Absorption, Distribution and Excretion
Amitriptyline is rapidly absorbed after oral administration (bioavailability is 30-60% due to first-pass metabolism). Peak plasma concentrations are reached 2-12 hours after oral or intramuscular administration. Steady-state plasma concentrations vary considerably, possibly due to genetic differences. Amitriptyline and its metabolites are primarily excreted in the urine. Almost all doses are excreted as glucuronide or sulfate conjugates, with approximately 2% of the unchanged drug appearing in the urine. 25-50% of a single oral dose is excreted in the urine as inactive metabolites within 24 hours. A small amount of the drug is excreted in the bile. The estimated apparent volume of distribution (Vd)β after intravenous administration is 1221 L ± 280 L; the range is 769-1702 L (16 ± 3 L/kg). Amitriptyline is widely distributed throughout the body. Amitriptyline and its major metabolite, nortriptyline, can cross the placental barrier and are present in small amounts in breast milk. The mean systemic clearance (Cls) was 39.24 ± 10.18 L/h (range: 24.53–53.73 L/h). Although aging may decrease clearance, the significant effect of aging on the pharmacokinetics of amitriptyline has not been determined. This study reports the pharmacokinetics of oral amitriptyline and its active metabolite nortriptyline in greyhounds. Five healthy greyhounds participated in a randomized crossover trial. Dogs were given a single oral dose of amitriptyline hydrochloride (mean dose 8.1 mg/kg) in either a fasting or fed state. Blood samples were collected at predetermined time points from 0 to 24 hours post-administration, and plasma drug concentrations were determined using liquid chromatography-mass spectrometry. Pharmacokinetic analysis was performed using a non-compartmental model. Two dogs in the fasting group experienced vomiting after amitriptyline administration and were therefore excluded from the analysis. The Cmax of amitriptyline in the remaining fasting dogs (n = 3) ranged from 22.8 to 64.5 ng/mL, while the Cmax in the fed dogs (n = 5) ranged from 30.6 to 127 ng/mL. The AUCINF of amitriptyline in the three fasting dogs ranged from 167 to 720 hr ng/mL, while the AUCINF in the fed dogs ranged from 287 to 1146 hr ng/mL. The relative bioavailability of amitriptyline in fasting dogs was 69-91% compared to fed dogs (n = 3). Exposure to the active metabolite nortriptyline was positively correlated with exposure to amitriptyline (R² = 0.84). Due to individual variability in pharmacokinetics and the small number of dogs included in this study, further research is needed to assess the effect of feeding on the pharmacokinetics of orally administered amitriptyline. Fasting dogs may be more prone to vomiting after administration of amitriptyline. A previous report described a 30-year-old woman with graft-versus-host disease who was unable to absorb oral amitriptyline. After four weeks of treatment with 50 mg amitriptyline daily, only trace plasma drug concentrations were detected. Subsequent treatment with 75 mg amitriptyline daily for 10 days also failed to increase the plasma concentration of the antidepressant. This study investigated the postmortem distribution of amitriptyline using a rat model. Two hours after a subcutaneous injection of 20 mg amitriptyline, rats (n=40) were anesthetized, and blood samples were collected from the femoral vein and heart. The rats were then euthanized with carbon dioxide and kept at room temperature for 0.1, 1, 2, 5, 24, 48, or 96 hours. High-performance liquid chromatography (HPLC) was used to analyze postmortem blood samples from the heart and inferior vena cava, as well as samples from the lungs, heart, liver, right kidney, thigh muscle, abdominal vein wall, and brain tissue. Results showed a significant increase in cardiac blood concentration within two hours postmortem, followed by a significant increase in inferior vena cava blood concentration. Ninety-six hours post-mortem, the concentrations in cardiac blood and inferior vena cava blood increased by 4.4 ± 0.5 times (p < 0.01) and 3.0 ± 1.1 times (p < 0.05), respectively, compared to pre-mortem values (mean ± standard error). In the lungs, the AMI concentration decreased from 148 ± 16.7 μmol/kg at 0.1 hours post-mortem to 49.1 ± 7.8 μmol/kg at 96 hours post-mortem (p < 0.01). A significant decrease in drug concentration was also observed in the peritoneal vein wall, while increases were observed in the myocardium and liver. In animals that underwent lung resection at the time of death (n = 7), the increase in cardiac blood concentration two hours post-mortem was significantly reduced. Using hairless (hr-1/hr-1) mice as an experimental model of human skin, the transdermal absorption of amitriptyline, nortriptyline, imipramine, and desipramine hydrochloride without a carrier was confirmed. Each compound was dissolved in 2 mg of distilled water and applied topically to the skin. After the water evaporated rapidly, concentrations in the heart, lungs, brain, liver, and blood were measured at 1, 2, 4, and 6 hours. The highest concentrations of all four compounds were consistently observed in the lungs, while the lowest concentrations were found in the heart and liver. During the 6-hour study period, the concentrations of all compounds in the heart remained essentially constant. Concentrations in solid tissues were far below those commonly seen after human overdose, while blood concentrations were close to low therapeutic to toxic levels. Transdermal absorption may provide a viable route of administration for tricyclic antidepressants, thereby improving patient adherence and reducing gastrointestinal side effects. Amitriptyline Hydrochloride
For more complete data on absorption, distribution, and excretion of amitriptyline (17 compounds), please visit the HSDB record page.

---

Metabolism/Metabolites
In in vitro metabolism, amitriptyline is primarily metabolized via demethylation (CYP2C19, CYP3A4) and hydroxylation (CYP2D6), followed by conjugation with glucuronic acid. Other isoenzymes involved in amitriptyline metabolism include CYP1A2 and CYP2C9. The metabolism of this drug is influenced by genetic polymorphism. The major active metabolite is the secondary amine nortriptyline. Nortriptyline exhibits stronger inhibition of norepinephrine than of serotonin, while amitriptyline shows comparable inhibition of both. Other metabolites, such as cis- and trans-10-hydroxyamitriptyline and cis- and trans-10-hydroxynortriptyline, share the same pharmacological characteristics with nortriptyline but have significantly reduced activity. Normethylnortriptyline and amitriptyline N-oxide are present in extremely low concentrations in plasma; the latter is essentially inactive. This article describes a method for determining amitriptyline and some of its metabolites in serum using reversed-phase liquid chromatography (RP-LC). This method uses a C-8 bonded phase as the stationary phase, water-methanol-dichloromethane-propylamine as the mobile phase, and performs UV detection at 254 nm. This article reports the serum concentrations of amitriptyline and its four major metabolites (nortriptyline, normethylnortriptyline, trans-10-hydroxyamitriptyline, and trans-10-hydroxynortriptyline) in patients who received a daily oral dose of 150 mg amitriptyline. The metabolic pathway of amitriptyline is the same as that of other tricyclic antidepressants; its N-monodemethylated metabolite, nortriptyline, is pharmacologically active. To investigate the metabolism of amitriptyline and nortriptyline…eight healthy Chinese volunteers received a single oral dose of 100 mg amitriptyline, and the area under the curve (AUC) ratio of amitriptyline and its three metabolites was evaluated. The results showed significant inter-individual differences in AUC. Furthermore, the hydroxylation of amitriptyline and nortriptyline may be regulated by similar enzymatic processes. This study investigated the biotransformation of amitriptyline to its demethylated product, nortriptyline, in vitro using human liver microsomes from four different donors. These donors were pre-screened to reflect different metabolic rates. The reaction rate followed an S-type Vmax model with respect to substrate concentration. Vmax varied from 0.42 to 3.42 nmol/mg/min, and Km varied from 33 to 89 μM amitriptyline. Ketoconazole was a potent inhibitor of N-demethylation, with an average Ki value of 0.11 ± 0.013 μM… while quinidine (at concentrations up to 50 μM), a CYP2D6 inhibitor, and α-naphthylflavonoid (at concentrations up to 5 μM), which only exhibits CYP1A2 inhibition at low concentrations, showed no inhibitory activity. All tested selective serotonin reuptake inhibitors inhibited the formation of nortriptyline. The mean Ki values were 4.37 (± 3.38) uM for sertraline, 5.46 (± 1.95) uM for norsertraline, 9.22 (± 3.69) uM for fluvoxamine, 12.26 (± 5.67) uM for norfluoxetine, 15.76 (± 5.50) uM for paroxetine, and 43.55 (± 18.28) uM for fluoxetine. A polyclonal rabbit antibody against rat liver CYP3A1 inhibited N-demethylation of amitriptyline at antibody/microsomal protein ratios ranging from 1:1 to 10:1, with an asymptotic maximum of 60%. For more complete metabolite/metabolite data on amitriptyline (8 metabolites), please visit the HSDB record page.
The known metabolites of amitriptyline include nortriptyline and E-10-hydroxyamitriptyline.
Amitriptyline is rapidly and well absorbed after oral administration. It is primarily metabolized in the liver, exhibiting a first-pass effect. Amitriptyline is demethylated in the liver to form its main active metabolite, nortriptyline.
Elimination pathway: Almost all doses are excreted as glucuronide or sulfate conjugates, with almost no unchanged drug in the urine. 25-50% of a single oral dose is excreted in the urine as inactive metabolites within 24 hours. A small amount of the drug is excreted in the bile.
Half-life: 10 to 50 hours, mean 15 hours.
The elimination half-life (t1/2β) after oral administration of amitriptyline is approximately 25 hours (24.65 ± 6.31 hours; range 16.49-40.36 hours).
The plasma half-life of amitriptyline is 10 to 50 hours. This study investigated the toxicokinetics of amitriptyline in nine Matthew-Lawson coma scale III-IV patients admitted after accidental ingestion of 1-5 grams of amitriptyline. The T1/2α and T1/2β of amitriptyline were 1.5–3.1 hours and 15–43 hours, respectively. … This preliminary study aimed to describe the individual and group pharmacokinetic parameters of healthy African grey parrots (Psittacus erithacus, n=3) and cockatoos (Cacatua, n=3) after single oral administration of 1.5 mg/kg, 4.5 mg/kg, and 9 mg/kg amitriptyline. All three birds received an initial oral dose of 1.5 mg/kg, and blood samples were collected at fixed time intervals over 24 hours. Serum concentrations of amitriptyline and its metabolites were determined using polarized immunofluorescence. After initial parameters were determined and a 14-day washout period was observed, two African Grey parrots and one cockatoo were administered a single oral dose of 4.5 mg/kg, and three cockatoos and one African Grey parrot were administered a single oral dose of 9 mg/kg. …Elimination half-lives ranged from 1.6 to 91.2 hours. …

Toxicity Summary
Identification and Uses: Amitriptyline is a tricyclic antidepressant in crystal form. Human Exposure and Toxicity: Overdose/poisoning symptoms may include: hypothermia, respiratory depression, seizures, abnormal tendon reflexes, disorientation, agitation, myoclonus, coma, pyramidal tract signs, arrhythmias, bundle branch block, cardiac arrest, hypotension, circulatory failure, dilated pupils, blurred vision, tachycardia, vasodilation, urinary retention, decreased gastrointestinal motility, decreased bronchial secretions, and dry mucous membranes and skin. A study in children showed that the initial symptoms and signs of acute amitriptyline poisoning appear severe, but most children recover with only supportive care; only a small number of children ingested high doses within days. However, short-term studies have shown that antidepressants increase the risk of suicidal ideation and behavior (suicidal tendencies) in children, adolescents, and young adults; these studies focused on major depressive disorder (MDD) and other mental illnesses. An amitriptyline study showed that the antidepressant reduces the release of nonneuronal acetylcholine in the human placenta, but this only occurs at concentrations approximately 30 times the therapeutic concentration. Therefore, caution is still advised when pregnant women use antidepressants. The genotoxicity of amitriptyline hydrochloride has been evaluated. This evaluation was conducted in somatic cells (bone marrow cells) and germ cells (spermatocytes), examining sperm morphology (i.e., head and tail) and sperm count. Results showed that the treatment induced chromosomal abnormalities, both structural and numerical, in both somatic cells (bone marrow) and germ cells (spermatocytes). Furthermore, different treatment regimens significantly reduced the mitotic index and meiotic activity. Amitriptyline significantly increased the incidence of sperm head and tail abnormalities and significantly reduced sperm count. These results indicate that the drug's effects are dose-dependent. Another study found that amitriptyline is not genotoxic at plasma concentrations. However, at concentrations of 4 and 40 times the plasma concentration, the frequency of chromosomal aberrations and sister chromatid exchanges significantly increased. Animal studies: Exposure symptoms in dogs included lethargy, tachycardia, vomiting, and hyperthermia. Symptoms in cats included dilated pupils and/or tachycardia, ataxia, lethargy, disorientation, and vomiting. In mice, amitriptyline caused rapid but reversible lens opacity if the eyes remained open and no measures were taken to prevent moisture evaporation. A canine study showed no hematological, biochemical, or anatomical evidence of drug toxicity observed at oral doses of 20 and 40 mg/kg/day for 6 months. Oral doses of 80 mg/kg/day were poorly tolerated: 2 out of 4 dogs died within 3 weeks of developing severe ataxia and sedation. Dose of 100 mg/kg/day or higher was tolerated for only a few days. Offspring of rats treated with amitriptyline showed reduced motor activity. In rats, oral doses of 25 mg/kg/day (equivalent to 8 times the maximum recommended human dose) caused delayed vertebral ossification in the fetus. In rabbits, an oral dose of 60 mg/kg/day (equivalent to 20 times the maximum recommended human dose) has been reported to cause incomplete ossification of the skull. Amitriptyline was tested for genotoxicity using the somatic mutation and recombinant assay (SMART) in Drosophila wing cells. The drug did not show genotoxicity at concentrations up to 100 mM. Amitriptyline is metabolized to nortriptyline, which almost equally inhibits the reuptake of norepinephrine and serotonin. Amitriptyline inhibits the membrane pump mechanisms responsible for the uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons. Pharmacologically, this effect may enhance or prolong neuronal activity, as the reuptake of these biogenic amines is physiologically crucial for terminating neurotransmitter activity. Some researchers believe that the antidepressant activity of amitriptyline is based on its interference with the reuptake of norepinephrine and/or serotonin.

---

Toxicity Data
LD50: 350 mg/kg (oral, mouse) (A308)Interactions
The teratogenicity, including internal and external malformations, of clozapine (Cdz) and amitriptyline (Amt) was investigated in combination. On day 8 of gestation, time-pregnant golden hamsters were administered a single intraperitoneal injection of either clozapine hydrochloride (28.5 mg/kg), amitriptyline hydrochloride (70.3 mg/kg), a clozapine-amitriptyline combination (28.5 mg/kg clozapine + 70.3 mg/kg amitriptyline, maintaining a 1:2.5 dose ratio commonly used in clinical formulations), or saline (control group). The fetuses were removed after the mothers were euthanized on day 15 of gestation. Skull deformity analysis was performed on fetuses fixed with Brunner's solution using coronal sections of each head (1 mm thick); visceral deformities were examined after full anatomical dissection of each fetus. Amitriptyline alone (Amt) significantly increased (P<0.05) the incidence of tail curvature and encephalocele, while cyclosporine (Cdz) significantly altered (P<0.05) the sex ratio of surviving fetuses compared to the saline-injected control group. Cyclosporine-amitriptyline combination therapy significantly increased the incidence of skull deformities, eye opening, tail curvature, pulmonary abnormalities, and genitourinary malformations. This article discusses the teratogenic effects of the components in this combination therapy, including external and internal malformations. Caution should be exercised when using this combination therapy if the patient is concurrently receiving high-dose acetaminophen. Transient delirium has been reported in patients receiving 1 gram of acetaminophen and 75 to 150 mg of amitriptyline hydrochloride. In some Caucasian populations, the biochemical activity of the drug-metabolizing isoenzyme cytochrome P450 2D6 (demethylisoquinoline hydroxylase) is reduced (approximately 7% to 10% of Caucasians are termed "metabolic asthenos"); there are currently no reliable estimates of the prevalence of reduced P450 2D6 isoenzyme activity in Asians, Africans, and other populations. Metabolically asthenos can experience higher-than-expected plasma drug concentrations when taking standard doses of tricyclic antidepressants (TCAs). Depending on the proportion of drug metabolized by P450 2D6, the increase in plasma drug concentration can be small or large (the plasma AUC of TCAs can increase up to 8-fold). Furthermore, some drugs inhibit the activity of this isoenzyme, causing normal metabolizers to behave like asthenos. Patients taking specific doses of tricyclic antidepressants (TCAs) and whose condition is stable may suddenly develop symptoms of toxicity if they concurrently take these inhibitors. Drugs that inhibit cytochrome P450 2D6 include some that are not metabolized by this enzyme (such as quinidine and cimetidine), as well as many substrate drugs of P450 2D6 (such as many other antidepressants, phenothiazines, and type 1C antiarrhythmics propafenone and flecainide). While all selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, sertraline, and paroxetine, inhibit P450 2D6, the degree of inhibition may vary. The extent of clinical problems that may arise from SSRI-TCA interactions depends on the degree of inhibition and pharmacokinetics of the SSRI. However, caution should be exercised when using TCAs in combination with any SSRI or when switching from one class of drugs to another. Particularly important is that for patients discontinuing fluoxetine, sufficient time must be allowed before initiating TCA therapy due to the long half-lives of its parent and active metabolites (potentially at least 5 weeks). When tricyclic antidepressants are used in combination with drugs that inhibit cytochrome P450 2D6, the usual dose of the tricyclic antidepressant or another drug may need to be reduced. Furthermore, once one of the drugs is discontinued, the dose of the tricyclic antidepressant may need to be increased. When TCAs are used in combination with drugs known to be P450 2D6 inhibitors, monitoring of TCA plasma concentrations is recommended. The combined use of ethanol and amitriptyline with tricyclic antidepressants resulted in greater impairment of three psychomotor functions in animals than either drug alone. Ethanol pretreatment also increased the total concentration of tricyclic antidepressants in the brain by 2.23%. For more complete data on interactions with amitriptyline (33 interactions in total), please visit the HSDB record page.

---

Non-human toxicity values
Mice intravenous LD50: 16 mg/kg
Mice subcutaneous LD50: 140 mg/kg
Mice intraperitoneal LD50: 56 mg/kg
Mice oral LD50: 140 mg/kg
For more complete non-human toxicity data for amitriptyline (6 in total), please visit the HSDB records page.

Therapeutic Uses
Adrenergic reuptake inhibitors; non-narcotic analgesics; tricyclic antidepressants. ClinicalTrials.gov is a registry and results database that tracks human clinical studies funded by public and private institutions worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov includes a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure under investigation); the title, description, and design of the study; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (for providing patient health information) and PubMed (for providing citations and abstracts of academic articles in the medical field). Amitriptyline is included in the database. Used to relieve depressive symptoms. Endogenous depression is more easily relieved than other depressive states. /Included in US product label/
Tricyclic antidepressants were previously used to treat attention deficit hyperactivity disorder (ADHD). /Tricyclic antidepressants; not included in US product label/
For more complete data on the therapeutic uses of amitriptyline (13 of them), please visit the HSDB record page.

---

Drug Warning
/Black Box Warning/ Suicidal Tendency and Antidepressants: In short-term studies of major depressive disorder (MDD) and other mental illnesses, antidepressants increased the risk of suicidal ideation and behavior (suicidal tendencies) in children, adolescents, and young adults compared to placebo. Anyone considering the use of amitriptyline hydrochloride tablets or any other antidepressant in children, adolescents, or young adults must weigh the risks against clinical need. Short-term studies have shown that antidepressant use did not increase the risk of suicide in adults 24 years of age and older compared to placebo; however, it did reduce the risk of suicide in adults 65 years of age and older compared to placebo. Depression and certain other mental illnesses are themselves associated with an increased risk of suicide. Patients of all ages starting antidepressant therapy should be appropriately monitored for worsening of their condition, suicidal ideation, or unusual behavioral changes. Family members and caregivers should be informed of the need for close monitoring and communication with the prescribing physician. Amitriptyline hydrochloride is not approved for use in children. In rare cases, NMS-like syndromes have been reported after starting or increasing the dose of amitriptyline hydrochloride, regardless of whether it is taken concurrently with medications known to cause neuroleptic malignant syndrome (NMS). Symptoms include muscle rigidity, fever, altered mental status, excessive sweating, tachycardia, and tremor. In rare cases, serotonin syndrome has been reported when amitriptyline hydrochloride is used in combination with other medications known to be associated with serotonin syndrome (SS). Amitriptyline hydrochloride…should be used with caution in patients with a history of epilepsy, and also with caution in patients with a history of urinary retention, angle-closure glaucoma, or elevated intraocular pressure due to its atropine-like effects. For patients with angle-closure glaucoma, even the average dose may induce a glaucoma attack. For more complete data on drug warnings for amitriptyline (39 in total), please visit the HSDB record page. Pharmacodynamics Efficacy in Pain and Depression Amitriptyline is a tricyclic antidepressant and analgesic. It has anticholinergic and sedative effects. Clinical studies have shown that oral amitriptyline provides good to moderate efficacy in at least two-thirds of patients with postherpetic neuralgia and three-quarters of patients with diabetic neuropathic pain, as well as in patients with neurogenic pain syndromes that are generally unresponsive to narcotic analgesics. Amitriptyline has also shown efficacy in a variety of chronic non-malignant pain conditions. Furthermore, some studies have shown its effectiveness in treating fibromyalgia (off-label use of the drug). Cardiovascular and Anticholinergic Effects Amitriptyline has potent anticholinergic properties and may cause electrocardiographic changes and quinidine-like cardiac effects. At higher micromolar therapeutic plasma concentrations, amitriptyline can inhibit ion channels (hERG channels) required for cardiac repolarization. Therefore, amitriptyline may increase the risk of arrhythmias. Orthostatic hypotension and tachycardia may occur in elderly patients taking normal doses of amitriptyline for depression. There is evidence in the literature that these adverse reactions may also occur rarely at lower doses used for pain treatment. Like other tricyclic antidepressants, amitriptyline can cause elevated blood glucose levels. Effects on Seizure Threshold This drug also lowers the seizure threshold and causes changes in EEG and sleep patterns.

C20H23N

277.40332

277.183

50-48-6

Amitriptyline hydrochloride;549-18-8

2160

Crystals

1.1±0.1 g/cm3

398.2±21.0 °C at 760 mmHg

196-197°C

174.0±18.9 °C

0.0±0.9 mmHg at 25°C

1.628

4.92

0

1

3

21

331

0

CN(C)CCC=C1C2=CC=CC=C2CCC3=CC=CC=C31

KRMDCWKBEZIMAB-UHFFFAOYSA-N

InChI=1S/C20H23N/c1-21(2)15-7-12-20-18-10-5-3-8-16(18)13-14-17-9-4-6-11-19(17)20/h3-6,8-12H,7,13-15H2,1-2H3

N,N-dimethyl-3-(2-tricyclo[9.4.0.03,8]pentadeca-1(15),3,5,7,11,13-hexaenylidene)propan-1-amine

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.

---

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).

View More

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)

---

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).

View More

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

---

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.

---

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