Absorption, Distribution and Excretion
The pharmacokinetics of citalopram for single and multiple doses are linear and dose-proportional within the dose range of 10 to 40 mg/day. Citalopram is primarily biotransformed in the liver, with a mean terminal half-life of approximately 35 hours. Steady-state plasma concentrations are reached approximately one week after once-daily administration. Based on the half-life, the steady-state accumulation of citalopram in plasma is expected to be 2.5 times the plasma concentration following a single oral dose. Peak plasma concentrations occur approximately 4 hours after a single oral dose of citalopram (40 mg tablets). The absolute bioavailability of citalopram is approximately 80% of the intravenous dose, and its absorption is not affected by food. After oral administration of citalopram, approximately 12% to 23% is excreted unchanged in the urine, and 10% is excreted in the feces. After intravenous administration of citalopram, approximately 10% of the recovered drug in the urine is in the form of citalopram, and approximately 5% is in the form of norepinephrine (DCT). The volume of distribution of citalopram is approximately 12 L/kg. The systemic clearance of citalopram is 330 mL/min, with approximately 20% cleared by the kidneys. Like other selective serotonin reuptake inhibitors, citalopram is a highly lipophilic compound and appears to be rapidly and adequately absorbed from the gastrointestinal tract after oral administration. Following a single 40 mg dose of citalopram tablets, the manufacturer states that the average peak plasma concentration is approximately 44 ng/mL, reached approximately 4 hours later. The absolute bioavailability of citalopram is approximately 80% of the intravenous dose. Citalopram tablets and solutions have been reported to be bioequivalent. Food has no significant effect on the absorption of citalopram. The distribution of citalopram and its metabolites in human tissues and fluids is not fully understood. However, limited pharmacokinetic data suggest that this highly lipophilic drug is widely distributed in human tissues.
/Breast Milk/ /The purpose of this study/ was to determine the milk/plasma (M/P) ratio and infant dose in lactating women taking citalopram for the treatment of depression, and to determine the plasma concentrations and effects of these drugs in their infants. This study included seven women (mean age 30.6 years) and their infants (mean age 4.1 months) who were taking citalopram (median dose 0.36 mg/kg/day). The concentrations of citalopram and desmethylcitalopram in plasma and breast milk were determined by high-performance liquid chromatography (HPLC) over a 24-hour dosing interval. Infant drug exposure was estimated using two different methods, calculated by multiplying the milk secretion rate by the drug concentration in breast milk and normalizing to body weight. The results were expressed as a percentage of the weight-adjusted maternal dose. The mean milk concentration/area under the curve (M/PAUC) values for citalopram and desmethylcitalopram were calculated to be 1.8 (range 1.2–3) and 1.8 (range 1.0–2.5), respectively. The mean maximum concentrations of citalopram and desmethylcitalopram in breast milk were 154 μg/L (95% CI, 102–207 μg/L) and 50 μg/L (23–77 μg/L), respectively. Depending on the calculation method, the average infant exposure to citalopram was 3.2% or 3.7%, and to desmethylcitalopram was 1.2% or 1.4%. Citalopram was detected in the bodies of 3 out of 7 infants (concentrations of 2.0, 2.3, and 2.3 μg/L, respectively). Desmethylcitalopram was detected in the plasma of two infants from the same batch (concentrations of 2.2 and 2.2 μg/L, respectively). …The mean total dose of citalopram and desmethylcitalopram passed to infants through breast milk (4.4–5.1% of the citalopram equivalent) was below 10% of the statutory concern level. ...
For more complete data on absorption, distribution, and excretion of citalopram (14 items in total), please visit the HSDB record page.

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Metabolism/Metabolites
Citalopram is primarily metabolized in the liver via N-demethylation by CYP2C19 and CYP3A4 to its major metabolite, desmethylcitalopram. Other metabolites include didesmethylcitalopram, citalopram N-oxide, and propionic acid, which are metabolized via CYP2D6. Citalopram is metabolized by monoamine oxidases A and B, as well as aldehyde oxidases, to produce derivatives. Compared to the parent drug, the pharmacological activity of citalopram metabolites is very low and unlikely to affect the clinical efficacy of citalopram.
In a 2002 study, 11 pregnant women took citalopram (20-40 mg/day); 10 of them took it throughout their pregnancy, and 1 woman started taking it at week 20 of gestation. The mean ratio of the two metabolites was significantly higher during pregnancy than at 2 months postpartum, indicating that the CYP2D6 isoenzyme was induced. The trough concentrations of citalopram, desmethylcitalopram, and bis-desmethylcitalopram in normal neonatal plasma were 64%, 66%, and 68% of the maternal concentrations, respectively. Citalopram (CT), an antidepressant, is a selective serotonin reuptake inhibitor and is administered as indicated on its label. Four healthy male volunteers were given a single oral dose of 14(C)-CT in 50 mL of aqueous solution (0.1 mmol/30 uCi/1.1 MBq). Radioactivity concentrations in whole blood and plasma were similar. …High-performance liquid chromatography analysis of urine components revealed the presence of three glucuronides in addition to the known metabolites of citalopram. The relative concentrations of CT and its metabolites in urine collected over 7 consecutive days were as follows: CT (26%), N-demethyl-CT (DCT, 19%), N,N-didemethyl-CT (DDCT, 9%), N-oxide (7%), quaternary ammonium glucuronide of CT (CT-GLN, 14%), N-glucuronide of DDCT (DDCT-GLN, 6%), and glucuronide of the acidic metabolite formed by deamination of N,N-dimethylamine (CT-acid-GLN, 12%). CT-GLN was separated by preparative chromatography and identified by LC-MS-MS and NMR. DDCT-GLN and CT-acid-GLN were identified by LC-MS. This study indicates that renal excretion is the primary clearance route, with only a small amount excreted in feces. A significant portion of the urinary excretion consists of N-glucuronide of CT and DDCT, and O-acylglucuronide of CT-acid. This study aimed to identify the enzyme system that ultimately catalyzes the local brain metabolism of citalopram. …The metabolism of citalopram, its enantiomers, and demethylated metabolites was investigated in rat brain microsomes and rat and human brain mitochondria. Cytochrome P-450-mediated transformation was not observed in the rat brain. …Oxidase activity of monoamine neurotransmitters was determined by stereoselectively measuring the production of citalopram propionate in the whole rat brain and in the frontal cortex, putamen, cerebellum, and white matter of five human brains. Except in the rat brain, all substrates were metabolized by two forms of monoamine oxidase (MAO), and monoamine oxidase B activity was not detected in the rat brain. In the human frontal cortex, the apparent Km and Vmax for the biotransformation of S-citalopram by monoamine oxidase B were 266 μM and 6.0 pmol min/mg protein, respectively, while those for monoamine oxidase A were 856 μM and 6.4 pmol min/mg protein, respectively. These Km values are within the same range as those for the metabolism of serotonin and dopamine by monoamine oxidase. ... Citalopram ... is partially demethylated by CYP2C19 to N-demethylcitalopram, and partially demethylated by CYP3A4. N-demethylcitalopram is further demethylated by CYP2D6 to a similarly inactive metabolite, didemethylcitalopram. Both metabolites are inactive. ... In vitro experiments show that citalopram does not inhibit CYP enzymes, or only slightly inhibits them. Multiple studies in healthy subjects and patients have confirmed this, as have in vivo experiments. Therefore, when citalopram is co-administered with CYP1A2 substrates (clozapine and theophylline), CYP2C9 substrates (warfarin), CYP2C19 substrates (imipramine and mephenytoin), CYP2D6 substrates (sparganum, imipramine, and amitriptyline), and CYP3A4 substrates (carbamazepine and triazolam), no pharmacokinetic changes have been observed, or only very minor changes have been observed. ...
For more complete data on the metabolism/metabolites of citalopram (7 metabolites in total), please visit the HSDB record page.
Known human metabolites of citalopram include N-demethylcitalopram and citalopram N-oxide.
Citalopram is primarily metabolized in the liver via N-demethylation to the major metabolite, demethylcitalopram. Other metabolites include bisdemethylcitalopram, citalopram N-oxide, and deaminopropionic acid derivatives. However, the main component in plasma is unmetabolized citalopram. Cytochrome P450 (CYP) 3A4 and 2C19 isoenzymes appear to be primarily involved in the formation of demethylcitalopram. Demethylcitalopram appears to be further demethylated by CYP2D6 to bis-demethylcitalopram. Compared to the parent compound, the pharmacological activity of citalopram metabolites is very low and unlikely to affect the clinical efficacy of the drug. Elimination pathway: After oral administration of citalopram, 12-23% is excreted in the urine as unmetabolized form, and 10% is excreted in the urine as unmetabolized form. A portion of the dose is excreted in the feces. Half-life: 35 hours. The mean terminal half-life of citalopram is approximately 35 hours.
Citalopram (CT), an antidepressant, is a selective serotonin reuptake inhibitor. It was administered orally in the labeled form 14(C)-CT to four healthy male volunteers via a single 50 mL aqueous solution (0.1 mmol/30 uCi/1.1 MBq). Radioactivity concentrations in whole blood and plasma were similar. The corresponding pharmacokinetic parameters were: ...half-lives of 90.2 ± 22.5 hours and 79.5 ± 14.9 hours, respectively. ...
In adults with normal renal and hepatic function, the mean elimination half-life of citalopram is approximately 35 hours.

Toxicity Summary
Identification and Uses: Citalopram is a solid dosage form. It is a serotonin reuptake inhibitor and belongs to the second-generation antidepressant class. Citalopram tablets are indicated for the treatment of depression. Human Studies: The most common symptoms of citalopram overdose (alone or in combination with other drugs and/or alcohol) include dizziness, sweating, nausea, vomiting, tremor, somnolence, and sinus tachycardia. In rarer cases, observed symptoms include amnesia, confusion, coma, seizures, hyperventilation, cyanosis, rhabdomyolysis, and ECG changes (including QTc interval prolongation, junctional rhythms, ventricular arrhythmias, and, in very rare cases, torsades de pointes). In very rare cases, citalopram overdose can lead to acute renal failure. Five male infants were exposed to citalopram (30 mg/day), paroxetine (10-40 mg/day), or fluoxetine (20 mg/day) during pregnancy, respectively, and developed withdrawal symptoms at birth or within days thereafter, lasting up to one month. Symptoms included irritability, persistent crying, tremors, increased muscle tone, difficulty feeding and sleeping, and seizures. Late pregnancy exposure to citalopram may lead to neonatal toxicity syndrome, which presents at birth or shortly thereafter and can sometimes be misdiagnosed as neonatal withdrawal syndrome. One infant weighing 3860 grams was delivered at 40 weeks of gestation. His mother had been taking citalopram 20 mg/day prior to delivery. In vitro human lymphocyte chromosome aberration assays showed that citalopram did not have chromosome breakage-inducing effects. Animal studies: Mice and rats were fed citalopram for 18 months and 24 months, respectively. No carcinogenicity of citalopram was found in mice at daily doses up to 240 mg/kg. In rats, daily intake of 8 or 24 mg/kg increased the incidence of small bowel cancer. The implications of these findings for humans are unclear. In a 2-year study of citalopram carcinogenicity, pathological changes (degeneration/atrophy) were observed in the retina of albino rats. In rabbit studies, no adverse effects on embryonic/fetal development were observed at daily intakes up to 16 mg/kg. From late gestation to weaning, female rats treated with citalopram (4.8, 12.8, or 32 mg/kg/day) showed increased mortality in the first 4 days after birth and persistent growth retardation in pups at the highest doses. In two rat embryonic/fetal development studies, oral administration of citalopram (32, 56, or 112 mg/kg/day) to pregnant animals during organogenesis resulted in decreased embryonic/fetal growth and survival, and increased fetal malformations (including cardiovascular and skeletal defects) in the high-dose group. In the in vitro bacterial reverse mutation assay (Ames test), citalopram was mutagenic in two of the five bacterial strains (Salmonella TA98 and TA1537) without metabolic activation. In the in vitro Chinese hamster lung cell chromosome aberration assay, citalopram was break-inducible regardless of metabolic activation. Citalopram did not show mutagenicity in the in vitro mammalian forward mutation assay (HPRT) of mouse lymphoma cells or in the in vitro/in vivo unplanned DNA synthesis (UDS) assay of rat liver. The antidepressant, anti-obsessive-compulsive, and anti-bulimia effects of citalopram are thought to be related to its inhibition of serotonin uptake by neurons in the central nervous system. Citalopram blocks the reuptake of serotonin by the serotonin reuptake pump on the neuronal membrane, thereby enhancing the effect of serotonin on its 5-HT1A autoreceptor. Compared with tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs) have significantly reduced affinity for histamine, acetylcholine, and norepinephrine receptors.

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Interactions
This study aimed to investigate the drug interaction between carvedilol and citalopram based on the in vitro metabolism of carvedilol and its in vivo pharmacokinetics (PKs) after oral monotherapy and combination therapy, and to reveal the effect of citalopram on the pharmacokinetics of carvedilol. Each rat was cannulated in the femoral vein and then connected to a BASi Culex ABC system. Carvedilol (3.57 mg/kg body weight) was administered orally to rats without citalopram or after multiple oral administrations of citalopram (1.42 mg/kg body weight). Plasma concentrations of carvedilol were determined by high-performance liquid chromatography-mass spectrometry (HPLC-MS) at specified time points after administration, and key pharmacokinetic parameters were calculated using a non-compartmental model analysis. Furthermore, the effect of citalopram on the metabolic rate of carvedilol was investigated using a rat mixed liver microsomal incubation system. During the combined administration, a significant increase in both the area under the plasma concentration-time curve (AUC) and peak plasma concentration was observed. The rat mixed liver microsomal incubation experiment demonstrated that citalopram reduces the metabolic rate of carvedilol. Citalopram combined administration resulted in significant changes in the pharmacokinetic characteristics of carvedilol in rats; in vitro experiments also confirmed that these changes may be due to CYP2D6 inhibition-mediated drug interactions.
…This article reports a case of death resulting from the concurrent use of two different types of antidepressants. A 41-year-old white male with a history of depression and suicide attempts was found dead at home. Multiple bottles of medication, including citalopram (Cipramil),… and a bottle of whiskey were found at the scene. The autopsy results were normal, but systematic toxicological analysis… revealed the presence of citalopram (and its metabolites)… A novel liquid chromatography separation method was developed… Blood and urine test results showed: demethylcitalopram 0.42 μg/mL and 1.22 μg/mL; citalopram 4.47 μg/mL and 19.7 μg/mL… and other substances. The cause of death was attributed to the synergistic toxicity of moclobemide and citalopram…/this/can lead to a potentially fatal hyperserotonergic state…
This study aimed to evaluate the effects of tobacco smoke on the pharmacokinetics of citalopram (CIT), demethylcitalopram (DCIT), and their enantiomers in animal models. High-performance liquid chromatography (HPLC) with a diode array detector (DAD) was used to identify and quantify the compounds under study. HPLC quantification of racemic mixtures of CIT was performed on a C18 column. The limits of detection (LOD) and quantitation (LOQ) were 7 ng/mL and 10 ng/mL, respectively. HPLC separation of the enantiomers (S- and R-CIT) of citalopram was performed on a Chirobiotic V column. The LOD and LOQ for R-citalopram and S-citalopram were 6 ng/mL and 15 ng/mL, respectively. Male Wistar rats were used in the experiment. Rats were exposed to tobacco smoke for 5 days (6 hours daily). After exposure, rats were administered citalopram at a dose of 10 mg/kg via intragastric gavage. The control group (unexposed group) was administered the same dose of citalopram in the same manner. Blood samples were collected from the animals at 9 time points. The results showed that tobacco smoke exposure inhibited the biotransformation of citalopram. After intragastric gavage, the half-life of the racemic citalopram mixture was prolonged by approximately 287%. The pharmacokinetic parameters of S-citalopram (the active isomer) showed a similar trend to those of the racemic mixture. No statistically significant changes in the pharmacokinetic parameters of R-citalopram were observed after exposure to tobacco smoke. The pharmacological parameters of desmethylcitalopram showed an opposite trend to those of the parent drug. Induction of metabolism of this compound was observed after exposure to tobacco smoke.
Concurrent or immediate use of selective serotonin reuptake inhibitors (SSRIs, such as citalopram) and other drugs affecting serotonergic neurotransmission may lead to life-threatening serotonin syndrome. Manifestations of serotonin syndrome may include altered mental status (e.g., agitation, hallucinations, delirium, coma), autonomic dysfunction (e.g., tachycardia, blood pressure fluctuations, dizziness, excessive sweating, flushing, high fever), neuromuscular symptoms (e.g., tremor, rigidity, myoclonus, hyperreflexia, ataxia), seizures, and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea). The exact mechanism of serotonin syndrome is not fully understood; however, it appears to be caused by excessive serotonergic activity in the central nervous system, possibly mediated by activation of the serotonin 5-HT1A receptor. Dopamine and 5-HT2 receptors may also be involved, but their roles are unclear. For more complete data on interactions of citalopram (34 in total), please visit the HSDB records page.

[1]. Enantioselective analysis of citalopram and escitalopram in postmortem blood together with genotyping for CYP2D6 and CYP2C19. J Anal Toxicol. 2009;33(2):65-76.

[2]. Citalopram. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in depressive illness. Drugs. 1991;41(3):450-477.

[3]. Assessment of citalopram and escitalopram on neuroblastoma cell lines. Cell toxicity and gene modulation. Oncotarget. 2017 Jun 27;8(26):42789-42807.

[4]. Mouse strain differences in SSRI sensitivity correlate with serotonin transporter binding and function. Sci Rep. 2017 Aug 17;7(1):8631.

Therapeutic Uses
Serotonin reuptake inhibitor; second-generation antidepressant. 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 patient health information) and PubMed (for citations and abstracts of academic articles in the medical field). Citalopram is listed in the database. Citalopram tablets are indicated for the treatment of depression. /Included in the US product label/ Citalopram has been used to treat obsessive-compulsive disorder. /Not included in the US product label/
For more complete therapeutic use data for citalopram (16 items in total), please visit the HSDB record page.

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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 citalopram or any other antidepressant in a child, adolescent, or young adult must weigh this risk against clinical need. Short-term studies showed no increased suicide risk in adults 24 years and older taking antidepressants compared to placebo; and a decreased suicide risk in adults 65 years and older taking antidepressants compared to placebo. Depression and some other mental illnesses are themselves associated with an increased risk of suicide. Patients of all ages starting antidepressants should be appropriately monitored for worsening of their condition, suicidal tendencies, or abnormal changes in behavior. Family members and caregivers should be informed of the need for close monitoring and communication with the prescribing physician. Citalopram is not approved for use in pediatric patients. Citalopram is contraindicated in patients with congenital long QT syndrome, bradycardia, hypokalemia or hypomagnesemia, recent acute myocardial infarction, or decompensated heart failure. Patients taking other medications that prolong the QTc interval should also avoid citalopram. These medications include Class 1A (e.g., quinidine, procainamide) or Class III (e.g., amiodarone, sotalol) antiarrhythmic drugs, antipsychotics (e.g., chlorpromazine, thioridazine), antibiotics (e.g., gatifloxacin, moxifloxacin), or any other known to prolong the QTc interval (e.g., pentamiprid, levomethadone acetate, methadone). Dosage of citalopram should be limited in certain populations. For patients with impaired CYP2C19 metabolism or those who may be taking cimetidine or other CYP2C19 inhibitors concurrently, the maximum dose should be limited, as higher citalopram exposure is expected in these patients. Maximum doses should also be limited in patients with impaired liver function and those over 60 years of age due to the anticipated higher drug exposure.
It has been reported that the use of selective norepinephrine reuptake inhibitors (SNRIs) and serotonin reuptake inhibitors (SSRIs) (including citalopram tablets) alone may induce life-threatening serotonin syndrome, especially when used concurrently with other serotonergic drugs (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, amphetamine, and St. John's wort) and drugs that impair serotonin metabolism (particularly monoamine oxidase inhibitors, including those used to treat mental illness, as well as others such as linezolid and intravenous methylene blue). Symptoms of serotonin syndrome may include altered mental status (e.g., agitation, hallucinations, delirium, and coma), autonomic dysfunction (e.g., tachycardia, blood pressure fluctuations, dizziness, excessive sweating, flushing, and high fever), neuromuscular symptoms (e.g., tremor, rigidity, myoclonus, hyperreflexia, and incoordination), seizures, and/or gastrointestinal symptoms (e.g., nausea, vomiting, and diarrhea). Patients should be monitored for serotonin syndrome. For more complete data on drug warnings for citalopram (49 total), please visit the HSDB record page. Pharmacodynamics: Citalopram belongs to a class of antidepressants called selective serotonin reuptake inhibitors (SSRIs). Studies have found that citalopram can relieve or control symptoms of various mood disorders, including depression, anxiety, eating disorders, and obsessive-compulsive disorder. The antidepressant, anti-anxiety, and other effects of citalopram are related to its inhibition of serotonin uptake in the central nervous system. Serotonergic abnormalities have been reported in patients with mood disorders. The behavioral and neuropsychological effects of serotonin include regulating mood, perception, reward, anger, aggression, appetite, memory, libido, and attention. Citalopram's onset of action in treating depression is approximately 1 to 4 weeks. Complete remission may require 8 to 12 weeks. In vitro studies have shown that citalopram is a potent and selective inhibitor of neuronal serotonin reuptake, with weaker effects on the central reuptake of norepinephrine and dopamine. Long-term use of citalopram has been shown to downregulate central norepinephrine receptors, similar to other effective medications for treating major depressive disorder. Citalopram does not inhibit monoamine oxidase.

C20H21FN2O

324.39

324.163

59729-33-8

Citalopram-d4 hydrobromide;1219803-58-3;Citalopram-d6;1190003-26-9;Citalopram hydrobromide;59729-32-7;Citalopram-d6 oxalate;1246819-94-2

2771

Colorless to light yellow ointment

1.2±0.1 g/cm3

428.3±45.0 °C at 760 mmHg

180 - 187ºC

212.8±28.7 °C

0.0±1.0 mmHg at 25°C

1.591

2.51

0

4

5

24

466

0

CN(C)CCCC1(C2=CC=C(C=C2)F)C3=C(C=C(C=C3)C#N)CO1

WSEQXVZVJXJVFP-UHFFFAOYSA-N

InChI=1S/C20H21FN2O/c1-23(2)11-3-10-20(17-5-7-18(21)8-6-17)19-9-4-15(13-22)12-16(19)14-24-20/h4-9,12H,3,10-11,14H2,1-2H3

1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-3H-2-benzofuran-5-carbonitrile

Lu-10-171 Lu10-171; Lu 10-171; Citalopram

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)

DMSO : ~100 mg/mL (~308.27 mM)

Solubility in Formulation 1: 2.5 mg/mL (7.71 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 sonication.
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 2: ≥ 2.5 mg/mL (7.71 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.)