D2 receptor blockade
[3]

Trifluoperazine is a widely used, "traditional" antipsychotic medication with a lengthy history. One extensively researched medication that has been utilized as a calmodulin inhibitor is trifluoperazine [3][4]. Trifluoperazine interferes with cellular CaM and/or CaM-dependent processes to operate as a reversible inhibitor of influenza virus morphogenesis, but not budding [5].

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In MDCK cells infected with influenza A NWS virus, TFP inhibited virus growth in a concentration-dependent manner within the range of 20-35 μM. At 35 μM, TFP caused a significant reduction in both supernatant and cell-associated virus yields when added at various time points post-infection (p.i.), including late stages (7.5, 10, and 12.5 h p.i.). [5]
- At 35 μM, TFP completely altered the cytoplasmic distribution pattern of viral hemagglutinin (HA) from a finely dotted pattern to aggregated spots, as visualized by immunofluorescence. Concomitantly, the appearance of HA on the cell surface was markedly reduced. [5]
- Scanning electron microscopy revealed that treatment with 35 μM TFP from 1 to 7.5 h p.i. resulted in few budding virus particles on the infected cell surface compared to untreated cells, where numerous budding virions were observed. The drug also suppressed the appearance of microvilli on uninfected and infected MDCK cells. [5]
- The inhibitory effect of TFP on virus growth and HA distribution was reversible. Within 60 minutes of drug removal, the cytoplasmic HA distribution returned to a normal finely dotted pattern, and HA gradually reappeared on the cell surface. This time course correlated with the recovery of supernatant infectivity. [5]
- The anti-influenza effect of 35 μM TFP was partially reversed by the simultaneous presence of purified calmodulin (CaM) in a concentration-dependent manner. Virus yield recovered to 47.2% of control with 5 μM CaM and to 12.8% with 2 μM CaM, while 0.5 μM CaM had a negligible effect. CaM alone (5 μM) did not affect virus yield. [5]
- Metabolic labeling with [³⁵S]methionine showed that TFP (35 μM) did not cause qualitative or quantitative differences in viral protein synthesis. [5]

Compared to placebo, trifluoperazine showed effectiveness in improving global state in people with schizophrenia. In three small short-term studies (3 months or less), the risk of not showing substantial improvement was lower with trifluoperazine (n=95, RR 0.62 CI 0.49 to 0.78, NNT 3 CI 2 to 4). In three medium-term studies (3 months to 1 year), the effect also favored trifluoperazine (n=320, RR 0.93 CI 0.86 to 1.0). [3]
In a single small study (n=23), people given trifluoperazine had a lower prevalence of delusions and hallucinations compared to those given placebo (RR 0.44 CI 0.19 to 0.99, NNT 3 CI 5 to 100). [3]
One small study (n=40) using the Wings Behaviour Rating Scale reported that trifluoperazine was more effective than placebo in improving behavior (RR 0.4 CI 0.23 to 0.68). [3]
Compared to other typical antipsychotic drugs (like chlorpromazine, haloperidol), trifluoperazine was not clearly different in terms of efficacy for 'no substantial improvement' in global state. This finding was consistent across 27 RCTs involving 1016 participants (RR 1.06 CI 0.98 to 1.14). The result was similar for both acutely ill and chronically ill patients. [3]
In a single six-week study comparing trifluoperazine with the atypical antipsychotic sulpiride (n=38), no clear differences were found in global state improvement (RR 0.89 CI 0.44 to 1.81) or in mental state measures. [3]
The mean daily dose of trifluoperazine used in the included studies was approximately 28mg/day (SD 20mg/day), with a range of 4 to 100mg/day, which aligns with American Psychiatric Association recommendations. [3]

Virus Growth Inhibition Assay: MDCK cell monolayers in 35-mm dishes were infected with influenza A NWS virus at a multiplicity of infection (MOI) of 0.1 PFU/cell. After a 45-min adsorption period, cells were washed and incubated in maintenance medium at 37°C. At various times post-infection, TFP (10-35 μM) was added to the medium. At 15 h p.i., supernatant and total (cells + supernatant after sonication) virus yields were collected and titrated by plaque assay on MDCK cells in the presence of trypsin. Cell-associated virus yield was calculated by subtracting supernatant yield from total yield. [5]
- Reversibility Experiment: MDCK cells were infected at an MOI of 5 PFU/cell. At 1 h p.i., cells were transferred to medium containing 35 μM TFP. At 4.5 h p.i., the medium was replaced with drug-free medium after washing. Supernatant virus yields were assayed at 30-minute intervals thereafter. [5]
- Immunofluorescence Microscopy: MDCK cells grown on coverslips were infected at an MOI of 5 PFU/cell and cultured with or without 35 μM TFP from 1 to 4.5 h p.i. For cytoplasmic staining, cells were fixed in acetone-methanol. For cell surface staining, cells were fixed in 1% paraformaldehyde. Cells were then incubated with anti-HA monoclonal antibody (B-4) followed by FITC-labeled anti-mouse IgG. The distribution of HA was examined using a fluorescence microscope. [5]
- Scanning Electron Microscopy: Infected cells cultured with or without 35 μM TFP from 1 to 7.5 h p.i. were fixed with glutaraldehyde and OsO₄, dehydrated, and critical-point dried. After gold sputtering, samples were examined with a scanning electron microscope to visualize virus particles and cell surface structures. [5]
- Calmodulin Reversal Assay: MDCK cells were infected at an MOI of 0.1 PFU/cell. At 5 h p.i., the medium was replaced with medium containing 35 μM TFP, 5 μM purified CaM, or a mixture of 35 μM TFP with various concentrations of CaM (0.5, 2, 5 μM). At 15 h p.i., supernatant virus yields were assayed by plaque titration. [5]

Xenograft Mouse Model:** Female NMRI-Foxn1^nu/Foxn1^nu (nude) mice were used. Ten million MiaPaCa-2 cells were inoculated subcutaneously. When tumors reached approximately 200 mm³, mice were treated daily with either vehicle or TFP. Tumor volumes were measured every 5 days. Mice were sacrificed after 30 days of treatment. [2]
- **Observation of Side Effects:** Mice treated with high doses of TFP were monitored for behavioral and physical signs of toxicity, which included strong lethargy and hunched posture. [2]

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Xenograft Mouse Model: Female NMRI-Foxn1^nu/Foxn1^nu (nude) mice were used. Ten million MiaPaCa-2 cells were inoculated subcutaneously. When tumors reached approximately 200 mm³, mice were treated daily with either vehicle or TFP. Tumor volumes were measured every 5 days. Mice were sacrificed after 30 days of treatment. [2]
- Observation of Side Effects: Mice treated with high doses of TFP were monitored for behavioral and physical signs of toxicity, which included strong lethargy and hunched posture. [2]

Absorption, Distribution and Excretion
Phenothiazine drugs have an extremely long final residence time in the body. /Phenothiazines/

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Metabolism/Metabolites
Hepatic metabolism.
Prolonged administration of piperazine-substituted phenothiazine drugs to rats resulted in the presence of drug metabolites in their tissues. These metabolites are substituted ethylenediamines formed by the cleavage of the piperazine ring through multiple oxidative dealkylation reactions. ...2-Trifluoromethyl analogues are generated from trifluoperazine in a similar manner.
In vivo degradation of the trifluoperazine piperazine ring leads to the formation of γ-(phenothiazinyl-10)-propylamine and its ring-substituted analogues CF3- and Cl-. The sulfoxides of these metabolites have been identified as biotransformation products in rat (chronic) urine.
Hepatic metabolism.
Half-life: 10-20 hours

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Biological half-life
10-20 hours

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Toxicity Summary
Trifluoperazine blocks postsynaptic dopamine D1 and D2 receptors in the mesolimbic system of the brain; it inhibits the release of hypothalamic and pituitary hormones and is thought to suppress the reticular activating system, thereby affecting basal metabolism, body temperature, arousal, vasomotor activity, and vomiting. Hepatotoxicity
A higher incidence of liver dysfunction has been reported in patients taking phenothiazines long-term, but elevations of liver function indicators exceeding three times the upper limit of normal are uncommon. Transaminase abnormalities are usually mild, asymptomatic, and transient, and can be reversed with continued use. There have been reports of rare, clinically significant acute liver injury caused by trifluoperazine, similar to that caused by chlorpromazine. Jaundice usually appears within 1 to 4 weeks, and serum enzyme elevations are typically cholestatic or mixed. Some cases have experienced immune allergic reactions (rash, fever, and eosinophilia), but these are mild and self-limiting; autoantibodies are rare.
Probability Score: D (Possibly a rare cause of clinically significant liver damage).

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Effects during Pregnancy and Lactation
◉ Overview of Use During Lactation
Limited information suggests that maternal administration of up to 10 mg of trifluoperazine daily does not affect breastfed infants. Very limited long-term follow-up data suggest no adverse developmental effects when used alone with other phenothiazines. The safety rating system recommends against the use of trifluoperazine during lactation. Due to the scarcity of reported experience with trifluoperazine use during lactation, other antipsychotic medications may be preferable, especially in breastfed newborns or preterm infants.
◉ Effects on Breastfed Infants
Two mothers received oral trifluoperazine at 5 mg/day and 10 mg/day, respectively, and began breastfeeding their infants at 1 week and 8 weeks of age, respectively. Mental and motor development was assessed at various time points before the infants reached 30 months of age, and the results showed normal development.
One mother was breastfeeding from birth while taking trifluoperazine 10 mg/day, clonazepam 0.25 mg/day, and valproic acid 500 mg/day. The mother did not report any adverse reactions in the infant (follow-up time not specified).
One mother started taking trifluoperazine (dosage not specified) 2 months postpartum while breastfeeding. She also started taking olanzapine 10 mg/day, paroxetine, and procyclophosphamide (dosage not specified). The infant did not experience any adverse reactions.
◉ Effects on Lactation and Breast Milk
Phenothiazines can cause galactorrhea in 26% to 40% of female patients. Hyperprolactinemia appears to be the cause of galactorrhea. Hyperprolactinemia is caused by the drug blocking the action of dopamine in the tuberous-infundibular pathway.

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Drug Interactions
When probucol is used in combination with phenothiazines, the cumulative QT interval prolongation may increase the risk of ventricular tachycardia.
Phenothiazines
Phenothiazines may produce additive photosensitizing effects when used in combination with other photosensitizing drugs. Furthermore, concomitant use of systemic methoxsalen, trisalicyline, or tetracyclines with phenothiazines may exacerbate intraocular photochemical damage to the choroid, retina, or lens.
Pre-use of phenothiazines may reduce the pressor effect of phenylephrine and shorten its duration of action.
In addition to increasing central nervous system and respiratory depression, concomitant use of opioid (narcotic) analgesics/phenothiazines may increase orthostatic hypotension and the risk of severe constipation, which may lead to paralytic ileus and/or urinary retention.
/Phenothiazines/
For more complete data on interactions of trifluoperazines (29 in total), please visit the HSDB record page.

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Non-human toxicity values
Mouse intraperitoneal injection LD50 175 mg/kg

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Trifluoperazine is a high-potency antipsychotic drug, and its propensity to induce extrapyramidal adverse effects (EPS), such as movement disorders, is well-documented. [3]
Compared to placebo, people taking trifluoperazine were more likely to experience extrapyramidal events (n=70, 2 RCTs, RR any movement disorder 2.27 CI 1.19 to 4.33, NNH 4 CI 2 to 23). Consequently, more people in the trifluoperazine group required antiparkinson drugs to alleviate these movement disorders (n=195, 4 RCTs, RR 5.06 CI 2.49 to 10.27, NNH 4 CI 2 to 9). [3]
Trifluoperazine may be more sedating than placebo (n=119, 3 RCTs, RR 2.94 CI 1.42 to 6.10, NNH 4 CI 2 to 18). [3]
When compared to other typical antipsychotics, the overall incidence of reporting at least one adverse event was similar, with about 60% of people in both groups reporting an event (n=585, 14 RCTs, RR 0.99 CI 0.87 to 1.13). [3]
Trifluoperazine was more likely to cause extrapyramidal adverse effects overall when compared specifically to low-potency antipsychotics such as chlorpromazine (n=130, 3 RCTs, RR 1.66 CI 1.03 to 2.67, NNH 6 CI 3 to 121). There was no significant difference in EPS incidence when compared to high-potency drugs like haloperidol. [3]
The risk of extrapyramidal reactions associated with trifluoperazine, such as pseudo-parkinsonism, acute dystonic reaction, akathisia, and tardive dyskinesia, is suggested to be higher than with other phenothiazines. [3]
Trifluoperazine has a low potency for cholinergic blockade, resulting in less frequent anticholinergic effects like dry mouth, blurred vision, and urinary retention compared to some other antipsychotics. It also causes less sedation and orthostatic hypotension due to its low histaminic and alpha-adrenergic antagonism. It is usually well tolerated. [3]
One small study (n=54) asked patients if they preferred a different medication. Between 50-60% in both the trifluoperazine and loxapine groups expressed a preference for the other medication, indicating no clear preference. [3]

[1]. Huerta-Bahena J, Villalobos-Molina R, García-Sáinz JA. Trifluoperazine and chlorpromazine antagonize alpha 1- but not alpha2- adrenergic effects. Mol Pharmacol. 1983;23(1):67-70.

[2]. Ligand-based design identifies a potent NUPR1 inhibitor exerting anticancer activity via necroptosis. J Clin Invest. 2019;129(6):2500-2513. Published 2019 Mar 28.

[3]. Marques LO, Lima MS, Soares BG. Trifluoperazine for schizophrenia. Cochrane Database Syst Rev. 2004;2004(1):CD003545.

[4]. Howland RH. Trifluoperazine: A Sprightly Old Drug. J Psychosoc Nurs Ment Health Serv. 2016;54(1):20-22.

[5]. Influence of trifluoperazine on the late stage of influenza virus infection in MDCK cells. Antiviral Res. 1991;15(2):149-160.

Trifluoperazine belongs to the phenothiazine class of compounds. Its structural characteristic is the introduction of a trifluoromethyl substituent at the 2-position of the phenothiazine and a 3-(4-methylpiperazin-1-yl)propyl substituent at the N-10 position. It possesses various pharmacological activities, including dopamine antagonist, antiemetic, EC 1.8.1.12 (trypanositol disulfide reductase) inhibitor, EC 5.3.3.5 (cholesterol delta-isomerase) inhibitor, calmodulin antagonist, and phenothiazine antipsychotic. It is an N-alkylpiperazine, N-methylpiperazine compound, belonging to the phenothiazine class, and is also an organofluorine compound. It is a phenothiazine drug with effects similar to chlorpromazine. It is used as an antipsychotic and antiemetic. Trifluoperazine is a phenothiazine drug. Trifluoperazine is a phenothiazine antipsychotic drug, currently no longer commonly used in clinical practice. Trifluoperazine is a rare cause of clinically significant acute cholestatic liver injury. It has been reported to have been found in Crotalaria pallida, with supporting data. Trifluoperazine is a phenothiazine derivative and a dopamine antagonist with antipsychotic and antiemetic activities. It exerts its antipsychotic effect by blocking central dopamine receptors, thus preventing symptoms such as delusions and hallucinations caused by dopamine overdose. It also acts as a calmodulin inhibitor, leading to increased cytoplasmic calcium ion concentration. Trifluoperazine is only found in individuals who have previously used or taken the drug. It is a phenothiazine drug with a mechanism of action similar to chlorpromazine. It is used as an antipsychotic and antiemetic. [PubChem] Trifluoperazine blocks postsynaptic mesolimbic dopamine D1 and D2 receptors in the brain; it inhibits the release of hypothalamic and pituitary hormones and is thought to inhibit the reticular activating system, thereby affecting basal metabolism, body temperature, arousal, vasomotor activity, and vomiting. A phenothiazine drug with a mechanism of action similar to chlorpromazine. It is used as an antipsychotic and antiemetic. See also: phenothiazines (subclass); trifluoperazine hydrochloride (salt form); trifluoperazine dimaleate (its active ingredient). Indications: Used to treat anxiety disorders, anxiety-induced depression, and agitation. Mechanism of Action: Trifluoperazine blocks postsynaptic mesolimbic dopamine D1 and D2 receptors in the brain; it inhibits the release of hypothalamic and pituitary hormones and is thought to inhibit the reticular activating system, thereby affecting basal metabolism, body temperature, arousal, vasomotor activity, and vomiting.
...Phenothiazines block dopamine receptors, increasing dopamine turnover in the striatum. This increased turnover is thought to be a result of neural feedback mechanisms. ...Dopaminergic neurons have been identified in the substantia nigra and ventral tegmentum. Spontaneous firing of these cells increases... /Phenothiazines/

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Therapeutic Uses
Antiemetics; Antipsychotics, phenothiazines; Dopamine antagonists
In the treatment of acute psychosis, the dose of antipsychotics is increased in the first few days to control symptoms. Then, in the following weeks, the dose is adjusted according to the patient's condition. /Phenothiazines/
Antipsychotics have achieved some success in the treatment of mania and depression. /Phenothiazines/
...Trifluoperazine... has been reported to be effective in children with severe autism, and differential diagnosis of these children from so-called minimal brain damage (MBD) syndrome is crucial.
For more (complete) data on the therapeutic uses of trifluoperazine (10 in total), please visit the HSDB records page.

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Drug Warnings
Phenothiazines should be used with extreme caution and are contraindicated in untreated epilepsy patients and patients who are withdrawing from central nervous system depressants (such as alcohol and barbiturates). Phenothiazines
…A small number of patients with angina have reported increased pain during treatment with trifluoperazine. Therefore, patients with angina should be closely monitored, and the drug should be discontinued immediately if adverse reactions occur. Hydrochloride drugs
…The potential adverse effects on fetal development from use during pregnancy have not been established. …Phenothiazines…should be used with extreme caution in patients with a history of glaucoma or benign prostatic hyperplasia. /Phenothiazines/
Most antipsychotic regimens should avoid routine use of anti-Parkinson's drugs. /Phenothiazines/
For more complete data on drug warnings for trifluoperazine (28 in total), please visit the HSDB records page.

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Pharmacodynamics
Trifluoperazine is a trifluoromethylphenothiazine derivative used to treat schizophrenia and other psychotic disorders. Trifluoperazine has not been proven effective in treating behavioral complications in patients with intellectual disabilities.

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Trifluoperazine is an inexpensive and widely accessible 'conventional' or 'typical' antipsychotic drug, long-established for the treatment of schizophrenia or related psychoses. It is considered a benchmark against which other antipsychotics are compared. [3]
It is a phenothiazine derivative, chemically related to chlorpromazine, but with a higher milligram potency and an adverse effect profile similar to haloperidol, particularly concerning extrapyramidal symptoms. [3]
Its therapeutic actions are primarily initiated by blocking postsynaptic D2 receptors in the mesolimbic and mesocortical projections of the brain. Blockade in the striatum is responsible for extrapyramidal effects, and blockade in the tuberoinfundibular system can cause hyperprolactinemia. [3]
The onset of clinical effects typically takes weeks, despite the immediate D2 blockade, probably due to the time required for homovanillic acid (the principal metabolite of dopamine) levels to decrease. [3]
Although it has been claimed that trifluoperazine is effective at low doses for patients with schizophrenia, the authors conclude that this claim does not appear to be based on good-quality trial-based evidence. [3]
The authors' conclusions state that despite shortcomings and gaps in the data, there is enough consistency to confirm that trifluoperazine is an antipsychotic of similar efficacy to other commonly used neuroleptics, with a similar adverse events profile. [3]
It is recommended as an alternative when newer and more expensive antipsychotics are not readily available, due to its comparable efficacy and lower cost. [3]

C21H24N3F3S

407.49556

407.164

117-89-5

Trifluoperazine dihydrochloride;440-17-5;Trifluoperazine dimaleate;605-75-4;Trifluoperazine-d8

5566

Typically exists as solid at room temperature

1.239g/cm3

506ºC at 760mmHg

Cream-colored, fine powder from absolute alcohol; MP: 242-243 °C; pH of 5% aq soln= 2.2, Hygroscopic /Dihydrochloride/ ; MP: 193-194 °C; crystals from alcohol /Dimaleate/ ; MP: 173-175 °C /Sulfoxide dihydrochloride trihydrate/

2.32E-10mmHg at 25°C

4.886

0

7

4

28

510

0

CN1CCN(CCCN2C3=CC=CC=C3SC4=C2C=C(C=C4)C(F)(F)F)CC1

ZEWQUBUPAILYHI-UHFFFAOYSA-N

InChI=1S/C21H24F3N3S/c1-25-11-13-26(14-12-25)9-4-10-27-17-5-2-3-6-19(17)28-20-8-7-16(15-18(20)27)21(22,23)24/h2-3,5-8,15H,4,9-14H2,1H3

10-[3-(4-methylpiperazin-1-yl)propyl]-2-(trifluoromethyl)phenothiazine

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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