K+ channel (KvQT1/minK) (IC50 = ~1 μM)

Mefloquine has an IC50 of roughly 10 μM, which preferentially inhibits the development of prostate cancer (PCa) cells. Moreover, mefloquine causes ROS generation and hyperpolarization of the mitochondrial membrane potential (MMP) [2]. In PC3 cells, mefloquine (10 μM)-mediated ROS concurrently stimulates ERK, JNK, and AMPK signaling and downregulates Akt phosphorylation [2]. In VeroE6/TMPRSS2 and Calu-3 cells, mefloquine exhibited more anti-SARS-CoV-2 activity than hydroxychloroquine, with IC50 values of 1.28 μM, IC90 values of 2.31 μM, and IC99 values of 4.39 μM in VeroE6/TMPRSS2 cells. ..Once the virus binds to its target cells, mefloquine prevents further viral entrance [3].

Mefloquine (5 mg/kg; intraperitoneal; daily; 14 days) reverses bone development and cancellous bone volume in the lower vertebra; in older mice, it has no effect on cortical bone volume, thickness, and moment of inertia [4].

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Aging is accompanied by imbalanced bone remodeling, elevated osteocyte apoptosis, and decreased bone mass and mechanical properties; and improved pharmacologic approaches to counteract bone deterioration with aging are needed. We examined herein the effect of mefloquine, a drug used to treat malaria and systemic lupus erythematosus and shown to ameliorate bone loss in glucocorticoid-treated patients, on bone mass and mechanical properties in young and old mice. Young 3.5-month-old and old 21-month-old female C57BL/6 mice received daily injections of 5 mg/kg/day mefloquine for 14 days. Aging resulted in the expected changes in bone volume and mechanical properties. In old mice mefloquine administration reversed the lower vertebral cancellous bone volume and bone formation; and had modest effects on cortical bone volume, thickness, and moment of inertia. Mefloquine administration did not change the levels of the circulating bone formation markers P1NP or alkaline phosphatase, whereas levels of the resorption marker CTX showed trends towards increase with mefloquine treatment. In addition, and as expected, aging bones exhibited an accumulation of active caspase3-expressing osteocytes and higher expression of apoptosis-related genes compared to young mice, which were not altered by mefloquine administration at either age. In young animals, mefloquine induced higher periosteal bone formation, but lower endocortical bone formation. Further, osteoclast numbers were higher on the endocortical bone surface and circulating CTX levels were increased, in mefloquine- compared to vehicle-treated young mice. Consistent with this, addition of mefloquine to bone marrow cells isolated from young mice led to increased osteoclastic gene expression and a tendency towards increased osteoclast numbers in vitro. Taken together our findings identify the age and bone-site specific skeletal effects of mefloquine. Further, our results highlight a beneficial effect of mefloquine administration on vertebral cancellous bone mass in old animals, raising the possibility of using this pharmacologic inhibitor to preserve skeletal health with aging [4].

Mefloquine is a quinoline antimalarial drug that is structurally related to the antiarrhythmic agent quinidine. Mefloquine is widely used in both the treatment and prophylaxis of Plasmodium falciparum malaria. Mefloquine can prolong cardiac repolarization, especially when coadministered with halofantrine, an antagonist of the human ether-a-go-go-related gene (HERG) cardiac K+ channel. For these reasons we examined the effects of mefloquine on the slow delayed rectifier K+ channel (KvQT1/minK) and HERG, the K+ channels that underlie the slow (I(Ks)) and rapid (I(Kr)) components of repolarization in the human myocardium, respectively. Using patch-clamp electrophysiology we found that mefloquine inhibited KvLQT1/minK channel currents with an IC50 value of approximately 1 microM. Mefloquine slowed the activation rate of KvLQT1/minK and more block was evident at lower membrane potentials compared with higher ones. When channels were held in the closed state during drug application, block was immediate and complete with the first depolarizing step. HERG channel currents were about 6-fold less sensitive to block by mefloquine (IC50 = 5.6 microM). Block of HERG displayed a positive voltage dependence with maximal inhibition obtained at more depolarized potentials. In contrast to structurally related drugs such as quinidine, mefloquine is a more effective antagonist of KvLQT1/minK compared with HERG. Block of KvLQT1/minK by mefloquine may involve an interaction with the closed state of the channel. Inhibition by mefloquine of KvLQT1/minK in the human heart may in part explain the synergistic prolongation of QT interval observed when this drug is coadministered with the HERG antagonist halofantrine [1].

Mefloquine (MQ) is a prophylactic anti-malarial drug. Previous studies have shown that MQ induces oxidative stress in vitro. Evidence indicates that reactive oxygen species (ROS) may be used as a therapeutic modality to kill cancer cells. This study investigated whether MQ also inhibits prostate cancer (PCa) cell growth. We used sulforhodamine B (SRB) staining to determine cell viability. MQ has a highly selective cytotoxicity that inhibits PCa cell growth. The antitumor effect was most significant when examined using a colony formation assay. MQ also induces hyperpolarization of the mitochondrial membrane potential (MMP), as well as ROS generation. The blockade of MQ-induced anticancer effects by N-acetyl cysteine (NAC) pre-treatment confirmed the role of ROS. This indicates that the MQ-induced anticancer effects are caused primarily by increased ROS generation. Moreover, we observed that MQ-mediated ROS simultaneously downregulated Akt phosphorylation and activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and adenosine monophosphate-activated protein kinase (AMPK) signaling in PC3 cells. These findings provide insights for further anticancer therapeutic options [2].

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Coronavirus disease 2019 (COVID-19) has caused serious public health, social, and economic damage worldwide and effective drugs that prevent or cure COVID-19 are urgently needed. Approved drugs including Hydroxychloroquine, Remdesivir or Interferon were reported to inhibit the infection or propagation of severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2), however, their clinical efficacies have not yet been well demonstrated. To identify drugs with higher antiviral potency, we screened approved anti-parasitic/anti-protozoal drugs and identified an anti-malarial drug, Mefloquine, which showed the highest anti-SARS-CoV-2 activity among the tested compounds. Mefloquine showed higher anti-SARS-CoV-2 activity than Hydroxychloroquine in VeroE6/TMPRSS2 and Calu-3 cells, with IC50 = 1.28 μM, IC90 = 2.31 μM, and IC99 = 4.39 μM in VeroE6/TMPRSS2 cells. Mefloquine inhibited viral entry after viral attachment to the target cell. Combined treatment with Mefloquine and Nelfinavir, a replication inhibitor, showed synergistic antiviral activity. Our mathematical modeling based on the drug concentration in the lung predicted that Mefloquine administration at a standard treatment dosage could decline viral dynamics in patients, reduce cumulative viral load to 7% and shorten the time until virus elimination by 6.1 days. These data cumulatively underscore Mefloquine as an anti-SARS-CoV-2 entry inhibitor [3].

Mice and treatment [4]
3.5-(young, n=8–9/group) and 21-month-old (old, n=10/group) C57BL/6 female mice were administered daily intraperitoneal injection of vehicle (1.5% ethanol) or 5mg/kg/day of mefloquine for 14 days. Mice were assigned an ID number and the age and treatment were recorded in a database. Investigators performing endpoint measurements were only given the mouse IDs, thus blinded to treatment and age. Mice were randomized and assigned to each experimental group based on matching spinal BMD. Animals were sacrificed 4–6 hours after receiving the last injection. Mice (5/cage) were fed a regular diet and water ad libitum, and maintained on a 12h light/dark cycle. All experiments were carried out as planned, with no adverse effects resulting from treatments. The mice received intraperitoneal injections of calcein (30 mg/kg) and alizarin red (50 mg/kg; Sigma) 7 and 2 days before sacrifice, respectively, to allow for dynamic histomorphometric measurements.

Absorption, Distribution and Excretion
Mefloquine is readily absorbed from the gastrointestinal tract; food significantly enhances absorption, increasing bioavailability by up to 40%. Tablets offer over 85% bioavailability compared to oral solutions. In healthy volunteers, peak plasma concentration (Cmax) is reached within 6 to 24 hours after a single dose. The mean plasma concentration ranges from 50 to 110 ng/ml/mg/kg. Steady-state plasma concentrations of 1000 to 2000 μg/L are achieved after weekly administration of 250 mg for 7 to 10 weeks. Mefloquine is primarily excreted via bile and feces. In healthy volunteers reaching steady-state mefloquine concentrations, 9% of the parent drug and 4% of its carboxylic acid metabolites are excreted. Concentrations of other metabolites could not be determined. In healthy adults, the apparent volume of distribution of mefloquine is approximately 20 L/kg, and it is widely distributed. Various estimates of the total apparent volume of distribution range from 13.3 to 40.9 L/kg. Mefloquine can accumulate in erythrocytes infected with Plasmodium. The systemic clearance of mefloquine ranges from 0.022 to 0.073 L/h/kg, with increased clearance during pregnancy. Prescription information mentions a clearance of 30 mL/min. Mefloquine is well absorbed from the gastrointestinal tract, but the time required to reach peak plasma concentrations varies significantly among individuals. …Mefloquine undergoes enterohepatic circulation. It binds to plasma proteins at approximately 98% and is widely distributed throughout the body. Malaria infection may alter the pharmacokinetics of mefloquine, leading to decreased absorption and accelerated clearance. …A small amount of mefloquine is secreted into breast milk. Its elimination half-life is relatively long, approximately 21 days, but shortens to approximately 14 days in malaria infection, likely due to disruption of enterohepatic circulation. Mefloquine is metabolized in the liver and excreted primarily via bile and feces. Pharmacokinetics showed that the racemic mixture exhibited enantioselectivity after administration, with the peak plasma concentration and area under the curve (AUC) of the SR enantiomer being higher than that of its RS enantiomer, while the volume of distribution and total clearance were lower. The bioavailability of the tablets was over 85% compared to the oral solution. The presence of food significantly improved the rate and extent of absorption, increasing bioavailability by approximately 40%. Following a single oral dose of mefloquine, peak plasma concentrations were reached within 6–24 hours (median approximately 17 hours). Maximum plasma concentrations in μg/L were roughly equivalent to those in mg (e.g., a single 1000 mg dose yielded a maximum concentration of approximately 1000 μg/L). A maximum steady-state plasma concentration of 1000–2000 μg/L was achieved after 7–10 weeks with a weekly dose of 250 mg.
Distributed in blood, urine, cerebrospinal fluid, and tissues; concentrated in erythrocytes…
In healthy adults, the apparent volume of distribution is approximately 20 L/kg, indicating widespread tissue distribution. Mefloquine may accumulate in parasitic erythrocytes, with an erythrocyte-to-plasma concentration ratio of approximately 2. Protein binding is approximately 98%. Mefloquine plasma concentrations of 620 ng/mL are considered to achieve a 95% preventative effect.
For more complete data on the absorption, distribution, and excretion of mefloquine (12 items in total), please visit the HSDB record page.

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Metabolic/Metabolic Substances
Mefloquine is primarily metabolized by the CYP3A4 enzyme in the liver. Two metabolites have been identified; the major metabolite is 2,8-bis-trifluoromethyl-4-quinolinecarboxylic acid, which is inactive against Plasmodium falciparum. The second metabolite is an alcohol, present in smaller quantities.
Biotransformation: Liver (partial); major metabolism is a carboxylic acid metabolite. Mefloquine is also extensively metabolized via the cytochrome P450 system in the liver. In vitro and in vivo studies strongly suggest that CYP3A4 is the major isoenzyme involved. Two mefloquine metabolites have been identified in humans. The major metabolite, 2,8-bis(trifluoromethyl)-4-quinolinecarboxylic acid, is inactive against Plasmodium falciparum. A study in healthy volunteers found that this carboxylic acid metabolite appeared in plasma 2 to 4 hours after a single oral dose of mefloquine. Peak plasma concentrations of this metabolite were reached after 2 weeks, approximately 50% higher than that of mefloquine. Thereafter, plasma concentrations of both the major metabolite and mefloquine decreased at similar rates. The area under the plasma concentration-time curve (AUC) of the major metabolite was 3 to 5 times that of the parent drug. The other metabolite, an alcohol, is present only in trace amounts.
Biological Half-Life
According to a pharmacokinetic review, the terminal elimination half-life of mefloquine is 0.9 to 13.8 days. In multiple studies conducted in healthy adults, the mean elimination half-life of mefloquine ranged from 2 to 4 weeks, with a mean half-life of approximately 21 days. In healthy volunteers… the absorption half-life of mefloquine ranged from 1 to 4 hours… the terminal elimination half-life ranged from 13.8 to 40.9 days (median 20 days). Half-life: elimination – 13 to 33 days (median 20 days); in severely ill patients (e.g., those with acute malaria), the half-life may be shorter. This study investigated the pharmacokinetics of mefloquine in 10 healthy subjects and 12 patients with severe acute Plasmodium falciparum malaria treated with 750 mg of oral mefloquine. Peak plasma concentrations of mefloquine were reached in both groups within 20–24 hours. The mean elimination half-life was 385 hours in healthy subjects and 493 hours in malaria patients, a significant difference. In multiple studies involving healthy adults, the mean elimination half-life of mefloquine ranged from 2 to 4 weeks, with an average of approximately 3 weeks. For more complete data on the biological half-life of mefloquine (out of 9), please visit the HSDB records page.

Hepatotoxicity
Long-term use of mefloquine can cause asymptomatic, transient elevations of serum enzymes in up to 18% of patients. These elevations are usually mild and resolve spontaneously without dose adjustment. Although mefloquine is widely used, it is rarely associated with clinically significant acute liver injury, and the number of reports is too small to describe the clinical characteristics of such injury. Cases of acute hepatocellular injury and cholestatic hepatitis have been associated with mefloquine use. Allergic reactions (rash, fever, eosinophilia) and autoantibody formation are rare. Probability score: D (likely a rare cause of clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of use during lactation: Very small amounts of mefloquine are excreted into breast milk; the dose is insufficient to harm the infant or protect the child from malaria. Breastfed infants should receive the recommended dose of mefloquine. ◉ Effects on breastfed infants: No published information was found as of the revision date.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.

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Protein binding
Mefloquine binds to plasma proteins at a rate exceeding 98%.

[1]. Interactions of the antimalarial drug mefloquine with the human cardiac potassium channels KvLQT1/minK andHERG. J Pharmacol Exp Ther. 2001 Oct;299(1):290-6.

[2]. Mefloquine exerts anticancer activity in prostate cancer cells via ROS-mediated modulation of Akt, ERK, JNK and AMPK signaling. Oncol Lett. 2013 May;5(5):1541-1545.

[3]. Mefloquine, a Potent Anti-severe Acute Respiratory Syndrome-Related Coronavirus 2 (SARS-CoV-2) Drug as an Entry Inhibitor in vitro. Front Microbiol. 2021 Apr 30;12:651403.

[4]. Reversal of loss of bone mass in old mice treated with mefloquine. Bone. 2018 Sep;114:22-31.

(-)-(11S,2'R)-erythro-mefloquine is the optically active form of [2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidinyl)methanol, with the (-)-(11S,2'R)-erythro-configuration. It is an antimalarial drug used in racemic form, acting as a blood schizonticide; its mechanism of action is not yet clear. It is an antimalarial drug. It is the enantiomer of (+)-(11R,2'S)-erythro-mefloquine. Malaria is a protozoan disease that places a significant burden on human health in endemic areas worldwide. The World Health Organization's 2020 Malaria Report showed that the global malaria mortality rate decreased by 60% between 2000 and 2019. Nevertheless, malaria remains a major cause of morbidity and mortality; 90% of malaria deaths occur in Africa. High-risk groups for malaria include: people who have never been infected with malaria, children under 5 years old, refugees in Central and East Africa, civilian and military travelers without immunity, pregnant women, and migrants returning to their country of origin. Mefloquine (brand name: Lareem) is an antimalarial drug used to prevent and treat malaria caused by Plasmodium vivax and Plasmodium falciparum. The drug was initially discovered by the Walter Reed Army Institute of Research (WRAIR) in a malaria drug development project conducted between 1963 and 1976. It was approved by the U.S. Food and Drug Administration (FDA) in 1989 and first marketed by Hoffman-Roche. It has been controversial due to concerns about its neurotoxic effects. Product information warns of potential serious neuropsychiatric side effects. Mefloquine is an antimalarial drug. Mefloquine is a quinoline derivative used to prevent and treat Plasmodium falciparum malaria. Mefloquine treatment is associated with a low incidence of transient and asymptomatic elevations in serum enzymes and is a rare cause of clinically significant acute liver injury.
It has been reported that mefloquine hydrochloride exists in Aspergillus nucleatus, and relevant data are available.
Mefloquine is a quinoline methanol derivative with antimalarial, anti-inflammatory, and potential chemosensitizing and radiosensitizing activities. Although its exact mechanism remains to be elucidated, mefloquine, as a weak base, preferentially accumulates in lysosomes, disrupting lysosomal function and integrity, thereby leading to host cell death. Similar to chloroquine, the chemosensitizing and radiosensitizing effects of this drug may be related to its inhibition of autophagy. Autophagy is a cellular mechanism involving lysosomal degradation that minimizes the production of reactive oxygen species (ROS) associated with tumor reoxygenation and tumor exposure to chemotherapeutic drugs and radiation. Compared to chloroquine, mefloquine has better blood-brain barrier (BBB) penetration.
A phospholipid-interacting antimalarial drug (antimalarial agent). It is highly effective against Plasmodium falciparum with minimal side effects.
See also: mefloquine hydrochloride (in salt form); mefloquine mesylate (its active ingredient).

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Drug Indications
Mefloquine is indicated for the treatment of mild to moderate malaria caused by Plasmodium falciparum and Plasmodium vivax. It is effective against chloroquine-resistant Plasmodium falciparum. Mefloquine is also indicated for the prevention of malaria caused by Plasmodium falciparum and Plasmodium vivax, including chloroquine-resistant Plasmodium falciparum.
FDA Label
Mechanism of Action
The mechanism of action of mefloquine is not fully elucidated. Some studies suggest that mefloquine specifically targets the 80S ribosome of Plasmodium falciparum, inhibiting protein synthesis and thus producing a schizontic effect. Other studies are available in the literature, but in vitro data on the mechanism of action of mefloquine are limited.
Mefloquine, like chloroquine and quinine, is a hemoschizontic agent effective during the intraerythrocyte stage of parasite development. Similar to chloroquine and quinine, mefloquine appears to interfere with the metabolism of Plasmodium and its ability to utilize hemoglobin in red blood cells. The antimalarial activity of mefloquine may depend on its ability to form hydrogen bonds with cellular components; structure-activity studies suggest that the relative orientation of the hydroxyl and amino groups in the mefloquine molecule may be crucial to its antimalarial activity. Although the exact mechanism of action of mefloquine is unclear, it may differ from that of chloroquine. This study used spectrophotometry to investigate the effects of the antimalarial drug mefloquine on Ca2+ uptake and release in canine brain microsomes. Mefloquine inhibited inositol-1,4,5-phosphate (IP3)-induced Ca2+ release with an IC50 value of 42 μM, but its inhibitory effect on Ca2+ entry into vesicles was weaker (IC50: 272 μM). These effects of mefloquine are the opposite of its effects on Ca2+ uptake and release in skeletal muscle microsomes, where its main function is to inhibit Ca2+ entry into vesicles. The study found that mefloquine, as a specific inhibitor of the release of IP3-sensitive Ca2+ reservoirs in canine brain microsomes, is more potent than quinine. The drug should be considered as potentially affecting intracellular IP3-related signal transduction processes.

C18H20F6N2O4S

474.417824745178

474.105

C, 45.57; H, 4.25; F, 24.03; N, 5.90; O, 13.49; S, 6.76

64003-26-5

53230-10-7;51773-92-3 (HCl);64003-26-5 (mesylate);

71587223

Typically exists as solid at room temperature

5.361

3

12

2

31

575

2

S(C)(=O)(=O)O.FC(C1=CC(=C2C=CC=C(C(F)(F)F)C2=N1)[C@@H]([C@H]1CCCCN1)O)(F)F

WESWYMRNZNDGBX-YLCXCWDSSA-N

InChI=1S/C17H16F6N2O.ClH/c18-16(19,20)11-5-3-4-9-10(15(26)12-6-1-2-7-24-12)8-13(17(21,22)23)25-14(9)11/h3-5,8,12,15,24,26H,1-2,6-7H21H/t12-,15+/m1./s1

C17H17ClF6N2O

Mefloquine mesylate; Mefloquine methanesulfonate; UNII-642Y4F6L0K; 642Y4F6L0K; 64003-26-5; DTXSID70213988; 4-Quinolinemethanol, alpha-(2R)-2-piperidinyl-2,8-bis(trifluoromethyl)-, (alphas)-rel-, methanesulfonate (1:1); 4-Quinolinemethanol, alpha-2-piperidinyl-2,8-bis(trifluoromethyl)-, (R*,s*)-(+/-)-, monomethanesulfonate (salt); Mefloquine (mesylate); WR-177,602 mesylate; WR142,490; WR177,602; Ro215998001; Roche Brand of Mefloquine mesylate

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.)