Sodium ion vitamin C transporter 2 (SVCT-2) is the transporter of L-ascorbic acid and determines its anticancer impact. Based on L-ascorbic acid diet and SVCT-2 expression, L-ascorbic acid (0.1 μM–2 mM) has anticancer effects. The sensitivity of human colorectal cancer cells to L-ascorbic acid varies, primarily based on the degree of SVCT-2 expression [4]. IPSC reprogramming is facilitated by L-ascorbic acid (10 μg) and L-ascorbic acid (50 μg/ml, 5 d) [5]. L-ascorbic acid (50 μg/ml, 9 d) facilitates fibroblast conversion to heart muscle cells[6]. (50 ng/ml, 4-6 d) encourages mice's terminal secretory B cells to develop into totipotent IPS cells[7].

The combination of L-ascorbic acid and tolbutamide was designed to cause hypotensive action in both normal (60 mg/kg) and diabetic (40 mg/kg) settings. Tobumide (20 mg/kg) had a longer duration of action and an earlier beginning of action in the presence of L-ascorbic acid when compared to the tolbutamide control [5].

Absorption, Distribution and Excretion
70% to 90%
The efficiency of absorption depends on the salt form, the amount administered, the dosing regimen and the size of iron stores. Subjects with normal iron stores absorb 10% to 35% of an iron dose. Those who are iron deficient may absorb up to 95% of an iron dose.
Ascorbic acid is readily absorbed from the gastrointestinal tract and is widely distributed in the body tissues. Plasma concentrations of ascorbic acid rise as the dose ingested is increased until a plateau is reached with doses of about 90 to 150 mg daily. Body stores of ascorbic acid in health are about 1.5 g although more may be stored at intakes above 200 mg daily. The concentration is higher in leucocytes and platelets than in erythrocytes and plasma. In deficiency states the concentration in leucocytes declines later and at a slower rate, and has been considered to be a better criterion for the evaluation of deficiency than the concentration in plasma.
Ascorbic acid is reversibly oxidized to dehydroascorbic acid; some is metabolized to ascorbate-2-sulfate, which is inactive, and oxalic acid which are excreted in the urine. Ascorbic acid in excess of the body's needs is also rapidly eliminated unchanged in the urine; this generally occurs with intakes exceeding 100 mg daily.
Ascorbic acid crosses the placenta and is distributed into breast milk. It is removed by hemodialysis.
The renal threshold for ascorbic acid is approx 14 ug/mL, but this level varies among individuals. When the body is saturated with ascorbic acid and blood concentrations exceed the threshold, unchanged ascorbic acid is excreted in the urine. When tissue saturation and blood concentrations of ascorbic acid are low, administration of the vitamin results in little or no urinary excretion of ascorbic acid. Inactive metabolites of ascorbic acid such as ascorbic acid-2-sulfate and oxalic acid are excreted in the urine ... Ascorbic acid is also excreted in the bile but there is no evidence for enterohepatic circulation ...
For more Absorption, Distribution and Excretion (Complete) data for L-Ascorbic Acid (29 total), please visit the HSDB record page.

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Metabolism / Metabolites
Hepatic. Ascorbic acid is reversibly oxidised (by removal of the hydrogen from the enediol group of ascorbic acid) to dehydroascorbic acid. The two forms found in body fluids are physiologically active. Some ascorbic acid is metabolized to inactive compounds including ascorbic acid-2-sulfate and oxalic acid.
Ascorbic acid-2-sulfate has ... been identified as metabolite of Vitamin C in human urine.
Ascorbate is oxidized to CO2 in rats and guinea pigs, but considerably less conversion can be detected in man. One route of metabolism of the vitamin in man involves its conversion to oxalate and eventual excretion in the urine; dehydroascorbate is presumably an intermediate.
... Young male guinea pigs /were fed/ diets containing either 2 g/kg (18 control animals) or 86 g/kg (29 treatment animals) of ascorbic acid for 275 days. The average weight gain was significantly higher in the control group. Eight control and eight treatment animals, chosen to maintain comparable weights between the groups, were then given a totally deficient ascorbic acid diet 24 hr before a metabolic study was initiated. In the metabolic study, (14)C-labeled L-ascorbic acid (628 g) was then injected intraperitoneally into both treatment and control guinea pigs to study the catabolism and excretion of the ascorbic acid. Catabolism of the labeled ascorbic acid to respiratory (14)CO2 was increased in treatment guinea pigs. The control and treatment animals were then divided into two groups. One group received 3 mg/kg ascorbic acid (chronic deficiency) for 68 days. The other received a diet devoid of ascorbic acid (acute deficiency) for 44 days. Four control and three treatment animals from the chronic deficiency group and three control and four treatment animals from the acute deficiency group were given a totally deficient ascorbic acid diet 24 hr before a second metabolic study was initiated. (14)C-labeled L-ascorbic acid (628 g) was injected intraperitoneally as above. Treatment animals in the chronic deficiency and the acute deficiency groups had increased catabolism of the labeled ascorbic acid to respiratory (14)CO2 compared to control animals in the chronic and acute deficiency groups. The amount of radioactivity recovered in the urine and feces was similar for both groups except for an increased urinary excretion of the label in treated animals exposed to the totally deficient diet. The treatment animals maintained higher tissue stores of ascorbic acid than the control animals. However, this difference was significant only in the testes. When subjected to a totally deficient diet the treatment animals were depleted of ascorbic acid at a faster rate than the control animals. The accelerated catabolism was not reversible by subnormal intakes of the vitamin ...
... Hartley guinea pigs approximately 30 days pregnant /were divided/ into a control group receiving 25 mg ascorbic acid and a treated group receiving 300 mg/kg/day ascorbic acid daily. All animals were fed a 0.05% ascorbic acid diet. The groups were maintained for 10 days on their respective diets. Pups (both sexes) were randomly chosen on either day 5 or day 10 for the metabolic study. L-l-(14)C-Ascorbic Acid (10 uCi/mM) was injected intraperitoneally into the pups and they were placed in a metabolic chamber for five hours to collect expired (14)CO2. From day 11 all pups were caged individually and weaned to a diet containing only traces of ascorbic acid. Every third day the animals were examined for physical signs of scurvy. Once signs appeared, the animals were examined daily until death. Necropsies were performed on all animals. Pups from the treated group demonstrated a marked increase in (14)CO2 excretion following the intraperitoneal injection. Signs of scurvy appeared 4 days earlier in the treated group and mortality of the treated pups occurred approximately one week earlier. When excretion of labeled CO2 in both groups was correlated with the day of onset of scurvy signs, a linear correlation was found between the two parameters, suggesting that the earlier appearance of signs of scurvy on the experimental pups is secondary to an increased rate of ascorbic acid catabolism ...
For more Metabolism/Metabolites (Complete) data for L-Ascorbic Acid (10 total), please visit the HSDB record page.
Ascorbic acid has known human metabolites that include Ascorbic acid-2-sulfate.

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Biological Half-Life
16 days (3.4 hours in people who have excess levels of vitamin C)
The plasma half-life is reported to be 16 days in humans. This is different in people who have excess levels of vitamin C where the half-life is 3.4 hours
Vitamin C has a 96 hr half-life in guinea pigs.
Due to homeostatic regulation, the biological half-life of ascorbate varies widely from 8 to 40 days and is inversely related to the ascorbate body pool.

Toxicity Summary
IDENTIFICATION: Origin of the substance: Ascorbic acid is of both natural and synthetic origin. Natural origin: ascorbic acid is found in fresh fruit and vegetables. Citrus fruits are a particularly good source of ascorbic acid and also hip berries, acerola and fresh tea leaves. Ascorbic acid exists as colorless, or white or almost white crystals. It is odorless or almost odorless. It has a pleasant, sharp acidic taste. It is freely soluble in water and sparingly soluble in ethanol. It is practically insoluble in ether and chloroform. HUMAN EXPOSURE: Main risks and target organs: The main target organs for toxicity are found in the gastrointestinal, renal and hematological systems. Summary of clinical effects: In individuals with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, hemolytic anemia may develop after administration of ascorbic acid. In individuals predisposed to renal stones, chronic administration of high doses may lead to renal calculi formation. In some cases, acute renal failure may be observed under both conditions. Indications: Prevention and treatment of scurvy. It has been used as a urinary acidifier and in correcting tyrosinemia in premature infants on high-protein diets. The drug may be useful to treat idiopathic methemoglobinemia. Contraindications: Ascorbic acid is contraindicated in patients with hyperoxaluria and G-6-PD deficiency. Routes of entry: Oral: Ascorbic acid is usually administered orally in extended-release capsule form, tablets, lozenges, chewable tablets, solutions and extended-release tablets and capsules Absorption by route of exposure: Ascorbic acid is readily absorbed after oral administration but the proportion does decrease with the dose. GI absorption of ascorbic acid may be reduced in patients with diarrhea or GI diseases. Distribution by route of exposure: Normal plasma concentrations of ascorbic acid are about 10 to 20 ug/mL. Total body stores of ascorbic acid have been estimated to be about 1.5 g with about a 30 to 45 mg daily turnover. Plasma concentrations of ascorbic acid rise as the dose ingested is increased until a plateau is reached with doses of about 90 to 150 mg daily. Ascorbic acid becomes widely distributed in body tissues with large concentrations found in the liver, leukocytes, platelets, glandular tissues, and the lens of the eye. In the plasma about 25% of the ascorbic acid is bound to proteins. Ascorbic acid crosses the placenta; cord blood concentration are generally 2 to 4 times the concentration in maternal blood. Ascorbic acid is distributed into milk. In nursing mothers on a normal diet the milk contains 40 to 70 ug/mL of the vitamin. Biological half-life by route of exposure: The plasma half-life is reported to be 16 days in humans. This is different in people who have excess levels of vitamin C where the half-life is 3.4 hours. Metabolism: Ascorbic acid is reversibly oxidized to dehydroascorbic acid in the body. This reaction, which proceeds by removal of the hydrogen from the enediol group of ascorbic acid, is part of the hydrogen transfer system. The two forms found in body fluids are physiologically active. Some ascorbic acid is metabolized to inactive compounds including ascorbic acid-2-sulfate and oxalic acid. Elimination by route of exposure: The renal threshold for ascorbic acid is approximately 14 ug/mL, but this level varies among individuals. When the body is saturated with ascorbic acid and blood concentrations exceed the threshold, unchanged ascorbic acid is excreted in the urine. When tissue saturation and blood concentrations of ascorbic acid are low, administration of the vitamin results in little or no urinary excretion of ascorbic acid. Inactive metabolites of ascorbic acid such as ascorbic acid-2-sulfate and oxalic acid are excreted in the urine. Ascorbic acid is also excreted in the bile but there is no evidence for enterohepatic circulation. Pharmacology and toxicology: Mode of action: Toxicodynamics: Hyperoxaluria may result after administration of ascorbic acid. Ascorbic acid may cause acidification of the urine, occasionally leading to precipitation of urate, cystine, or oxalate stones, or other drugs in the urinary tract. Urinary calcium may increase, and urinary sodium may decrease. Ascorbic acid reportedly may affect glycogenolysis and may be diabetogenic but this is controversial. Pharmacodynamics: In humans, an exogenous source of ascorbic acid is required for collagen formation and tissue repair. Vitamin C is a co-factor in many biological processes including the conversion of dopamine to noradrenaline, in the hydroxylation steps in the synthesis of adrenal steroid hormones, in tyrosine metabolism, in the conversion of folic acid to folinic acid, in carbohydrate metabolism, in the synthesis of lipids and proteins, in iron metabolism, in resistance to infection, and in cellular respiration. Vitamin C may act as a free oxygen radical scavenger. Toxicity: Human data: Adults: Diarrhea may occur after oral dosage of large amounts of ascorbic acid. Interactions: Concurrent administration of more than 200 mg of ascorbic acid per 300 mg of elemental iron increases absorption of iron from the GI tract. Increased urinary excretion of ascorbic acid and decreased excretion of aspirin occur when the drugs are administered concurrently. Ascorbic acid increases the apparent half-life of paracetamol. Interference with anticoagulant therapy has been reported. Carcinogenicity: It has been reported that there is no evidence of carcinogenicity. Some studies suggest that vitamin C may amplify the carcinogenic effect of other agents. L-ascorbic acid increases the oral carcinoma size induced by dimethylbenz(a)anthracene. Also, butylated hydroxyanisole induced forestomach carcinogenesis in rats. Teratogenicity: There is no evidence of teratogenicity. Mutagenicity: Ascorbic acid is reported to increase the rate of mutagenesis in cultured cells but this only occurs in cultures with elevated levels of Cu(2+) or Fe(2+). This effect may be due to the ascorbate induced generation of oxygen-derived free radicals. However, there is no evidence of ascorbate induced mutagenesis in vivo.

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Vitamin C is a normal component of human milk and is a key milk antioxidant. The recommended vitamin C intake in lactating women is 120 mg daily, and for infants aged 6 months or less is 40 mg daily. High daily doses up to 1000 mg increase milk levels, but not enough to cause a health concern for the breastfed infant and is not a reason to discontinue breastfeeding. Nursing mothers may need to supplement their diet to achieve the recommended intake or to correct a known deficiency. Maternal doses of vitamin C in prenatal vitamins at or near the recommended intake do not alter milk levels.
Freezing (-20 degrees C) freshly expressed mature milk from hospitalized mothers of term and preterm infants does not change milk vitamin C levels for at least 3 months of freezer storage. After 6 to 12 months of freezing (-20 degrees C), vitamin C levels can decrease by 15 to 30%. Storage at -80 degrees C preserves vitamin C levels for up to 8 months, with 15% loss by 12 months.
◉ Effects in Breastfed Infants
Sixty healthy lactating women between 1 and 6 months postpartum exclusively breastfeeding their infants were given vitamin C 500 mg plus vitamin E 100 IU once daily for 30 days, or no supplementation. Infants of supplemented mothers had increased biochemical markers of antioxidant activity in their urine. Clinical outcomes were not reported.
Eighteen preterm infants, seven of whom were less than 32 weeks gestational age, who were fed pooled, Holder-pasteurized donor milk beginning during the first three days of life had their average blood plasma ascorbic acid concentrations decrease from 15.5 mg/L at birth to 5.4 mg/L by 1 week of age, and to 4.1 mg/L by 3 weeks of age. The authors described the 1- and 3-week levels as subtherapeutic (<6 mg/L) and indicative of inadequate intake, potentially jeopardizing postnatal growth potential. Although this study was conducted before advances in the provision of parenteral nutrition and enteral milk fortification for preterm infants, contemporary studies suggest that inadequate vitamin C intake from pooled, pasteurized donor milk may be a potential health problem for preterm infants receiving donor milk.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
25%

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Interactions
BALB/c male mice (288) were allocated into four groups: group 1 (48 animals), control diet; group 2 (48 animals), control diet and 500 ppm 2-acetylaminofluorene (2-AAF); group 3 (96 animals), control diet and 250 mg/mL of ascorbic acid in water; group 4 (96 animals), control diet, 2-AAF, and ascorbic acid. Food and water consumptions were measured at weekly intervals. The animals were killed at 28 days and necropsied. There were no detectable differences in relative food consumption due to the addition of ascorbic acid or to an interaction of ascorbic acid with 2-AAF. However the presence of ascorbic acid in the water was associated with a significant reduction in relative water consumption. The addition of 2-AAF caused a significant increase in relative water consumption, and a significant interaction of ascorbic acid with 2-AAF was detected. Major histological findings were restricted to the urinary bladder. Vacuolization of the transitional epithelium, simple and nodular urothelial hyperplasia, fibrosis, and chronic inflammation of the lamina propria were found in varying degrees in the urinary bladders of mice receiving 2-AAF alone and in combination with ascorbic acid. The most severe lesions were seen in the mice given the combination of 2-AAF and ascorbic acid. The urinary bladders of mice receiving the control diet and ascorbic acid alone were normal. The chronic inflammation and fibrosis were restricted primarily to the fundus of the urinary bladder. The lamina propria contained an increased amount of collagen, an increase in the vasculature and an infiltration of mononuclear inflammatory cells ...
Effect of ascorbic acid on metal toxicity.
Table: Effect of Ascorbic Acid on Metal Toxicity [Table#2228]

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Non-Human Toxicity Values
LD50 Rat oral 11,900 mg/kg
LD50 Rat oral > 5000 mg/kg bw /From table/
LD50 Rat sc 5,000 mg/kg bw /From table/
LD50 Rat iv 1,000 mg/kg bw /From table/
For more Non-Human Toxicity Values (Complete) data for L-Ascorbic Acid (24 total), please visit the HSDB record page.

[1]. Michael T Nelson, et al. Molecular mechanisms of subtype-specific inhibition of neuronal T-type calcium channels by ascorbate. J Neurosci. 2007 Nov 14;27(46):12577-83.
[2]. Aleksander Hinek, et al. Sodium L-ascorbate enhances elastic fibers deposition by fibroblasts from normal and pathologic human skin. J Dermatol Sci. 2014 Sep;75(3):173-82.
[3]. Sungrae Cho, et al. Hormetic dose response to L-ascorbic acid as an anti-cancer drug in colorectal cancer cell lines according to SVCT-2 expression. Sci Rep. 2018 Jul 27;8(1):11372.
[4]. Satyanarayana Sreemantula, et al. Influence of antioxidant (L- ascorbic acid) on tolbutamide induced hypoglycaemia/antihyperglycaemia in normal and diabetic rats. BMC Endocr Disord. 2005 Mar 3;5(1):2.
[5]. Sebastian J Padayatty, et al. Vitamin C as an antioxidant: evaluation of its role in disease prevention. J Am Coll Nutr. 2003 Feb;22(1):18-35.
[6]. Esteban MA, Wang T, Qin B, et al. Vitamin C enhances the generation of mouse and human induced pluripotent stem cells. Cell Stem Cell. 2010;6(1):71-79. doi:10.1016/j.stem.2009.12.001
[7]. Talkhabi M, Pahlavan S, Aghdami N, Baharvand H. Ascorbic acid promotes the direct conversion of mouse fibroblasts into beating cardiomyocytes. Biochem Biophys Res Commun. 2015;463(4):699-705.
[8]. Stadtfeld M, Apostolou E, Ferrari F, et al. Ascorbic acid prevents loss of Dlk1-Dio3 imprinting and facilitates generation of all-iPS cell mice from terminally differentiated B cells. Nat Genet. 2012;44(4):398-S2.

Therapeutic Uses
Antioxidants; Free Radical Scavengers
Prophylaxis and treatment of scurvy
Ascorbic acid 100 to 200 mg daily may be given with desferrioxamine in the treatment of patients with thalassemia, to improve the chelating action of desferrioxamine, thereby increasing the excretion of iron.
In iron deficiency states ascorbic acid may increase gastrointestinal iron absorption and ascorbic acid or ascorbate salts are therefore included in some oral iron preparations.
For more Therapeutic Uses (Complete) data for L-Ascorbic Acid (30 total), please visit the HSDB record page.

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Drug Warnings
Large doses are reported to cause diarrhea and other gastrointestinal disturbances. It has also been stated that large doses may result in hyperoxaluria and the formation of renal calcium oxalate calculi, and ascorbic acid should therefore be given with care to patients with hyperoxaluria. Tolerance may be induced with prolonged use of large doses, resulting in symptoms of deficiency when intake is reduced to normal. Prolonged or excessive use of chewable vitamin C preparations may cause erosion of tooth enamel.
Large doses of ascorbic acid have resulted in hemolysis in patients with G6PD deficiency.
Vitamin C intakes of 250 mg/day or higher have been associated with false-negative results for detecting stool and gastric occult blood. Therefore, high dose vitamin C supplements should be discontinued at least two weeks before physical exams to avoid interference with blood and urine tests.
Supplemental vitamin C may reduce the effectiveness of cancer chemotherapy, and its effectiveness in reducing risk from cancer and related death is unclear.
For more Drug Warnings (Complete) data for L-Ascorbic Acid (25 total), please visit the HSDB record page.

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Pharmacodynamics
Ascorbic Acid (vitamin C) is a water-soluble vitamin indicated for the prevention and treatment of scurvy, as ascorbic acid deficiency results in scurvy. Collagenous structures are primarily affected, and lesions develop in bones and blood vessels. Administration of ascorbic acid completely reverses the symptoms of ascorbic acid deficiency.
The major activity of supplemental iron is in the prevention and treatment of iron deficiency anemia. Iron has putative immune-enhancing, anticarcinogenic and cognition-enhancing activities.

C6H8O6

176.12

176.032

50-81-7

L-Ascorbic acid;50-81-7;L-Ascorbic acid sodium salt;134-03-2;L-Ascorbic acid calcium dihydrate;5743-28-2;L-Ascorbic acid;50-81-7

54670067

Crystals (usually plates, sometimes needles, monoclinic system)
White crystals (plates or needles)
White to slightly yellow crystals or powder ... gradually darkens on exposure to light

2.0±0.1 g/cm3

552.7±50.0 °C at 760 mmHg

190-194 °C (dec.)

238.2±23.6 °C

0.0±3.4 mmHg at 25°C

1.711

-2.41

4

6

2

12

232

2

O1C(C(=C([C@@]1([H])[C@]([H])(C([H])([H])O[H])O[H])O[H])O[H])=O

CIWBSHSKHKDKBQ-JLAZNSOCSA-N

InChI=1S/C6H8O6/c7-1-2(8)5-3(9)4(10)6(11)12-5/h2,5,7-10H,1H2/t2-,5+/m0/s1

(2R)-2-[(1S)-1,2-dihydroxyethyl]-3,4-dihydroxy-2H-furan-5-one

ascorbate; Vitamine C; L-ascorbic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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 (~567.79 mM)
H2O : ≥ 100 mg/mL (~567.79 mM)

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.)