Inhibits uridine nucleoside ribohydrolase from Trichomonas vaginalis, with an IC50 value of 0.3 μM [1].
Inhibits gastric H⁺/K⁺ ATPase (proton pump) by irreversible inactivation, leading to inhibition of intracellular proton efflux [2].
Inhibits phosphorylation of extracellular signal-regulated protein kinase 1/2, resulting in decreased cell viability and apoptosis [2].

Following a 16-hour exposure to 0.2 mM of rabeprazole, human gastric cancer cells exhibit reduced vitality [2]. In MKN-28 cells, rabeprazole totally suppressed ERK1/2 phosphorylation. For two hours, the gastric cancer cell line MKN-28 was grown in an acidic media (pH 5.4). In MKN-28 cells, rabeprazole pretreatment (0.2 mM, 2 hours) significantly reduced ERK1/2 phosphorylation [2].

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Gastric cancer cell lines (KATO III, MKN-28, MKN-45) showed higher tolerance to acidic culture media (pH 5.5) compared to non-cancer cells (GES-1). The viability of GES-1 cells dropped to 20.30 ± 4.05%, while gastric cancer cells maintained high viability at pH 5.5 [2].
Rabeprazole (0.2 mM for 16 h) reduced the viability of human gastric cancer cell lines KATO III, MKN-28, and MKN-45. The antiproliferative effect was most potent on MKN-28 cells, whose viability was significantly lower than that of KATO III and MKN-45 cells (P < 0.05) [2].
Rabeprazole (0.2 mM) induced apoptotic cell death in AGS gastric cancer cells in a time-dependent manner. After 72 hours of treatment, the apoptosis rate reached 72.21 ± 3.24%, compared to 3.20 ± 0.26% in the control group (P < 0.01). Flow cytometry analysis indicated that Rabeprazole mainly induced early apoptosis in AGS cells [2].
Western blot analysis showed that treatment with Rabeprazole (0.2 mM, pre-treatment for 2 h) in acidic media (pH 5.4) completely inhibited ERK1/2 phosphorylation in MKN-28 cells. However, this effect was not observed in KATO III or MKN-45 cells. Rabeprazole also suppressed ERK1/2 phosphorylation in AGS cells [2].
Treatment of AGS cells with the ERK1/2 inhibitor PD98059 significantly reduced cell viability at pH 5.4 and effectively inhibited ERK1/2 phosphorylation, similar to the effects observed in the Rabeprazole-treated group [2].
RT-PCR analysis revealed that the α-subunit of H⁺/K⁺ ATPase was strongly expressed in KATO III and MKN-28 cells, but weakly expressed in MKN-45 cells. The β-subunit was equally expressed across the tested cancer cell lines [2].
Rabeprazole inhibited T. vaginalis UNH enzyme activity with an IC50 value of 0.3 μM, providing a possible molecular mechanism for its antiprotozoal activity [1].
The inhibitory activity of Rabeprazole on UNH was determined in an in vitro enzyme assay at pH 6.5. At this pH, its prodrug activation as a PPI is negligible over the assay timeframe, indicating a mechanism distinct from its gastric acid suppression [1].

In female mice, courses of rabeprazole (10 mg/kg; oral; every 48 hours for 18 weeks) led to significant reductions in serum calcium levels, secondary parathyroid disease, and bone mineral density (BMD). hyperthyroidism [3].

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In female mice, long-term (18 weeks) oral administration of Rabeprazole (10 mg/kg every 48 h) resulted in significant reduction in bone mineral density, accompanied by decreased serum calcium levels and secondary hyperparathyroidism [3].
Histopathological examination of femurs from Rabeprazole-treated mice showed widely separated, thin-walled bone trabeculae with widened intertrabecular spaces and an increased number of osteoclasts [3].
Immunohistochemical analysis demonstrated increased optical density of TRAP staining (indicating higher osteoclastic activity) and a significant increase in the percentage area of osteopontin immunostaining in the bones of the Rabeprazole-treated group [3].

UNH Enzyme Activity Assay [1]: A 19F NMR-based activity assay was developed to monitor the UNH enzyme reaction. 5-Fluorouridine was used as a substrate instead of uridine due to its lower Km (15 μM) compared to uridine (54 μM), providing a lower hit threshold. The reaction mixture contained 50 mM potassium phosphate (pH 6.5), 0.3 M KCl, 10% D2O, 80 nM UNH, and test compounds. The reaction was initiated by adding 5-fluorouridine to a final concentration of 50 μM and quenched after 40 minutes with 10 μL of 1.5 M HCl. Enzyme activity was determined by measuring the signal intensities of the product 5-fluorouracil (169.2 ppm) and remaining substrate 5-fluorouridine (165.8 ppm) via 19F NMR spectroscopy. For IC50 determinations, compounds were tested at concentrations ranging from 200 μM to 0.04 μM [1].
RT-PCR for H⁺/K⁺ ATPase Subunits [2]: Total RNA from gastric cancer cell lines was extracted using TRIzol reagent. First-strand cDNA synthesis was carried out with reverse transcriptase using 2 μg total RNA. Specific primers were used to amplify cDNA for human H⁺/K⁺ ATPase α- and β-subunits. PCR amplifications were performed with an initial denaturation at 94°C for 5 min, followed by 38 cycles of 94°C for 1 min, 55°C for 30 sec, and 72°C for 1 min, with a final extension at 72°C for 10 min. The amplified products were subjected to electrophoresis in 1% agarose gels and visualized by ethidium bromide staining. GAPDH was used as an internal control [2].
Immunohistochemistry for Bone Markers [3]: Femur samples were decalcified, embedded, and sectioned. Primary monoclonal antibodies against TRAP or rabbit polyclonal antibodies against osteopontin were added to tissue sections and incubated overnight at 4°C. After washing, sections were incubated with appropriate secondary antibodies for 20 min at room temperature, followed by incubation with streptavidin for 10 minutes. The reaction was detected with 3,3'-diaminobenzidine, and counterstaining was performed with Mayer's hematoxylin. Optical density of TRAP immunostaining and area percentage of osteopontin immunostaining were measured using digital image analysis software [3].

Cell Viability Assay[2]
Cell Types: Three gastric cancer cell lines KATO III, MKN-28 and MKN-45
Tested Concentrations: 0.2 mM
Incubation Duration: 16 hrs (hours)
Experimental Results: Treatment resulted in diminished viability of all cancer cell lines tested, with KATO III and Compared with MKN-45 cells, the cell viability of MKN-28 cells was Dramatically diminished.

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Cell viability assay[2]
Cell Types: Three gastric cancer cell lines (KATO III, MKN-28 and MKN-45)[2]
Tested Concentrations: 0.2 mM
Incubation Duration: 2 hrs (hours) pretreatment
Experimental Results: Result in strong inhibition of ERK 1/2 Phosphorylated in MKN-28 cells, but no similar effect was observed in KATO III and MKN-45 cells.

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Cell Viability Assay : Cells were cultured in media with various pH levels (7.5, 6.5, 5.5) for 24 h, or further cultured at various pH levels (7.4, 6.4, 5.4) for 16 h following treatment with Rabeprazole or PD98059 for 2 h. Cell viability was determined by a dye exclusion assay using trypan blue. The viability percentage was calculated as (number of viable unstained cells / total number of cells) × 100 [2].
Apoptosis Detection: Induction of apoptosis was detected using an Annexin V-FITC/PI apoptosis assay kit. Treated and control AGS cells were harvested, washed, and incubated with 20 μl Annexin V-FITC and 20 μl PI for 15 min at room temperature in the dark. Cells were then evaluated by flow cytometry, and data were analyzed using WinMDI 2.9 software. FITC-positive cells were classed as early apoptotic, and FITC/PI-double positive cells as late apoptotic [2].
Western Blot Analysis: Treated and control cells were harvested, washed, and lysed in cold lysis buffer. Lysates were centrifuged, and supernatants were collected. Protein concentrations were determined using a BCA protein assay kit. Samples containing 50 μg of protein were electrophoresed on 12% SDS-polyacrylamide gels and transferred to PVDF membranes. Membranes were blocked and then incubated with specific primary antibodies against phosphorylated-ERK and total ERK overnight at 4°C [2].

Animal/Disease Models: Female Swiss albino mice (body weight 18-26 g) [3]
Doses: 10 mg/kg
Route of Administration: Oral; every 48 hrs (hrs (hours)) for 18 weeks
Experimental Results: Serum calcium levels compared with vehicle-treated group Dramatically lower (5.5±2.07 vs. 9.68±2.77).

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Mouse Model of Rabeprazole-Induced Osteopenia and Intervention Study [3]: 80 female Swiss albino mice were divided into 4 groups (n=20/group) for an 18-week treatment period. Group I (Vehicle): received distilled water (12 ml/kg, P.O.). Group II (Rabeprazole control): received Rabeprazole (10 mg/kg every 48 h, P.O.). Group III (Rabeprazole + Calcium): received Rabeprazole (10 mg/kg every 48 h, P.O.) along with dietary calcium carbonate (0.5% w/w mixed with chow). Group IV (Rabeprazole + Alendronate): received Rabeprazole (10 mg/kg every 48 h, P.O.) and alendronate (1 mg/kg per week, i.p.). At the end of the experiment, blood was collected by intracardiac puncture, and animals were sacrificed. The right femurs were kept for X-ray examination, and the left femurs were kept for histopathological examination [3].

Absorption, Distribution and Excretion
Absolute bioavailability is approximately 52%. Following a single oral dose of 20 mg of 14C-labeled rabeprazole, approximately 90% of the drug is excreted in the urine, primarily as thiocarboxylic acid, its glucuronide, and thiouric acid metabolites. Excretion: With normal renal function: approximately 1 to 2 hours. With impaired hepatic function: 2 to 6 hours. Protein binding: Very high; approximately 96% bound to human plasma proteins. Because rabeprazole is unstable in acid, it is administered in extended-release tablet form to allow it to pass through the stomach relatively intact. Rabeprazole is absorbed within 1 hour after administration. Bioavailability is approximately 52%. It is unclear whether rabeprazole is distributed into human milk. However, in lactating rats, the concentration of rabeprazole in milk is 2 to 7 times higher than in blood. For more complete data on the absorption, distribution, and excretion of rabeprazole (10 items in total), please visit the HSDB record page.

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Metabolism/Metabolites
Hepatic Metabolism
Approximately 90% of the dose of rabeprazole is excreted in the urine as metabolites. These metabolites primarily include thiocarboxylic acid (TCA), glucuronide of TCA, and mercaptouric acid.
Rabeprazole is extensively metabolized. The major metabolites detected in human plasma are thioethers and sulfones. No significant antisecretory activity of these metabolites has been observed. In vitro studies have shown that rabeprazole is primarily metabolized in the liver by cytochrome P450 3A (CYP3A) to sulfone metabolites, and by cytochrome P450 2C19 (CYP2C19) to desmethylrabeprazole. Thioether metabolites are generated by the reduction of rabeprazole rather than enzymatic reaction. CYP2C19 exhibits known genetic polymorphisms due to CYP2C19 deficiency in certain subpopulations (e.g., 3%–5% of Caucasians and 17%–20% of Asians). In these subpopulations, rabeprazole is metabolized slowly, hence they are referred to as poor metabolizers of the drug. Rabeprazole is a known human metabolite of rabeprazole (rabeprazole thioether). Biological half-life: 1–2 hours (in plasma). The plasma half-life is 1–2 hours. This study aimed to determine the absolute bioavailability of 20 mg rabeprazole tablets in healthy subjects and to compare it with intravenous 20 mg rabeprazole. …Each subject was randomly assigned at the start of the study to receive a single 20 mg rabeprazole intravenous or oral dose in phase one. …The intravenous dose was administered via a continuous infusion over 5 minutes. The elimination half-life after oral administration of rabeprazole sodium (1.47±0.82 hours) was significantly longer than that after intravenous administration (1.02±0.63 hours), which may be due to the slower absorption rate compared to the elimination rate.

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Hepatotoxicity
Despite its widespread use, cases of liver injury caused by rabeprazole are rare. In large-scale long-term rabeprazole trials, the incidence of elevated serum ALT was less than 1%, similar to that in placebo or control groups. In large case series of drug-induced liver injury, rabeprazole caused only a few cases of symptomatic acute liver injury. Currently, only a few cases of clinically significant liver disease caused by rabeprazole have been reported, and the characteristics of this injury are not yet fully understood, but appear similar to those associated with other proton pump inhibitors (PPIs). Clinically significant liver injury caused by PPIs typically appears within the first 4 weeks of treatment, with symptoms including jaundice, nausea, and fatigue, as well as hepatocellular or mixed-type elevations in serum enzymes. Recovery is usually rapid upon discontinuation of the drug. Rash, fever, and eosinophilia are rare, as is autoantibody formation. Relapses have been reported after re-administration. Probability Score: D (Possibly a rare cause of clinically significant liver injury).

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Effects during pregnancy and lactation
◉ Overview of use during lactation
Since there is currently no information on the use of rabeprazole during lactation, it is recommended to choose other medications, especially when breastfeeding newborns or premature infants.
◉ Effects on breastfed infants
As of the revision date, no relevant published information was found.
◉ Effects on lactation and breast milk
A retrospective claims database study in the United States found an increased risk of gynecomastia in users of proton pump inhibitors.
The Spanish pharmacovigilance system reported a case of gynecomastia in a 90-year-old man after taking rabeprazole between 1982 and 1983. This reaction occurred 32 days after treatment and subsided upon discontinuation of the drug.
A review article reported that a search of the European Pharmacovigilance Center database revealed 11 cases of gynecomastia, 3 cases of galactorrhea, 2 cases of breast pain, and 1 case of breast enlargement associated with rabeprazole. A search of the World Health Organization's Global Pharmacovigilance Database revealed 38 cases of gynecomastia, 29 cases of galactorrhea, 28 cases of breast pain, and 5 cases of breast enlargement associated with rabeprazole. One woman was prescribed metronidazole 400 mg three times daily for diarrhea and indigestion, and a combination therapy containing rabeprazole 20 mg and domperidone 30 mg once daily. After 3 days of treatment, she developed bilateral galactorrhea. The combined use of rabeprazole and domperidone is considered the cause of the adverse reaction. Protein binding rate: 96.3% (bound to human plasma proteins). Drug interactions: Warfarin: Potential pharmacokinetic interactions. Proton pump inhibitors may inhibit the metabolism of warfarin. No clinically significant interactions were observed in single-dose studies, but there have been reports of elevated international normalized ratio (INR) and prothrombin time (PT) in patients taking these medications concurrently; monitoring of INR and PT may be necessary during co-administration with rabeprazole. Rabeprazole may increase gastrointestinal pH; co-administration of digoxin and rabeprazole in normal subjects resulted in a 29% increase in peak serum concentrations. Rabeprazole may increase gastrointestinal pH; co-administration of ketoconazole with rabeprazole resulted in a 30% decrease in rabeprazole bioavailability. In vitro human liver microsomal incubation assays showed that rabeprazole inhibited cyclosporine metabolism with an IC50 of 62 μmol, a concentration more than 50 times higher than the Cmax achieved after 14 consecutive days of 20 mg rabeprazole in healthy volunteers. This level of inhibition was similar to that of an equivalent concentration of omeprazole. Co-administration of rabeprazole, amoxicillin, and clarithromycin resulted in elevated plasma concentrations of both rabeprazole and 14-hydroxyclarithromycin.

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Long-term (18 weeks) Rabeprazole treatment (10 mg/kg every 48 h, P.O.) in female mice led to osteopenia, characterized by a significant reduction in bone mineral density [3].
Rabeprazole treatment resulted in significantly decreased serum calcium levels (5.5 ± 2.07 vs. vehicle 9.68 ± 2.77) and induced secondary hyperparathyroidism (PTH levels increased to 43.98 ± 19.23 pg/ml vs. vehicle 18.69 ± 4.19 pg/ml) [3].
Histopathological examination revealed that Rabeprazole treatment caused widely separated, thin-walled bone trabeculae and an increased number of osteoclasts in the femur [3].
Immunohistochemical results showed that Rabeprazole increased the expression of TRAP (a marker of osteoclast activity) and osteopontin (a marker of bone turnover) in bone [3].

[1]. Identification of Proton-Pump Inhibitor Drugs That Inhibit Trichomonas Vaginalis Uridine Nucleoside Ribohydrolase. Bioorg Med Chem Lett. 2014 Feb 15;24(4):1080-4.

[2]. Rabeprazole Exhibits Antiproliferative Effects on Human Gastric Cancer Cell Lines. Oncol Lett. 2014 Oct;8(4):1739-1744.

[3]. Supplement With Calcium or Alendronate Suppresses Osteopenia Due to Long Term Rabeprazole Treatment in Female Mice: Influence on Bone TRAP and Osteopontin Levels. Front Pharmacol. 2020 May 13;11:583.

Therapeutic Uses
Rabeprazole is indicated for short-term treatment (4-8 weeks) to relieve symptoms and promote healing of erosive or ulcerative gastroesophageal reflux disease (GERD). For patients whose GERD has not healed, rabeprazole may be administered for an additional 8 weeks. Rabeprazole is also indicated for maintaining healing of erosive or ulcerative GERD. /Included on US product label/ Rabeprazole is indicated for long-term treatment of pathological hypersecretion states, including Zollinger-Ellison syndrome. /Included on US product label/ Rabeprazole is indicated for short-term treatment (up to 4 weeks) to promote healing and relieve symptoms in patients with active duodenal ulcers. /Included on US product label/

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Drug Warnings Caution should be exercised when using this medication in patients with severe hepatic impairment, especially given the lack of clinical data for this patient population. However, the usual daily dose of 20 mg is unlikely to cause rabeprazole accumulation, and no dose adjustment is required in patients with mild to moderate hepatic impairment.
Symptom relief with rabeprazole does not rule out the possibility of occult gastric cancer. Approximately 4% of patients did not develop intestinal metaplasia during follow-up (up to 40 months), and no persistent changes were observed.
Use of proton pump inhibitors is associated with an increased risk of certain infections, such as community-acquired pneumonia.
FDA Pregnancy Risk Category: B / No evidence of risk to humans. Although adverse reactions have been observed in animal studies, adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal malformations; or, in the absence of adequate human studies, animal studies have shown no fetal risk. The possibility of fetal harm is small but still exists. /
For more complete data on drug warnings for rabeprazole (12 of 12), please visit the HSDB record page.

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Pharmacodynamics
Rabeprazole inhibits gastric acid secretion. It can relieve symptoms in patients with gastroesophageal reflux disease (GERD) or ulcers and prevent esophageal or gastric damage. Rabeprazole is also indicated for conditions of excessive gastric acid secretion, such as Zollinger-Ellison syndrome. Rabeprazole can also be used in combination with antibiotics to eliminate bacteria associated with certain ulcers. Rabeprazole is a selective and irreversible proton pump inhibitor that suppresses gastric acid secretion by specifically inhibiting H+,K+-ATPase on the secretory surface of parietal cells. This inhibits the eventual transport of hydrogen ions (through exchange with potassium ions) into the gastric lumen.

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Rabeprazole is a second-generation proton pump inhibitor that irreversibly inactivates gastric H⁺/K⁺ ATPase through covalent binding, causing rapid and sustained inhibition of intracellular proton efflux and raising extracellular pH [2].
Compared to other commonly used PPIs like omeprazole or lansoprazole, Rabeprazole has a relatively higher pKa, allowing for faster activation and higher accumulation even in weakly acidic environments [2].
Due to the acidic microenvironment of tumors, PPIs like Rabeprazole can be specifically activated within tumor tissues, selectively inducing apoptosis in gastric cancer cells without significant side effects on non-cancer cells [2].
The anticancer effect of Rabeprazole was linked to the inhibition of the ERK1/2 signaling pathway, in addition to its known target H⁺/K⁺ ATPase [2].
Rabeprazole was identified as an inhibitor of T. vaginalis UNH, which may explain its previously reported antiprotozoal activity [1].
The FDA has raised concerns about a potentially increased risk of osteoporotic fractures with long-term PPI use. This study provides in vivo evidence in mice supporting this concern and explores the protective effects of calcium or alendronate [3].

C18H21N3O3S

359.4426

359.13

117976-89-3

Rabeprazole sodium;117976-90-6;Rabeprazole-d4;934295-48-4;Rabeprazole Sulfide;117977-21-6

5029

Light green to green solid powder

1.3±0.1 g/cm3

603.9±65.0 °C at 760 mmHg

202-204°C

319.1±34.3 °C

0.0±1.7 mmHg at 25°C

1.655

1.83

1

6

8

25

440

0

YREYEVIYCVEVJK-UHFFFAOYSA-N

InChI=1S/C18H21N3O3S/c1-13-16(19-9-8-17(13)24-11-5-10-23-2)12-25(22)18-20-14-6-3-4-7-15(14)21-18/h3-4,6-9H,5,10-12H2,1-2H3,(H,20,21)

2-[[4-(3-methoxypropoxy)-3-methylpyridin-2-yl]methylsulfinyl]-1H-benzimidazole

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.)