IC50: 2.4±0.6 μM (PI3K γ), 3.0±0.0 μM (PI3K δ), 5.4±0.3 μM (PI3K β)[1]

Quercetin hydrate is a phytochemical or plant-based substance that is added to foods, beverages, and supplements. It has been shown in multiple studies to possess antioxidant and anti-inflammatory qualities, and a host of other possible health advantages are being investigated. The IC50 of quercetin hydrate, a PI3K inhibitor, ranges from 2.4 to 5.4 μM. Strong inhibitions of PI3K and Src kinase, moderate inhibition of Akt1/2, and minor effects on PKC, p38, and ERK1/2 are observed with quercetin hydrate[1]. Quercetin hydrate reduces the production of LDH% in response to TNF, the adherence of neutrophils to bovine pulmonary artery endothelial cells (BPAEC) that is dependent on EC, and the synthesis and proliferation of BPAEC DNA [2].

The growth of PC-3 cell xenograft tumors and human prostate cancer LNCaP was more effectively inhibited when quercetin hydrate (75 mg/kg) and 2-methoxyestradiol were combined [3].

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In the present study, researchers determined whether their combination could inhibit LNCaP and PC-3 xenograft tumor growth in vivo and explored the underlying mechanism. Human prostate cancer LNCaP and PC-3 cells were inoculated subcutaneously in male BALB/c nude mice. When xenograft tumors reached about 100 mm3, mice were randomly allocated to vehicle control, quercetin or 2-Methoxyestradiol singly treated and combination treatment groups. After therapeutic intervention for 4 weeks, combination treatment of quercetin and 2-ME i) significantly inhibited prostate cancer xenograft tumor growth by 46.8% for LNCaP and 51.3% for PC-3 as compared to vehicle control group, more effective than quercetin (28.4% for LNCaP, 24.8% for PC3) or 2-ME (32.1% for LNCaP, 28.9% for PC3) alone; ii) was well tolerated by BALB/c mice and no obvious toxic reactions were observed; iii) led to higher Bax/Bcl-2 ratio, cleaved caspase-3 protein expression and apoptosis rate; and iv) resulted in lower phosphorylated AKT (pAKT) protein level, vascular endothelial growth factor protein and mRNA expression, microvascular density and proliferation rate than single drug treatment. These effects were more remarkable compared to vehicle group. Therefore, combination of quercetin and 2-ME can serve as a novel clinical treatment regimen owning the potential of enhancing antitumor effect on prostate cancer in vivo and lessening the dose and side effects of either quercetin or 2-ME alone. These in vivo results will lay a further solid basis for subsequent researches on this novel therapeutic regimen in human prostate cancer.[3]

alpha(2)beta(1) and alpha(IIb)beta(3) integrins, that support platelet adhesion to collagen and fibrinogen, respectively, share common signaling molecules. The effect of quercetin on platelet static adhesion to collagen and fibrinogen was assessed and correlated with its kinase inhibitory activity. Quercetin strongly abrogated PI3K and Src kinases, mildly inhibited Akt1/2, and slightly affected PKC, p38 and ERK1/2. Quercetin or the combined use of adenosine diphosphate and thromboxane A(2) inhibitors abrogated platelet spreading on these surfaces to a similar extent. We suggest that the inhibitory effect of quercetin on platelet kinases blocks early signaling events preventing a complete platelet spreading.[1]

The purpose of this study was to evaluate the inhibition of RTEC senescence and renal fibrosis by quercetin/strong> and explore the underlying mechanisms. We found that quercetin attenuated RTEC senescence induced by angiotensin II (AngII) in vitro and unilateral ureteral obstruction in vivo. Moreover, we demonstrated that mitochondrial abnormalities such as elevated reactive oxygen species, decreased membrane potential, and fragmentation and accumulation of mitochondrial mass, occurred in AngII-treated RTECs. Quercetin treatment reversed these effects. Furthermore, quercetin enhanced mitophagy in AngII-treated RTECs, which was markedly reduced by treatment with mitophagy-specific inhibitors. Sirtuin-1 (SIRT1) was involved in quercetin-mediated PTEN-induced kinase 1 (PINK1)/Parkin-associated mitophagy activation. Pharmacological antagonism of SIRT1 in AngII-treated RTECs blocked the effects of quercetin on mitophagy and cellular senescence. Finally, quercetin alleviated kidney fibrosis by reducing RTEC senescence via mitophagy. Collectively, the antifibrotic effect of quercetin involved inhibition of RTEC senescence, possibly through activation of SIRT1/PINK1/Parkin-mediated mitophagy. These findings suggest that pharmacological elimination of senescent cells and stimulation of mitophagy represent effective therapeutic strategies to prevent kidney fibrosis[4].

Before the formal in vivo experiment, we evaluated the toxicity of two combined drugs and vehicle that would be administrated simultaneously using two groups of male BALB/c nude mice (n = 5 each). Solvent for quercetin was 25% hydroxypropyl-β-cyclodextrin (HPβCD, w/v in ddH2O) and for 2-Methoxyestradiol was 25% HPβCD containing 0.5% carboxymethyl cellulose (CMC, w/v in ddH2O). Drug group were given the two drugs, namely dissolved quercetin and 2-ME, and vehicle control group were given two drug-free vehicles, namely 25% HPβCD containing or not containing 0.5% CMC. After operation, toxic reaction was observed in the mice of both groups represented as poor mental state, lightly twisting the body, convulsion and occasional moderate haematuria that were in consistent with the description of Ehteda A and may be attributed to high concentration of HPβCD. For this reason, in the subsequent experiment, combination of quercetin and 2-ME was carried out in this way: quercetin was given on day 1, followed by 2-ME given on day 2.[3]
Mice were inoculated subcutaneously with 5×105 PC-3 cells suspended in 100μL PBS and 2×108 LNCaP cells suspended in 100μL of matrigel and PBS mixture (1:1) on the right back. When xenograft tumors reached a volume of approximately 100mm3, mice were randomly assigned to four groups (n = 8 each group) and treated intraperitoneally. Therapeutic schedule based on our in vitro results, preliminary experiments and many other researchers' studies was as follows: (1) Vehicle control group: vehicle of quercetin on day 1, vehicle of 2-ME on day 2, (2) Quercetin treated group: quercetin 75mg/kg on day 1, vehicle of 2-ME on day 2, (3) 2-ME treated group: vehicle of quercetin on day 1, 2-ME 150mg/kg on day 2, (4) Combination treatment group: quercetin 75mg/kg on day 1, 2-ME 150mg/kg on day 2. Two days was a treatment cycle and the whole treatment process lasted for 4 weeks. Tumor sizes were monitored every 2 days using caliper and tumor volume were calculated according to the formula: L×S2×0.5, in which L represents the longest diameter and S represents the shortest diameter of tumor. Mice were weighed as well. At the end of treatment procedure, on day 29, mice were anesthetized with chloral hydrate and sacrificed by cervical dislocation. Xenograft tumors were taken out quickly and weighed. One part of it was put into liquid nitrogen immediately for future biomarker analysis and the other part was fixed in 10% neutral buffered formalin for immunohistochemical analysis. Serum biochemical parameters such as ALT, AST, creatinine and urea nitrogen that reflected drug toxicity were also detected.[3]

[1]. Effect of quercetin on platelet spreading on collagen and fibrinogen and on multiple platelet kinases. Fitoterapia. 2010 Mar;81(2):75-80.

[2]. Inhibitory effects of protein kinase C inhibitors on tumor necrosis factor induced bovine pulmonary artery endothelial cell injuries. Yao Xue Xue Bao. 1996;31(3):176-81.

[3]. Combination of Quercetin and 2-Methoxyestradiol Enhances Inhibition of Human Prostate Cancer LNCaP and PC-3 Cells Xenograft Tumor Growth. PLoS One. 2015 May 26;10(5):e0128277.

[4]. Quercetin alleviates kidney fibrosis by reducing renal tubular epithelial cell senescence through the SIRT1/PINK1/mitophagy axis. Life Sci. 2020 Jul 20;118116.

Quercetin is a yellow needle-like or yellow powder. It converts to its anhydrous form at 203-207 °F (95-98 °C). Its alcoholic solution has an extremely bitter taste. (NTP, 1992) National Toxicology Program (NTP), Institute of Environmental Health Sciences, National Institutes of Health. 1992. National Toxicology Program Chemical Database. Research Triangle Park, North Carolina. Quercetin is a five-hydroxyflavonoid with its five hydroxyl groups located at positions 3, 3', 4', 5, and 7. It is one of the most abundant flavonoids in edible vegetables, fruits, and wines. It possesses a variety of activities, including antibacterial, antioxidant, protein kinase inhibitor, antitumor agent, EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor, phytome, phytoestrogen, free radical scavenger, chelating agent, Aurora kinase inhibitor, and anti-aging agent. It is a penthydroxyflavonoid and 7-hydroxyflavonol, and also the conjugate acid of quercetin-7-ol ester. Quercetin is a flavonol widely found in plants and, like many other phenolic heterocyclic compounds, possesses antioxidant properties. Its glycosylated forms include rutin and quercetin. Quercetin is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain). Quercetin is a flavonoid compound found in many foods and herbs and is a common component of a normal diet. Quercetin extract has been used to treat or prevent a variety of diseases, including cardiovascular disease, hypercholesterolemia, rheumatic diseases, infections, and cancer, but clinical trials have not yet confirmed its effectiveness for any disease. As a nutritional supplement, quercetin is well tolerated, and no events of elevated serum enzymes or clinically significant liver injury have been found.

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Quercetin has been reported to be found in tansina, hydrangea, and other organisms with relevant data. Quercetin is a polyphenolic flavonoid with potential chemopreventive activity. It is widely found in plant-based food sources and is a major bioflavonoid in the human diet. It may exert its antiproliferative effect by regulating EGFR or estrogen receptor-mediated signal transduction pathways. Although its mechanism of action is not fully elucidated, in vitro experiments have confirmed that this compound has the following effects: reducing the expression of mutant p53 protein and p21-ras oncogene, inducing cell cycle arrest at the G1 phase, and inhibiting the synthesis of heat shock proteins.

Furthermore, in vitro experiments have shown that this compound, when used in combination with chemotherapy drugs, exhibits a synergistic effect and can reverse multidrug resistance phenotypes. Quercetin also exerts anti-inflammatory and anti-allergic effects by inhibiting lipoxygenase and cyclooxygenase pathways, thereby preventing the production of pro-inflammatory mediators. Quercetin is a flavonoid compound widely found in various plants and fruits, including red grapes, citrus fruits, tomatoes, broccoli and other leafy green vegetables, as well as various berries such as raspberries and cranberries. Quercetin itself (quercetin aglycone) is not a normal component of the diet; rather, it is quercetin glycoside. Quercetin glycoside is converted into phenolic acids as it passes through the gastrointestinal tract. Quercetin has not been scientifically proven to have a specific therapeutic effect on any disease, nor has it received approval from any regulatory agency. The U.S. Food and Drug Administration (FDA) has also not approved any health claims regarding quercetin. However, following numerous epidemiological studies showing a negative correlation between dietary flavonol and flavonoid intake and the incidence and mortality of cardiovascular disease and cancer, interest in dietary flavonoids has grown significantly. In recent years, a wealth of experimental and clinical data has accumulated regarding the effects of flavonoids on endothelial cells under physiological and pathological conditions. A meta-analysis of seven prospective cohort studies concluded that, after adjusting for known risk factors and other dietary components, individuals in the top third of dietary flavonol intake had a lower risk of death from coronary heart disease compared to those in the bottom third. Currently, studies are underway using small-scale interventions with flavonoid compounds and flavonoid-containing foods and extracts to treat various pathological conditions. (A7896)A7896: Perez-Vizcaino F, Duarte J, Andriantsitohaina R: Endothelial function and cardiovascular disease: effects of quercetin and wine polyphenols. Free Radic Res. 2006 Oct;40(10):1054-65. PMID:17015250

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Quercetin is a metabolite found or produced in Saccharomyces cerevisiae and is a flavonol widely found in plants. Like many other phenolic heterocyclic compounds, it has antioxidant properties. Glycosylated forms include rutin and quercetin.

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Therapeutic Uses
Quercetin is used medically to reduce capillary fragility. International Agency for Research on Cancer (IARC). Monographs on Risk Assessment of Carcinogenic Chemicals in Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972 to present. (Multi-volume). URL: https://monographs.iarc.fr/ENG/Classification/index.php, Volume V73, page 498 (1999)
/EXPL THER/ ... In a randomized, double-blind, placebo-controlled trial.../In patients with Class III chronic prostatitis syndrome (nonbacterial chronic prostatitis and prostatodynia)/...as measured by the NIH Chronic Prostatitis Score, significant improvement was achieved in the treatment group. Approximately 67% of the treated subjects experienced at least a 25% improvement in symptoms, compared to only 20% in the placebo group. In a follow-up, open-label, unblinded study...quercetin was used in combination with bromelain and papain, which may enhance its absorption. In this study, 82% of the subjects experienced at least a 25% improvement in symptoms.

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Drug Warning
While quercetin appears to have potential as an anticancer agent, further research is needed because most studies are based on in vitro experiments using high concentrations of quercetin that are not achievable through dietary intake, and its benefits for cancer remain inconclusive in animal and/or human studies. Coates, PM, Blackman, MR, Cragg, GM, Levine, M., Moss, J., White, JD (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 580 (2005)
...Quercetin has been shown to protect low-density lipoprotein (LDL) from oxidation and prevent platelet aggregation. Quercetin has been reported to inhibit the proliferation and migration of smooth muscle cells… Quercetin has been reported to significantly reduce plasma lipid, lipoprotein, and liver cholesterol levels, inhibit the production of oxidized low-density lipoprotein (oxLDL) caused by oxidative stress, and protect an enzyme that hydrolyzes oxidized lipoproteins and specific lipid peroxides in atherosclerotic lesions… It induces endothelial-dependent vasodilation of the rat aorta by increasing nitric oxide production… Quercetin and its glycosides have also been reported to inhibit angiotensin-converting enzyme activity and angiotensin II-induced JNK activation, thereby inhibiting vascular smooth muscle cell (VSMC) hypertrophy… However, because the concentration of quercetin in most studies is too high to be achieved through dietary intake, some effects may be impractical or negligible under physiological conditions… The beneficial effects of quercetin on cardiovascular disease remain inconclusive in human studies. Following a single oral dose… In four male and two female volunteers, 4 g of quercetin was administered. Within the first 24 hours, quercetin and its conjugates were undetectable in blood or urine; within 72 hours, 53% of the dose was excreted in feces. Following a single intravenous injection of 100 mg of quercetin in six volunteers, plasma concentrations showed a biphasic decline with half-lives of 8.8 minutes and 2.4 hours, respectively; protein binding exceeded 98%. In urine, within 9 hours, 0.65% of the intravenous dose was excreted unchanged as quercetin, and 7.4% as conjugates; no further excretion was observed within 24 hours… International Agency for Research on Cancer (IARC). Monographs on Risk Assessment of Human Carcinogenic Chemicals. Geneva: International Agency for Research on Cancer, World Health Organization, 1972–present. (Multi-volume). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, page 10. V73 P501 (1999)
When 14C-quercetin is orally administered to ACI rats, approximately 20% of the administered dose is absorbed by the digestive tract, over 30% is broken down to 14-CO2, and approximately 30% is excreted unchanged in feces.

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Metabolism/Metabolites
Glycosides are hydrolyzed in vivo to the corresponding aglycones, which are then further metabolized via heterocyclic cleavage to produce 3,4-dihydroxyphenyl-substituted acids…The location of ring cleavage depends on the structure…For flavonols (quercetin), cleavage occurs at the 1,2 and 3,4 bonds, producing high-alcohol catechins…These acids are further metabolized via β-oxidation, O-methylation and demethylation of the acyl side chains, as well as aromatic dehydroxylation. Parke, DV, Biochemistry of Exogenous Compounds. Oxford: Pergamon Press, 1968, p. 151.
The β-hydroxyethylated derivatives of quercetin were isolated from urine samples and separated by high-performance liquid chromatography (HPLC). The 5,7,3',4'-tetracycline was separated from the 3,7,3',4'-tetracycline derivative. The 7,3',4'-tricycline and the 7'-monocycline produced a common peak, which was separated from the peak of the 7,4'-dicycline.

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Biological half-life
A male and a female volunteer consumed a diet containing quercetin glycoside (64.2 mg as aglycone)...distribution phase half-life of 3.8 hours, elimination phase half-life of 16.8 hours.../quercetin glycoside/International Agency for Research on Cancer (IARC). 《Monographs on Risk Assessment of Human Carcinogenic Chemicals》. Geneva: World Health Organization, International Agency for Research on Cancer, 1972–present. (Multi-volume). Accessible at: https://monographs.iarc.fr/ENG/Classification/index.php, Volume V73, page 501 (1999). The elimination half-life of quercetin is approximately 25 hours. Mechanism of action: Quercetin is a specific inhibitor of quinone reductase 2 (QR2), an enzyme (along with its human QR1 homolog) that catalyzes the metabolism of toxic quinolines. Inhibition of QR2 in Plasmodium may lead to lethal oxidative stress. Inhibition of the antioxidant activity of Plasmodium may help kill the parasite. The 5', 7', 3', and 4'-hydroxyl groups on quercetin can donate electrons, thereby scavenging various reactive oxygen species (ROS) and other free radicals... Oxygen free radicals (superoxide, hydrogen peroxide, hydroxyl radicals, and other related free radicals)... are scavenged by... antioxidant systems, including antioxidant compounds. These systems balance the redox state of cells and participate in cellular homeostasis processes... Typically, in vitro assessment of the antioxidant activity of flavonoids requires consideration of three criteria: First, two adjacent hydroxyl groups on ring B; second, a 2,3-double bond, a 4-oxo group, and a 3-hydroxyl group on ring C; and third, a 5,7-dihydroxyl group on ring A. Quercetin meets all three criteria, indicating stronger antioxidant activity… This flavonol has been reported to protect carbohydrates, proteins, nucleotides, and lipids from free radical damage… Glucuronide conjugates found in plasma have also been reported to have potent antioxidant activity, suggesting that their activity may depend on the binding site… Coates, PM, Blackman, MR, Cragg, GM, Levine, M., Moss, J., White, JD (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 579 (2005)
Cytokines, such as tumor necrosis factor-associated apoptosis-inducing ligands (TRAIL), can induce apoptosis in colon cancer cells by activating death receptors. However, many types of cancer exhibit the characteristic of evading apoptosis induced by anticancer drugs. This necessitates combination therapy. This study investigated whether the flavonoid quercetin could enhance the sensitivity of human colon adenocarcinoma cell lines to TRAIL-induced apoptosis. Studies have found that quercetin enhances TRAIL-induced apoptosis by promoting the redistribution of DR4 and DR5 receptors to lipid rafts. Meanwhile, the cholesterol sequestrant nystatin inhibits quercetin-induced death receptor aggregation and the sensitivity of colon adenocarcinoma cells to TRAIL-induced apoptosis. The combination of quercetin and TRAIL activates the mitochondrial-dependent death pathway, manifested as the cleavage of Bid protein and the release of cytochrome c into the cytosol. In summary, these findings suggest that quercetin, through its ability to redistribute death receptors on the cell surface, promotes the formation of the death-inducing signaling complex and the activation of caspases, thereby responding to death receptor stimulation. Based on these results, this study provides a challenging approach to improving the efficiency of TRAIL-based therapies.

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Preparation Methods
Quercetin…is obtained by rapidly extracting oak bark powder with dilute ammonia, followed by boiling the extract with sulfuric acid. It can be used as a natural colorant (Natural Yellow 10)…The first successful synthesis of quercetin was reported in 1962…In this process, 2-methoxyacetylphloroglucinol reacts with O-benzylvanillic anhydride in triethylamine, followed by treatment with potassium hydroxide to produce 5,7-dihydroxy-4'-benzyloxy-3,3'-dimethylflavonoid. The benzyl ether is cleaved with acetic acid-hydrochloric acid, and the methyl ether is further cleaved with hydroiodic acid to produce quercetin.

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Hepatotoxicity
Although there are few studies on the hepatotoxicity of quercetin, quercetin supplementation has not been found to be associated with elevated serum transaminases during treatment. Furthermore, no published reports of clinically significant liver injury caused by quercetin have been found. In fact, many in vitro and in vivo studies have shown that quercetin can protect the liver from damage caused by drugs and toxins, including acetaminophen and anticancer chemotherapy drugs. These hepatoprotective effects have not been confirmed in prospective human clinical trials. Probability Score: E (Unlikely to be a clinically significant cause of liver injury). Other Names: Commonly used as a component of bioflavonoid extracts. Drug Category: Herbal and dietary supplement.

C15H10O7.XH2O

320.2510

320.053

849061-97-8

Quercetin;117-39-5; Quercetin-d3;263711-79-1; 117-39-5; Quercetin dihydrate;6151-25-3;Quercetin hydrate;849061-97-8; Quercetin-d5;263711-78-0;Quercetin-13C3

16212154

Light yellow to yellow solid powder

714.6ºC at 760 mmHg

>300ºC

386ºC

1.923

6

8

1

23

488

0

O=C1C2C(=CC(=CC=2O)O)OC(C2C=C(O)C(O)=CC=2)=C1O.O

OKXFBEYCJRMINR-UHFFFAOYSA-N

InChI=1S/C15H10O7.H2O/c16-7-4-10(19)12-11(5-7)22-15(14(21)13(12)20)6-1-2-8(17)9(18)3-6;/h1-5,16-19,21H;1H2

2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate

Quercetin hydrate; 849061-97-8; 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one hydrate; 1001001-36-0; Quercetin hydrate; Quercetin (hydrate); 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate; Quercetin monohydrate;

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.)