Absorption, Distribution and Excretion
This drug is rapidly and completely absorbed. Due to first-pass metabolism in the liver and intestinal wall, its absolute bioavailability is approximately 50%. Peak plasma concentrations are reached approximately 2 hours after oral administration. Food has minimal effect on the absorption of mirtazapine, and no dose adjustment is required when taken with food. Steady-state plasma concentrations are reached approximately 5 days after the first dose. The pharmacokinetics of mirtazapine vary with sex and age. Studies have shown that plasma concentrations are higher in women and older adults than in men and younger adults. The drug is primarily excreted by the kidneys, with 75% excreted in the urine and 15% in the feces. One pharmacokinetic study determined the volume of distribution after an oral steady-state dose to be 107 ± 42 L. A clinical pharmacokinetic study found a total clearance of 31 L/h in men after intravenous administration. **Clearance in Elderly Patients** Mirtazapine is cleared more slowly in older adults than in younger adults. Therefore, caution should be exercised when using this drug in elderly patients. One clinical trial showed that the clearance of mirtazapine was significantly lower in older men compared to younger men taking the same dose. The difference in clearance rates between older women and younger women taking mirtazapine was smaller. **Clearance Rate in Patients with Hepatic or Renal Impairment** Clearance is reduced in patients with hepatic or renal impairment, and dose adjustments may be necessary. Moderate renal and hepatic impairment can reduce mirtazapine clearance by approximately 30%. Severe renal impairment can reduce mirtazapine clearance by 50%.

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Metabolism / Metabolites
Mirtazapine is extensively metabolized in the human body. Demethylation, hydroxylation, and subsequent glucuronidation are the main metabolic pathways of mirtazapine. In vitro human liver microsomal studies show that cytochrome P450 2D6 and 1A2 can generate the 8-hydroxy metabolite of mirtazapine. The CYP3A enzyme metabolizes this drug into N-demethyl and N-oxide metabolites. Several other pharmacologically active non-conjugated metabolites also exist, but their concentrations in the blood are low. Known human metabolites of mirtazapine include 8-hydroxymirtazapine, mirtazapine N-oxide, and N-demethylmirtazapine. Mirtazapine is primarily metabolized via demethylation, hydroxylation, and subsequent glucuronidation. Cytochrome P450 2D6 and cytochrome P450 1A2 are involved in the generation of the 8-hydroxy metabolite of mirtazapine, while cytochrome P450 3A4 is responsible for the generation of the N-demethyl and N-oxide metabolites. Many metabolites possess pharmacological activity, but their plasma concentrations are extremely low. Excretion route: This drug is known to be primarily excreted via the kidneys (75%). Half-life: 20-40 hours.

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Biological Half-Life
20-40 hours

Toxicity Summary
Mirtazapine is a relatively safe medication, although its toxicity is slightly higher than most selective serotonin reuptake inhibitors (SSRIs) (except citalopram). Deaths from mirtazapine overdose are rare. The reported lethal toxicity index for mirtazapine is 3.1 deaths per million prescriptions (95% confidence interval), similar to observations of SSRIs. A study involving 267 patients with mirtazapine overdose reported tachycardia, mild hypertension, and mild central nervous system depression associated with overdose, with more severe toxicities observed in patients taking other substances concurrently. Unlike tricyclic antidepressants, mirtazapine does not produce significant cardiovascular adverse effects even at doses up to 22 times its maximum recommended dose. Some case reports show that mirtazapine overdose at 30 to 50 times the prescribed dose has relatively lower toxicity compared to tricyclic antidepressants. Signs and symptoms of mirtazapine overdose include disorientation, somnolence, bradycardia, and memory loss. As mentioned above, doses exceeding the recommended dosage, especially mixed overdose, can have serious consequences, including death. Clinicians should provide supportive care for patients who have overdosed on mirtazapine. There is currently no specific antidote for mirtazapine. Please contact a poison control center (1-800-222-1222) for the latest advice. Treatment: * Ensure an open airway, oxygenation, and ventilation. * Monitor heart rhythm and vital signs. * Treat arrhythmias according to Advanced Life Support (ACLS) and Pediatric Advanced Life Support (PALS) protocols. Mirtazapine, as an antagonist of the presynaptic α2 receptor in the central nervous system, inhibits negative feedback in the presynaptic neurite, leading to increased norepinephrine (NE) release. Blocking the heterologous α2 receptor present in serotonergic neurons enhances the release of serotonin (5-HT) and increases the interaction between 5-HT and 5-HT_sub>1 receptors, thereby enhancing the anxiolytic effect of mirtazapine. Mirtazapine has a weak antagonistic effect on 5-HT1 receptors, while exhibiting a potent antagonistic effect on 5-HT2 receptors (especially subtypes 2A and 2C) and 5-HT3 receptors. Blocking these receptors may explain the low incidence of adverse reactions to mirtazapine, such as anxiety, insomnia, and nausea. Furthermore, mirtazapine also has a significant antagonistic effect on H1 receptors, thus producing a sedative effect. Mirtazapine has no effect on the reuptake of norepinephrine or serotonin, and its activity on dopaminergic and muscarinic receptors is extremely low.

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Hepatotoxicity
Up to 10% of patients taking mirtazapine have reported liver dysfunction, but the elevations are usually small and rarely require dose adjustment or discontinuation. Rare cases of acute, clinically significant liver injury with markedly elevated liver enzymes have been reported in patients taking mirtazapine, with or without jaundice. The onset time of liver injury varies widely, ranging from months to years. The pattern of serum enzyme elevation is usually hepatocellular, but mixed patterns have also been reported. Autoimmune (autoantibodies) and immunoallergic features (rash, fever, eosinophilia) are uncommon. Probability score: C (Possibly a rare cause of clinically significant liver disease).

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Effects During Pregnancy and Lactation
◉ Summary of Use During Lactation
Limited information suggests that even with daily doses up to 120 mg, low concentrations of the drug in breast milk are not expected to have any adverse effects on breastfed infants, especially those older than 2 months. If the mother needs to take mirtazapine, this is not a reason to discontinue breastfeeding. A safety rating system considers mirtazapine safe for use during lactation. If this medication is used during lactation, the behavioral side effects and growth and development of the exclusively breastfed infant should be monitored.
◉ Effects on Breastfed Infants
A 14-week-old infant was breastfed 6 times daily while the mother was treated with 30 mg mirtazapine daily. After 6 weeks of treatment, the infant's psychomotor development was normal, and no adverse reactions, including sedation or abnormal weight gain, were observed.
Eight infants with a mean age of 6.3 months (range 1.5 to 13 months) were breastfed by mothers taking mirtazapine at a mean dose of 495 μg/kg daily for 6 to 129 days. At the time of the study, the average Denver developmental age of the seven infants was 101% of the normal range. No adverse reactions were observed in any of the infants. One 6-week-old infant was exclusively breastfed by a mother who took 22.5 mg of mirtazapine nightly starting 4 weeks postpartum. The infant was followed weekly and no sedation or abnormal weight gain was observed, although the infant's weight had been below the 25th percentile before starting mirtazapine. One 2-month-old infant was breastfed by a mother (feeding extent not specified) who took 15 mg of mirtazapine daily during pregnancy and lactation. This mother reported that the infant had a higher birth weight, gained weight faster than her previous three children, and, unlike her other children, slept through the night at this age. The authors note that these observations may not necessarily be attributable to mirtazapine. In a case series study involving 55 women who took mirtazapine during pregnancy and postpartum, 24 of their 56 infants were exclusively breastfed and 20 were partially breastfed. In infants exposed to mirtazapine in utero during late pregnancy, the incidence of neonatal maladaptive syndrome was lower in partially or exclusively breastfed infants than in exclusively formula-fed infants. No sleep or feeding problems were observed in any of the infants.
Another case series reported on eight women taking paroxetine 20 mg and mirtazapine 15 mg daily for various psychiatric disorders. These women breastfed their infants, who were an average of 4.3 weeks old (the extent of breastfeeding was not specified). Infants were followed up 3 to 6 weeks after discontinuation of mirtazapine. One infant developed restlessness 5 days after treatment, as described by the mother. Symptoms did not improve after discontinuation of mirtazapine, but disappeared after discontinuation of paroxetine. No other adverse reactions were observed in other infants.
◉ Effects on lactation and breast milk
An 89-year-old male developed gynecomastia, hyperprolactinemia, and galactorrhea after 21 months of daily mirtazapine administration of 30 mg. Symptoms resolved and prolactin levels returned to normal one month after discontinuation of the drug. A 28-year-old female hospitalized patient developed galactorrhea, breast pain, fatigue, and extensive subcutaneous edema of the trunk and extremities after her mirtazapine dose was adjusted to 30 mg daily for 4 weeks. At this time, her morning serum prolactin level was not elevated; however, after 12 days, her morning serum prolactin level rose to 32.1 mcg/L (normal range 4.79-23.3 mcg/L). After discontinuing mirtazapine and starting escitalopram, her serum prolactin level returned to normal, and the edema and galactorrhea symptoms subsided within a week. A pituitary tumor has been ruled out. Mirtazapine is likely the cause of the patient's symptoms. The clinical significance of these findings for lactating women is unclear. For mothers who have established lactation, prolactin levels may not affect their ability to breastfeed. An observational study investigated the outcomes of 2859 women who had taken antidepressants for two years prior to pregnancy. Compared to women who did not take antidepressants during pregnancy, mothers who took antidepressants in all three stages of pregnancy were 37% less likely to breastfeed at discharge. Mothers who took antidepressants only in the third trimester were 75% less likely to breastfeed at discharge. Mothers who took antidepressants only in the first and second trimesters were not less likely to breastfeed at discharge. The study did not specify the type of antidepressant used by the mothers. A retrospective cohort study analyzed hospital electronic medical records from 2001 to 2008, comparing women who took antidepressants in the third trimester (n = 575; mirtazapine n = 12), women with mental illness but not taking antidepressants (n = 1552), and mothers without a diagnosed mental illness (n = 30,535). The results showed that women taking antidepressants were 37% less likely to breastfeed at discharge than women without a diagnosed mental illness, but there was no difference in the likelihood of breastfeeding compared to mothers without a diagnosed mental illness but not receiving treatment. A study of 80,882 Norwegian mother-infant pairs between 1999 and 2008 showed that 392 women reported starting antidepressant use postpartum, and another 201 women reported starting antidepressant use during pregnancy. Compared to a control group unexposed to antidepressants, antidepressant use in late pregnancy was associated with a 7% lower rate of breastfeeding initiation, but had no effect on the duration of breastfeeding or the rate of exclusive breastfeeding. Compared to a control group unexposed to antidepressants, starting or restarting antidepressant use postpartum was associated with a 63% lower rate of breastfeeding as the primary breastfeeding method at 6 months, a 51% lower rate of breastfeeding of any method, and a 2.6-fold increased risk of abrupt cessation of breastfeeding. The study did not mention any specific antidepressants. What is mirtazapine? Mirtazapine is a medication used to treat major depressive disorder and hyperemesis gravidarum (gestational vomiting). The brand name for mirtazapine is Remeron®. The MotherToBaby website provides information on mirtazapine for treating hyperemesis gravidarum: Depression (https://mothertobaby.org/fact-sheets/depression-pregnancy/) and hyperemesis gravidarum (https://mothertobaby.org/fact-sheets/nausea-vomiting-pregnancy-nvp/). Sometimes, when people find out they are pregnant, they consider changing their medication regimen or even stopping it altogether. However, it is essential to consult your healthcare provider before changing your medication regimen. Your healthcare provider can discuss with you the benefits of treating your condition and the risks of not treating it during pregnancy. Some people may experience a relapse of symptoms if they stop taking this medication during pregnancy. ◈ I am taking mirtazapine. Will taking mirtazapine affect my ability to get pregnant?
In some people, mirtazapine may raise levels of a hormone called prolactin. High levels of prolactin can suppress ovulation (the process by which the ovary releases an egg during the menstrual cycle). This can make it more difficult to conceive. If you have any concerns, your healthcare provider can test your prolactin levels.
◈ Does taking mirtazapine increase the risk of miscarriage?
Miscarriage is common and can occur in any pregnancy for a variety of reasons. One study found no association between taking mirtazapine and an increased risk of miscarriage. Depression itself may increase the risk of miscarriage.
◈ Does taking mirtazapine increase the risk of birth defects?
There is a 3-5% risk of birth defects in every pregnancy. This is called background risk. Studies and case reports have investigated nearly 5,000 pregnancies in which mirtazapine was taken and no increased risk of birth defects was found.
◈ Does taking mirtazapine during pregnancy increase the risk of other pregnancy-related problems?
Some studies suggest that taking mirtazapine throughout pregnancy may increase the risk of other pregnancy-related problems, such as preterm birth (delivery before 37 weeks of gestation) or low birth weight (birth weight less than 5 pounds 8 ounces [2500 grams]). Studies have also shown that untreated prenatal depression can increase the risk of pregnancy complications such as premature birth, low birth weight, and preeclampsia (high blood pressure and organ problems such as kidney problems), the latter of which can lead to seizures (called eclampsia). Therefore, it is difficult to determine whether medication, an underlying medical condition, or other factors increase the risk of these problems.
◈ I need to take mirtazapine throughout my pregnancy. Will my baby experience withdrawal symptoms after birth?
Taking mirtazapine during pregnancy may cause temporary symptoms in newborns shortly after birth. These symptoms are sometimes called withdrawal reactions. Symptoms may include sensitivity to light and sound (called hyperexcitability), a rapid heart rate, tremors, and thermoregulation disorders shortly after birth. In most cases, these symptoms are mild and disappear on their own. Some infants may require treatment in the neonatal intensive care unit until the symptoms disappear. Not all infants exposed to mirtazapine will experience these symptoms. It is important that your healthcare provider knows you are taking mirtazapine so that your baby can receive optimal care if symptoms occur.
◈ Will taking mirtazapine during pregnancy affect my child's future behavior or learning?
Currently, there are no studies indicating whether mirtazapine causes behavioral or learning problems in children.
◈ Breastfeeding while taking mirtazapine:
Small amounts of mirtazapine pass into breast milk. Most breastfed infants have not reported side effects from the drug in their breast milk. If you suspect your baby is experiencing any symptoms (such as excessive sleepiness), contact your child's healthcare provider. Be sure to discuss all your breastfeeding questions with your healthcare provider.
◈ Does mirtazapine affect fertility or increase the risk of birth defects if the man is taking it?
It is currently unclear whether mirtazapine affects male fertility (the ability to impregnate a partner) or increases the risk of birth defects (above background risk). Generally, contact with the father or sperm donor is unlikely to increase the risk of pregnancy. For more information, see the “Father Contact” fact sheet on the MotherToBaby website: https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/.

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Protein Binding
Mirtazapine binds to plasma proteins at a rate of approximately 85%.

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Toxicity Data
LD50: 600-720 mg/kg (oral, mouse) (L1855)
LD50: 320-490 mg/kg (oral, rat) (L1855)

Mirtazapine is a benzodiazepine tetracyclic antidepressant. It has various pharmacological effects, including dream-inducing, anti-anxiety, alpha-adrenergic antagonism, H1 receptor antagonism, histamine antagonism, and serotonergic antagonism. Mirtazapine is a tetracyclic piperazine benzodiazepine antidepressant, initially approved in the Netherlands in 1994 for the treatment of major depressive disorder (MDD). Originally manufactured by Organon, it was approved by the U.S. Food and Drug Administration (FDA) for the treatment of MDD in 1997. The drug's effects can be seen as early as one week after starting treatment. In addition to its efficacy against depression, mirtazapine has been reported to be used to treat a variety of other conditions (out-of-care treatment). It may improve symptoms of neurological disorders, reverse disease-induced weight loss, improve sleep, and prevent postoperative nausea and vomiting. Mirtazapine is a tetracyclic antidepressant with a unique mechanism of action. Mirtazapine treatment may cause a transient, asymptomatic increase in serum transaminase levels and has been associated with rare cases of clinically significant acute liver injury. Mirtazapine is a synthetic tetracyclic derivative of piperazine-azapine compounds with antidepressant activity. Although its mechanism of action is not fully understood, mirtazapine may enhance central adrenergic and serotonergic neurotransmission by antagonizing presynaptic α2-adrenergic inhibitory autoreceptors and heteroreceptors. This drug is a potent antagonist of serotonin type 2 (5-HT2), 5-HT3, and histamine 1 (H1) receptors, and a moderate antagonist of peripheral α1-adrenergic and muscarinic receptors. Mirtazapine was introduced by Organon International in 1996 for the treatment of moderate to severe depression. With a tetracyclic chemical structure, mirtazapine is classified as a noradrenergic and specific serotonergic antidepressant (NaSSA). It is the only tetracyclic antidepressant approved by the U.S. Food and Drug Administration (FDA) for the treatment of depression. It is a piperazine-azapine tetracyclic compound that enhances the release of norepinephrine and serotonin by blocking presynaptic α2-adrenergic receptors. It also blocks 5-HT2 and 5-HT3 serotonin receptors and is a potent histamine H1 receptor antagonist. It is used to treat depression and may also be effective in treating anxiety disorders. See also: Mianserin (related drug); Opimidazole (related drug); Lofepramine (related drug)... See more...

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Drug Indication
This medication is indicated for the treatment of major depressive disorder and related symptoms. Mirtazapine has been used to treat a variety of conditions, including panic disorder, generalized anxiety disorder, dysphoric mood, tension headaches, hot flashes, post-traumatic stress disorder (PTSD), sleep disorders, substance abuse disorders, and sexual dysfunction.
FDA Label
Mirtazapine is an atypical antidepressant primarily used to treat major depressive disorder. It was first synthesized in 1989 and approved in the Netherlands in 1994 for the treatment of major depressive disorder. In 1996, mirtazapine was approved by the U.S. Food and Drug Administration (FDA) for the treatment of moderate to severe depression. Mirtazapine has not yet been approved by the FDA for use in children.

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Mechanism of Action
**Overview** The mechanism of action of mirtazapine is not fully understood, but it may be related to its effects on central adrenergic and serotonergic activity. This drug has a rapid onset of action, significant efficacy, manageable side effects, and exhibits dual noradrenergic and serotonergic activity, unlike other antidepressants. **Effects on Multiple Receptors** Studies have shown that mirtazapine administration enhances both noradrenergic and serotonergic activity. These results indicate that mirtazapine antagonizes both presynaptic α2-adrenergic inhibitory autoreceptors and heteroreceptors in the central nervous system. This is thought to enhance noradrenergic and serotonergic activity, which is known to improve depressive symptoms and forms the basis of antidepressant treatment. Mirtazapine is a potent antagonist of serotonin type 2 (5-HT2) and type 3 (5-HT3) receptors. Although significant binding to serotonin type 1A (5-HT1A) and type 1B (5-HT1B) receptors has not yet been found, it can indirectly enhance 5-HT1A receptor transmission. In addition to the above effects, mirtazapine is also a peripheral α1-adrenergic receptor antagonist. This effect may explain the orthostatic hypotension that occurs after taking mirtazapine. Miralzapine is also a potent histamine H1 receptor antagonist, which may be related to its strong sedative effect. The analgesic effect of mirtazapine may be related to its action on opioid receptors.

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Pharmacodynamics
**General Effects and Suicide Risk Warnings** Mirtazapine is effective in treating moderate to severe depression and can alleviate many associated symptoms. These symptoms may include sleep disturbances, loss of appetite, anhedonia, and anxiety. It is important to note that, as with other antidepressants, suicidal ideation and behavior may occur or worsen while taking mirtazapine. This risk is particularly pronounced in young adults. Patients, healthcare professionals, and family members should closely monitor patients for suicidal thoughts, worsening depression, anxiety, agitation, sleep changes, irritability, aggression, impulsivity, restlessness, and other unusual behaviors when taking this medication or adjusting the dosage. Do not give mirtazapine to children. The increased risk of suicidal ideation and behavior, especially in young adults, should be carefully considered when deciding whether to prescribe this medication. **Effects on Appetite and Weight Gain** In addition to the above effects, mirtazapine also has an appetite-stimulating effect and has been used to increase appetite and reduce nausea in cancer patients. Some studies and case reports have shown that when used in combination with psychotherapy and/or other psychotropic medications, this medication can improve eating habits and increase weight in patients with anorexia nervosa. In a clinical trial, female patients with depression who received mirtazapine treatment for 6 weeks experienced clinically significant increases in weight, body fat mass, and leptin concentration, without affecting glucose homeostasis. **Effects on Sleep** Mirtazapine is used to treat sleep disorders through its sedative effect, a common side effect of this medication. Studies have shown that the sedative effect of mirtazapine can improve sleep latency, sleep duration, and sleep quality. Insomnia is a common symptom of depression, and mirtazapine has been proven effective in treating this condition.

C17H19N3

265.35

265.158

61337-67-5

4205

White to off-white solid powder

1.2±0.1 g/cm3

432.4±45.0 °C at 760 mmHg

114-116 °C ; 114 - 116 °C

215.3±28.7 °C

0.0±1.0 mmHg at 25°C

1.668

2.75

0

3

0

20

345

0

CN1CCN2C(C1)C3=CC=CC=C3CC4=C2N=CC=C4

RONZAEMNMFQXRA-UHFFFAOYSA-N

InChI=1S/C17H19N3/c1-19-9-10-20-16(12-19)15-7-3-2-5-13(15)11-14-6-4-8-18-17(14)20/h2-8,16H,9-12H2,1H3

5-methyl-2,5,19-triazatetracyclo[13.4.0.02,7.08,13]nonadeca-1(15),8,10,12,16,18-hexaene

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.)