Drug compounds have included stable heavy isotopes of carbon, hydrogen, and other elements, mostly as quantitative tracers while the drugs were being developed. Because deuteration may have an effect on a drug's pharmacokinetics and metabolic properties, it is a cause for concern [1].

Absorption, Distribution and Excretion
This study investigated the distribution of low-dose dietary bisphenol A (BPA). Following oral administration of 50 μg/kg (14)C-BPA to female rats, radioactive material was distributed throughout the body, with particularly high levels in the uterus. Pre-administration of estradiol or the estrogen antagonist ICI 182,780 significantly reduced radioactivity in the uterus. Gas chromatography-mass spectrometry (GC-MS) analysis confirmed that most BPA in the uterus was aglycone (with receptor activity). Subsequently, administration of 0.5, 5, or 50 μg/kg (14)C-BPA to mice resulted in higher radioactivity in the uterus compared to other non-metabolic tissues. Female mice receiving 50 μg/kg (14)C-BPA for 1, 7, or 28 days, with measurements taken 24 hours after the last administration, showed significantly increased radioactivity in the uterus, liver, and kidneys after repeated administration. These data collectively demonstrate the interaction between BPA and estrogen receptors in vivo. They also showed that repeated low-dose administration increased BPA levels in reproductive tissues. Widespread human exposure to bisphenol A (BPA)—an endocrine disruptor that interferes with developmental processes—has raised concerns about the health risks of fetal exposure to BPA. In humans, BPA concentrations vary considerably in the placental-fetal system. However, the extent of human fetal exposure to BPA remains unclear. This study aimed to characterize the exchange of bisphenol A (BPA) and its major metabolite, bisphenol A glucuronide (BPA-G), in the placenta using a non-circulating twin placental perfusion technique. Lipid-soluble BPA exhibited high bidirectional permeability in the placenta, strongly suggesting passive diffusion in both the maternal-fetal and feto-maternal directions, resulting in a calculated ratio of approximately 1 between fetal and maternal free BPA concentrations. In contrast, BPA-G exhibited limited placental permeability, particularly in the maternal-fetal direction. Therefore, fetal exposure to BPA conjugates can primarily be attributed to the limited ability of the fetus to expel BPA-G. When administered via gavage to male CFE rats, 28% of the 14C-labeled bisphenol A was excreted in the urine (mainly as glucosamine) and 56% in the feces (20% free bisphenol A, 20% hydroxylated bisphenol A, and the remainder unidentified conjugates). No carbon-labeled residues were detected in animals euthanized after 8 days. The toxicokinetics of radiolabeled 14C bisphenol A in Rana temporaria were investigated at two experimental temperatures (7°C and 19°C). During the 96-hour experiment, tadpoles grew very slowly at 7°C, but at 19°C, their body weight nearly doubled. At all tested exposure concentrations (0.2, 1.5, 10, and 100 μg/L), the conditional uptake rate constant (ku) at 7 °C was 69% to 82% lower and the elimination rate (ke) was 79% to 90% lower than at 19 °C. Conversely, the bioaccumulation factor (BCF) was higher at 7 °C than at 19 °C. The total accumulation of bisphenol A in individuals was higher at 19 °C, consistent with the higher ku value at 19 °C. Exposure concentration had no significant effect on BCF at either temperature. These results suggest that higher temperatures increase the amount and total amount of chemicals absorbed by frog tadpoles, but do not necessarily lead to a higher BCF. Higher temperatures may result in a greater increase in growth rate than in uptake rate, leading to a net dilution of bisphenol A in tadpole tissues. The observed differences in bioaccumulation factor (BCF) may also be due to temperature-induced changes in allometric growth relationships (increased surface area to volume ratio) and/or more efficient clearance by more mature tadpoles at higher temperatures. For more complete data on the absorption, distribution, and excretion of bisphenol A (27 types), please visit the HSDB record page. Metabolism/Metabolites…This study investigated the metabolism of bisphenol A [2,2-bis(4-hydroxyphenyl)propane] (BPA) in CD1 mouse liver microsomes and S9 fraction. Nine metabolites were isolated and identified using high-performance liquid chromatography (HPLC) and mass spectrometry. Many of these metabolites were identified in mammals for the first time, including isopropylhydroxyphenol (produced by bisphenol A cleavage), bisphenol A glutathione conjugate, glutathioneylphenol, glutathioneyl-4-isopropylphenol, and bisphenol A dimer. This study used reversed-phase high-performance liquid chromatography-fluorescence detection to analyze the bisphenol A (BPA) content in urine samples from 30 healthy Koreans (15 males, age 42.6 ± 2.4 years; 15 females, age 43.0 ± 2.7 years). These samples were treated with β-glucuronidase and/or sulfatase, or were untreated. The total BPA concentrations (including free BPA and urinary conjugates) were similar in men and women (2.82 +/- 0.73 and 2.76 +/- 0.54 ng/mL, respectively), but the levels of BPA conjugates in urine differed between the sexes. The levels of bisphenol A-glucuronide (BPA) in males (2.34 ± 0.85 ng/mL) were significantly higher than those in females (1.00 ± 0.34 ng/mL), while the levels of BPA-sulfate (1.20 ± 0.32 ng/mL) in females were higher than those in males (0.49 ± 0.27 ng/mL). This study aimed to determine whether the pharmacokinetics and metabolism of 10 or 100 mg/kg of 14C-labeled bisphenol A (BPA) in Fischer 344 rats were route-dependent after a single oral (po), intraperitoneal (ip), or subcutaneous (sc) administration. The results showed that the pharmacokinetics of BPA were significantly route-dependent. Compared with subcutaneous or intraperitoneal administration, oral administration significantly reduced the relative bioavailability and plasma radioactivity of BPA. Following oral administration, the main component of plasma radioactivity is bisphenol A (BPA) monoglucuronide conjugates (accounting for 68-100% of plasma radioactivity). After subcutaneous or intraperitoneal injection, the plasma BPA concentration reaches its peak (Cmax), second only to BPA monoglucuronide in the plasma of female animals administered intraperitoneally. Up to four unidentified metabolites are also present in the plasma of animals administered intraperitoneally or subcutaneously. One of these was only found after intraperitoneal injection and has been preliminarily identified as a BPA monosulfate conjugate. Monoglucuronide conjugates are the main metabolite in urine; unmetabolized BPA is the main excreted component in feces. ...
Previous studies have shown that after oral administration of bisphenol A (BPA) to adult rats, the clearance rate of BPA in the blood is rapid, with its main metabolite being BPA monoglucuronide (BPA-glucuronide). Since the development of glucuronyl transferase (GT) varies with age, this study investigated the pharmacokinetics of bisphenol A (BPA) in newborn animals. (14) C-BPA was administered by gavage to rats at pnd 4, pnd 7, and pnd 21 (pnd 4, pnd 7, pnd 21) or to 11-week-old adult rats (at a dose of 10 mg/kg only). Blood (newborn and adult animals) and selected tissues (newborn animals) were collected at 0.25, 0.75, 1.5, 3, 6, 12, 18, and 24 hours after administration. BPA and BPA-glucuronide in plasma were quantified by high performance liquid chromatography; radioactivity in plasma and tissues was quantified by liquid scintillation counting. The data showed that newborn rats of all three age groups were able to metabolize bisphenol A to bisphenol A-glucuronide, but the quantity and concentration of plasma metabolites were age-dependent, consistent with individual development of GT. Except for 24 hours after administration, the concentrations of bisphenol A-glucuronide and bisphenol A in the plasma of neonatal rats were higher than those in adult rats, suggesting that the hepatic excretion function of neonatal rats is immature. …Furthermore, dose-dependent metabolism and pharmacokinetics of bisphenol A were observed in neonatal rats. At a dose of 1 mg/kg, bisphenol A was almost completely metabolized to bisphenol A-glucuronide (94-100% of plasma radioactivity). This contrasts sharply with the observation of up to 13 different plasma metabolites at a dose of 10 mg/kg. …
For more complete data on the metabolism/metabolites of bisphenol A (a total of 8 metabolites), please visit the HSDB record page.
Known human metabolites of bisphenol A include (2S,3S,4S,5R)-3,4,5-trihydroxy-6-[4-[2-(4-hydroxyphenyl)prop-2-yl]phenoxy]oxecyclohexane-2-carboxylic acid. Bisphenol A (BPA) is rapidly absorbed from the gastrointestinal tract after ingestion and then converted into various metabolites in the liver, primarily BPA glucuronide. BPA metabolites include isopropyl hydroxyphenol (produced by BPA cleavage), BPA-glutathione conjugate, glutathione phenol, glutathione 4-isopropylphenol, and BPA dimer. Monoglucuronide conjugate is the main urinary metabolite; unmetabolized BPA is the main component excreted in feces (A287, A288).

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Biological Half-Life
...After a single oral or intravenous (iv) administration of 100 μg/kg (circular-(14)C(U)) radiolabeled bisphenol A ((14)C-BPA) to male and female cynomolgus monkeys...the terminal elimination half-life after intravenous administration (t(1/2iv) = 13.5 to 14.7 hours) was longer than that after oral administration (t(1/2oral) = 9.63 to 9.80 hours). The fast-phase half-life of total radioactivity after intravenous administration (t(1/2f)) was 0.61 to 0.67 hours. The half-life of unmetabolized (14)C-BPA in females (t_1/2f) (0.39 hours) was shorter than that in males (0.57 hours).
...Oral bioavailability of bisphenol A was determined after intravenous (0.1 mg/kg) and oral (10 mg/kg) administration of relatively low doses to rats. ...The apparent terminal elimination half-life of bisphenol A following oral administration (21.3 ± 7.4 h) was significantly longer than that following intravenous administration.
...Bisphenol A was intravenously administered to mice, rats, rabbits, and dogs at doses of 1–2 mg/kg. In all these animals, the obtained serum concentration-time curves were well described by a biexponential equation, with mean half-lives of 39.9 min, 37.6 min, 40.8 min, and 43.7 min in mice, rats, rabbits, and dogs, respectively. ...Simple allometric scaling and different time-transformation methods predicted human half-lives (t_1/2) ranging from 43.6 to 196.2 min. ...The toxicokinetics of bisphenol A (BPA) in F344 rats, cynomolgus monkeys, and chimpanzees were investigated. ...After oral administration of 10 mg/kg BPA, the Cmax and AUC of BPA metabolites were in the following order: cynomolgus monkeys > chimpanzees > rats, and the terminal elimination half-life (T1/2) in rats was greater than that in cynomolgus monkeys and chimpanzees, indicating that BPA exists in enterohepatic circulation in rats.

Toxicity Summary
Identification and Uses: Bisphenol A (BPA) is a solid. It is used in the manufacture of epoxy resins and polycarbonates for food packaging. Human Studies: Reports of allergic contact dermatitis caused by PVC gloves are rare, with only two cases identified as sensitizers. One clinical report describes a group of eight outdoor workers experiencing photosensitivity contact dermatitis due to BPA. Urinary BPA may be associated with decreased semen quality and increased sperm DNA damage. An association has been observed between environmental exposure to BPA and the occurrence of fetal malformations. Maternally bound BPA has also been associated with an increased risk of aneuploid and euploid miscarriage. BPA is an endocrine disruptor with estrogenic properties that can adversely affect meiotic spindle assembly. Data suggest that exposure to BPA in female patients may interfere with oocyte quality during in vitro fertilization (IVF). Male exposure to bisphenol A (BPA) may affect embryo quality during IVF. Studies have found that BPA is cytotoxic to human cell lines but not genotoxic. Animal studies: BPA caused severe eye damage in rabbits, but its skin irritation was negligible. A large-scale two-generation oral reproductive toxicity study in rats evaluated the effects of BPA on fertility. No clinical symptoms of toxicity or effects on lactational weight gain were observed in F1 and F2 generation pups. No treatment-related changes were observed in litter size, survival rate, sex ratio, anorectal distance, and reflex development. In a spontaneously developing transgenic mouse model of tumors, BPA significantly accelerated the development of mammary tumors. In mice, exposure to low doses of BPA during pregnancy alone had immediate and durable transgenerational effects on mRNA in the brain and social behavior. Prenatal exposure to bisphenol A (BPA) primarily affected male rats and eliminated sex differences in upright behavior in the open field test and struggling behavior in the forced swimming test. In mice, prenatal exposure to BPA affected the development of female pituitary gonadotropins. Experiments using test strains of Salmonella typhimurium (TA 98, TA 100, and TA 102) with or without metabolic activation showed that BPA was not mutagenic. However, exposure to BPA in rats resulted in a significant increase in micronucleus frequency in polychromatic erythrocytes, chromosomal structural aberrations in bone marrow cells, and DNA damage in blood lymphocytes. Exposure to BPA in rodents has been shown to induce obesity. Furthermore, feeding male fruit flies with BPA significantly inhibited the expression of insulin-like peptides. Ecotoxicity studies: Bisphenol A (BPA) exhibited a sex reversal effect on the gonads of F1 generation embryos of Japanese quail (Coturnix japonica). Induction of vitellogenin expression in rainbow trout after intraperitoneal injection of BPA has also been reported. Japanese medaka (Oryzias latipes) were exposed to sublethal concentrations of BPA of 2.28, 13.0, 71.2, 355, and 1820 μg/L during the early life stage from fertilization to 60 days post-hatching. Observation of external secondary sexual characteristics revealed no male individuals in the 1820 μg/L treatment group. Furthermore, histological examination showed that 32% of the fish in the 1820 μg/L group possessed a testis-oocyte complex composed of testicular germ cells and oocytes. The effects of bisphenol A (BPA) on gene expression in Arabidopsis thaliana were determined using microarray analysis and quantitative gene PCR. Many hormone-responsive genes showed altered expression after BPA treatment. BPA interferes with flowering through a mechanism potentially involving disruption of auxin signaling. Bisphenol is an endocrine disruptor. Low doses of BPA can mimic human hormones and may have negative health effects. Therefore, there are concerns that long-term low-dose exposure to BPA may produce chronic toxicity in humans (L705).

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Toxicity Data
LC (mice)> 1,700 mg/m3/2h (inhalation);
LD50: 2230 mg/kg (oral, rabbit) (T249)

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Interactions
We investigated whether genetic alterations in mice exposed to bisphenol A (BPA) (alone or in combination with X-rays) before conception could be transmitted through sperm. Male mice were exposed to BPA, X-rays, or both for 8 weeks and then mated with unexposed female mice. We examined prenatal and postnatal development in offspring of exposed male mice. Both exposure to BPA alone and in combination had a slight effect on postnatal development. In combination, the mortality rate was twice as high as that of BPA alone; while BPA exposure resulted in decreased body weight and reduced sperm quality in F1 mice. This study aimed to investigate the effects of two-week exposure to bisphenol A (BPA) alone or in combination with X-rays on sperm count, quality, and the induction of DNA strand breaks in somatic and germ cells in male mice. Pzh:SFIS male mice were exposed to X-rays (0.05 and 0.10 Gy), BPA (5, 10, 20, and 40 mg/kg), or a combination of both (0.05 Gy + 5 mg/kg body weight BPA and 0.10 Gy + 10 mg/kg body weight BPA). Both X-rays and BPA alone reduced sperm count and quality. X-rays induced DNA strand breaks in spleen cells, while bisphenol A (BPA) induced DNA strand breaks in lymphocytes, spleen, kidney, and lung cells, as well as germ cells. After combined exposure to both substances, sperm count and quality were similar to those after exposure to either substance alone, but significantly lower than in the control group. Compared with BPA alone, combined exposure to both lower and higher doses significantly reduced the levels of DNA damage in somatic and germ cells. The results confirmed the mutagenicity of BPA. Combined exposure to X-rays and BPA prevented DNA damage in mouse somatic and germ cells. Bisphenol A (BPA) is used in the manufacture of epoxy resins, polyester-styrene resins, and polycarbonate resins, which are used in the production of baby bottles, water bottles and reusable containers, food and beverage packaging, dental fillings, and sealants. This study aimed to investigate the effects of exposure to BPA alone and combined exposure to BPA with X-rays for 8 weeks (one complete spermatogenesis cycle) on the reproductive organs and germ cells of adult and adolescent male mice. Pzh:Sfis male mice were exposed to BPA (5, 10, and 20 mg/kg), X-rays (0.05 Gy), or a combination of both (0.05 Gy + 5 mg/kg body weight BPA), respectively. Parameters measured included sperm count, sperm motility, sperm morphology, and DNA damage in male gametes. Both BPA and X-ray exposure alone reduced sperm quality. Compared with adult mice, BPA exposure significantly reduced sperm count in adolescent male mice, and degenerative changes were detected in the seminiferous epithelium. This may indicate that the germ cells of young male mice are more sensitive to the effects of BPA. Combined treatment with BPA and X-rays enhanced the detrimental effects of BPA alone on adult male germ cells, while low-dose radiation sometimes showed a protective or additive effect in adolescent mice. This study aimed to investigate whether BPA induces oxidative stress in the rat liver, and whether concurrent administration of the antioxidant vitamin C could prevent oxidative stress. Rats were orally administered BPA (0.2, 2.0, and 20 μg/kg body weight/day) and BPA + vitamin C (0.2, 2.0, and 20 μg + 40 mg/kg body weight/day), respectively, for 30 consecutive days. Twenty-four hours after the last administration, rats were euthanized by anesthesia with an overdose of ether. No significant changes were observed in animal body weight or liver weight. The activities of antioxidant enzymes (including superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase) in the mitochondrial and microsomal components of the liver were decreased. Compared with the corresponding control groups, the levels of hydrogen peroxide and lipid peroxidation were increased in the treatment group rats. The activity of alanine aminotransferase, a marker of liver injury, was unchanged in the treatment group rats compared with the corresponding control groups. After co-administration of bisphenol A with vitamin C, the activities of superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase, as well as the levels of hydrogen peroxide and lipid peroxidation, were not changed compared with the corresponding control groups. For more complete data on interactions with bisphenol A (12 items in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 of rats (male, F344): 4100 mg/kg
Oral LD50 of rats (female, F344): 3300 mg/kg
Oral LD50 of mice (male): 5280 mg/kg
Oral LD50 of mice (female, B6C3F1): 4100 mg/kg
For more complete (9) non-human toxicity values of bisphenol A, please visit the HSDB record page.

[1]. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019 Feb;53(2):211-216.

[2]. Bisphenol A and its analogues bisphenol S, bisphenol F and bisphenol AF induce oxidative stress and biomacromolecular damage in human granulosa KGN cells. Chemosphere. 2020 Apr 9;253:126707.

[3]. Bisphenol A: an endocrine disruptor with widespread exposure and multiple effects. J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):27-34.

According to data from the National Toxicology Program's Center for Human Reproduction Risk Assessment, bisphenol A (BPA) may cause developmental toxicity. According to an independent committee of scientific and health experts, it may cause female reproductive toxicity. 4,4'-Isopropylidene diphenol is a white to light brown flake or powder with a slightly medicinal odor and sinks in water. (US Coast Guard, 1999) Bisphenol A is a bisphenol with the chemical formula 4,4'-methylenediphenol, in which the methylene hydrogen is replaced by two methyl groups. It is an exogenous estrogen, environmental pollutant, exogenous substance, and endocrine disruptor. Bisphenol A is a diphenylmethane derivative containing two hydroxyphenyl groups. Bisphenol A (BPA) is a colorless solid used in the synthesis of commercial plastics, including polycarbonates and epoxy resins, which are widely used in various consumer products. Ingestion of bisphenol A (BPA) may have estrogen-like effects. Exposure to BPA may increase the risk of certain cancers. Bisphenol A (BPA), commonly abbreviated as BPA, is an organic compound containing two phenolic hydroxyl groups. It is a bifunctional structural unit in several important plastics and plastic additives. With an annual production of 2 to 3 million tons, BPA is a crucial monomer in polycarbonate production. Because BPA is used in reusable polycarbonate food containers, such as buckets, baby bottles, and kitchen utensils, it can become a food contaminant. Since the 1930s, concerns about the harmful effects of BPA on humans have existed. In 2008, after reports from some national governments questioned its safety, news media began to frequently report on concerns about the use of BPA in consumer products, and some retailers removed baby bottles and other children's products made with BPA from their shelves. See also: isoprene monomer (monomer); polycarbonate (note moved to)... See more...

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Mechanism of Action
This study evaluated the effects of bisphenol A (BPA) on the differentiation of human endometrial stromal fibroblasts (ESF) and the expression of genes related to estrogen metabolism. Human estradiol fibroblasts (ESFs) were isolated from eight hysterectomy specimens, cultured, and treated with 5-100 μmol/L BPA (with or without estradiol or 8-bromo-cAMP) for 48 hours. mRNA expression was analyzed using real-time reverse transcription PCR. 8-bromo-cAMP-induced decidualization of human ESFs was confirmed by the expression of insulin-like growth factor binding protein-1 (IGFBP1) and prolactin secretion. Short-term exposure (48 hours) reduced human ESF proliferation (P<0.04), but this was not due to apoptosis. High-dose bisphenol A (BPA) significantly induced IGFBP1 mRNA and protein expression, decreased P450scc mRNA expression, and reversed, in a dose-dependent manner, the 8-bromocyclic adenosine monophosphate (8-br-cAMP)-induced increase in HSD17B2 (estradiol to estrone) expression while downregulating HSD17B1 (estradiol to estradiol) expression (P = 0.03). 8-br-cAMP significantly enhanced this effect (P = 0.028). BPA had no significant effect on the expression of aromatase and PPARγ. The estrogen receptor antagonist ICI had no effect on gene expression in BPA-treated cells, while high-dose BPA significantly downregulated estrogen receptor α (but not estrogen receptor β) expression (P = 0.028). BPA has endocrine-disrupting effects on human endocrine function and gene expression, but its underlying mechanism does not appear to involve estrogen-mediated pathways.

C15H12D4O2

232.14

102438-62-0

Bisphenol A;80-05-7

6623

White to off-white solid powder

1.1±0.1 g/cm3

400.8±25.0 °C at 760 mmHg

307 to 313 °F (NTP, 1992)
160 °C
MP: 150-155 °C (solidification range)
156 - 157 °C
150-157 °C
307-313 °F

192.4±17.8 °C

0.0±1.0 mmHg at 25°C

1.599

3.43

2

2

2

17

209

0

IISBACLAFKSPIT-UHFFFAOYSA-N

InChI=1S/C15H16O2/c1-15(2,11-3-7-13(16)8-4-11)12-5-9-14(17)10-6-12/h3-10,16-17H,1-2H3

4-[2-(4-hydroxyphenyl)propan-2-yl]phenol

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.)