produce (mild) antidepressant and anti-Parkinsonian effects. This effect may also lead to psychomotor agitation and exacerbation of psychotic symptoms (rarely seen in clinical practice). Drug Interactions…Patients taking chlorpromazine may need to increase the dose of their oral hypoglycemic agents…
QT interval prolonging drugs, including cisapride, erythromycin, and quinidine, may produce additive QT interval prolongation when used in combination with phenothiazines, increasing the risk of arrhythmias.
Phenothiazines may produce additive photosensitizing effects when used in combination with other photosensitizing drugs. Furthermore, phenothiazines may enhance intraocular photochemical damage to the choroid, retina, or lens when used in combination with systemic methoxsalen, triamcinolone, or tetracyclines.
Prior use of phenothiazines may reduce the pressor effect of phenylephrine and shorten its duration of action.
For more complete interaction data on chlorpromazine (37 interactions total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats: 225 mg/kg
Oral LD50 in rats: 142 mg/kg
Intraperitoneal LD50 in rats: 58 mg/kg
Subcutaneous LD50 in rats: 75 mg/kg
For more complete non-human toxicity data for chlorpromazine (out of 10), please visit the HSDB record page.

[1]. Multifaceted effect of chlorpromazine in cancer: implications for cancer treatment. Oncotarget. 2021 Jul 6;12(14):1406-1426.

[2]. The antipsychotic agent chlorpromazine induces autophagic cell death by inhibiting the Akt/mTOR pathway in human U-87MG glioma cells. Carcinogenesis. 2013 Sep;34(9):2080-9.

[3]. Cancer cell-intrinsic XBP1 drives immunosuppressive reprogramming of intratumoral myeloid cells by promoting cholesterol production. Cell Metab. 2022 Nov 2:S1550-4131(22)00461-2.

[4]. Mechanism of inhibition by chlorpromazine of the human pain threshold sodium channel, Nav1.7. Neurosci Lett. 2017 Feb 3;639:1-7.

[5]. The antipsychotic drug chlorpromazine inhibits HERG potassium channels. Br J Pharmacol. 2003 Jun;139(3):567-74.

[6]. Comparison of the anti-dopamine D₂ and anti-serotonin 5-HT(2A) activities of chlorpromazine, bromperidol, haloperidol and second-generation antipsychotics parent compounds and metabolites thereof. J Psychopharmacol. 2013 Apr;27(4):396-400.

Therapeutic Uses

Antiemetic; Antipsychotic, phenothiazines; Dopamine antagonist
/Chlorpromazine is indicated for/the treatment of schizophrenia. /US product label contains/
/Chlorpromazine is indicated for/the control of nausea and vomiting. /US product label contains/
/Chlorpromazine is indicated for/the relief of preoperative agitation and anxiety. /US product label contains/
For more complete data on the therapeutic uses of chlorpromazine (16 in total), please visit the HSDB record page.

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Drug Warnings
Older patients with dementia-related psychosis receiving antipsychotic medication have an increased risk of death. An analysis of 17 placebo-controlled trials (mean duration 10 weeks) showed that the risk of death in the drug treatment group was 1.6 to 1.7 times higher than in the placebo group. These trials primarily involved patients taking atypical antipsychotic medications. In a typical 10-week controlled trial, the mortality rate was approximately 4.5% in the drug treatment group and approximately 2.6% in the placebo group. Although the causes of death vary, most deaths appear to be related to cardiovascular diseases (e.g., heart failure, sudden death) or infectious diseases (e.g., pneumonia). Observational studies have shown that, similar to atypical antipsychotics, conventional antipsychotic treatment may also increase mortality. However, it is unclear to what extent the increased mortality observed in observational studies is attributable to the antipsychotics themselves or to certain patient characteristics. Chlorpromazine hydrochloride injection (USP) is not approved for the treatment of patients with dementia-related psychosis.
...Extrapyramidal reactions...quite common, usually of three types...Parkinsonian syndrome...dystonia and movement disorders, including torticollis, tics, and other involuntary muscle movements...akathisia, manifested as restlessness...hyperreflexia has been reported in newborns.../Phenothiazines/
The antiemetic effect of chlorpromazine may mask the signs and symptoms of other drug overdose and may interfere with the diagnosis and treatment of other conditions (e.g., intestinal obstruction, brain tumors, and Reye's syndrome). When chlorpromazine is used in combination with anticancer chemotherapy drugs, its antiemetic effect may mask vomiting symptoms caused by the toxicity of these drugs. Chlorpromazine is contraindicated in patients with known hypersensitivity to phenothiazines. It is contraindicated in the presence of coma or large amounts of central nervous system depressants (alcohol, barbiturates, anesthetics, etc.). For more complete data on chlorpromazine (55 total), please visit the HSDB records page. Pharmacodynamics: Chlorpromazine is a psychotropic drug used to treat schizophrenia. It also has sedative and antiemetic effects. Chlorpromazine acts on various levels of the central nervous system—primarily the subcortical level—and multiple organ systems. Chlorpromazine has strong antiadrenergic activity and weak peripheral anticholinergic activity; its ganglion blocking effect is relatively weak. It also has mild antihistamine and antiserotonin activity.

C17H19CLN2S

318.864161729813

318.095

C, 64.04; H, 6.01; Cl, 11.12; N, 8.79; S, 10.05

50-53-3

Chlorpromazine hydrochloride;69-09-0;Chlorpromazine-d6 hydrochloride;1228182-46-4;Chlorpromazine-d6 oxalate;1276197-23-9

2726

White to off-white solid

1.2±0.1 g/cm3

450.1±45.0 °C at 760 mmHg

192 - 196ºC (decomposes)

226.0±28.7 °C

0.0±1.1 mmHg at 25°C

1.623

5.2

0

3

4

21

339

0

CN(C)CCCN1C2=CC=CC=C2SC3=C1C=C(C=C3)Cl

ZPEIMTDSQAKGNT-UHFFFAOYSA-N

InChI=1S/C17H19ClN2S/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

10H-Phenothiazine-10-propanamine, 2-chloro-N,N-dimethyl-

BC-135; BC135; BC 135

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : 100 mg/mL (313.62 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.84 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.

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Solubility in Formulation 2: 2.5 mg/mL (7.84 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
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 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: ≥ 2.5 mg/mL (7.84 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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)