p-Cresol inhibited MPAG formation in a potent and competitive manner (Ki=5.2 µM in pooled human liver microsomes) and the interaction was primarily mediated by UGT1A9. This interaction was estimated to increase plasma MPA exposure in patients by approximately 1.8-fold, which may result in MPA toxicity. The mechanism of inhibition for AcMPAG formation was noncompetitive (Ki=127.5 µM) and less likely to be clinically significant. p-Cresol was the most potent inhibitor of MPA-glucuronidation compared with other commonly studied uremic toxins (eg, indole-3-acetic acid, indoxyl sulfate, hippuric acid, kynurenic acid, and 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid) and its metabolites (ie, p-cresol sulfate and p-cresol glucuronide).[1]

After oral administration of tyrosine feed to PBC (primary biliary cholangitis) mice, PCS (p-Cresol sulfate) increased, liver inflammatory factors were decreased, and anti-inflammatory factors were increased. Furthermore, Kupffer cells in the liver polarized form M1 transitioned to M2. PCS can damage normal bile duct epithelial cells and suppress the immune response of Kupffer cells. But PCS protects bile duct epithelial cells damaged by LPS through Kupffer cells.[2]

Mycophenolic acid (MPA) is commonly prescribed for preventing graft rejection after kidney transplantation. The primary metabolic pathways of MPA are hepatic glucuronidation through UDP-glucuronosyltransferase (UGT) enzymes in the formation of MPA-glucuronide (MPAG, major pathway) and MPA-acyl glucuronide (AcMPAG). p-Cresol, a potent uremic toxin known to accumulate in patients with renal dysfunction, can potentially interact with MPA via the inhibition of glucuronidation. We hypothesized that the interaction between MPA and p-cresol is clinically relevant and that the estimated exposure changes in the clinic are of toxicological significance. Using in vitro approaches (ie, human liver microsomes and recombinant enzymes), the potency and mechanisms of inhibition by p-cresol towards MPA glucuronidation were characterized. Inter-individual variabilities, effects of clinical co-variates, in vitro-in vivo prediction of likely changes in MPA exposure, and comparison to other toxins were determined for clinical relevance. p-Cresol inhibited MPAG formation in a potent and competitive manner (Ki=5.2 µM in pooled human liver microsomes) and the interaction was primarily mediated by UGT1A9. This interaction was estimated to increase plasma MPA exposure in patients by approximately 1.8-fold, which may result in MPA toxicity. The mechanism of inhibition for AcMPAG formation was noncompetitive (Ki=127.5 µM) and less likely to be clinically significant. p-Cresol was the most potent inhibitor of MPA-glucuronidation compared with other commonly studied uremic toxins (eg, indole-3-acetic acid, indoxyl sulfate, hippuric acid, kynurenic acid, and 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid) and its metabolites (ie, p-cresol sulfate and p-cresol glucuronide). Our findings indicate that the interaction between p-cresol and MPA is of toxicological significance and warrants clinical investigation.[1]

Gas chromatography-mass spectrometry (GC-MS) was used to detect differences in tyrosine, phenylalanine, tryptophan, PCS, and p-Cresyl glucuronide (PCG) between the serum of PBC patients and healthy controls. In vivo experiments, mice were divided into the normal control, PBC group, and PBC tyrosine group. GC-MS was used to detect PCS and PCG. Serum and liver inflammatory factors were compared between groups along with the polarization of liver Kupffer cells. Additionally, PCS was cultured with normal bile duct epithelial cells and Kupffer cells, respectively. PCS-stimulated Kupffer cells were co-cultured with lipopolysaccharide-injured bile duct epithelial cells to detect changes in inflammatory factors.[2]

Levels of tyrosine and phenylalanine were increased, but PCS level was reduced in PBC patients, with PCG showing a lower concentration distribution in both groups. PCS in PBC mice was also lower than those in normal control mice. After oral administration of tyrosine feed to PBC mice, PCS increased, liver inflammatory factors were decreased, and anti-inflammatory factors were increased. Furthermore, Kupffer cells in the liver polarized form M1 transitioned to M2. PCS can damage normal bile duct epithelial cells and suppress the immune response of Kupffer cells. But PCS protects bile duct epithelial cells damaged by LPS through Kupffer cells.[2]

Absorption, Distribution and Excretion
Under normal circumstances, the human body excretes approximately 50 mg of p-cresol daily in urine. P-cresol is endogenously synthesized by anaerobic bacteria in the gastrointestinal tract using tyrosine. Normal individuals excrete 16 to 39 mg of p-cresol daily. Cresol compounds are slightly more corrosive to the skin and eyes than phenol, but their systemic effects may be slightly weaker due to slower absorption. On average, healthy individuals excrete approximately 50 mg (range 16-74 mg) of p-cresol daily in urine. Endogenous p-cresol is synthesized by anaerobic bacteria in the gut using tyrosine (an amino acid found in most proteins). Free p-cresol formed in this way is absorbed by the intestines and excreted in urine as a conjugate. For more complete data on the absorption, distribution, and excretion of p-cresols (9 types in total), please visit the HSDB records page.

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Metabolisms/Metabolites
p-cresol fed to rabbits is excreted in urine as a conjugate of glucuronide (60%) and sulfate (15%), with approximately 10% oxidized to p-hydroxybenzoic acid and trace amounts hydroxylated to 3,4-dihydroxytoluene.
In rabbits, p-cresol is converted to p-cresol-β-D-glucuronide, p-cresol sulfate, p-hydroxybenzyl alcohol, 4-methylcatechol, and p-methyl anisole.
In humans, p-cresol is converted to p-cresol sulfate.
In rats, 4-methylphenol can be converted to p-cresol sulfate and p-methyl anisole.
For more complete data on the metabolism/metabolites of p-cresol (18 metabolites in total), please visit the HSDB record page.
Known human metabolites of 4-methylphenol include 4-methyl-2,5-cyclohexadien-1-one, (2S,3S,4S,5R)-3,4,5-trihydroxy-6-(4-methylphenoxy)oxacyclohexane-2-carboxylic acid, 4-methylhydroquinone, and 4-hydroxybenzyl alcohol.
4-Methylphenol is a known human metabolite of toluene.
Cresol compounds can be absorbed through inhalation, oral ingestion, and skin contact. Once in the body, they can be rapidly distributed to many organs and tissues. Cresol is oxidatively metabolized in the liver and rapidly excreted, primarily in the urine as sulfate or glucuronide conjugates. Oxidative activation of cresol involves tyrosinase and thyroid peroxidase, generating active quinone methylates. Experiments with recombinant P-450 enzymes have shown that the metabolism of cresol is mediated by multiple P-450 enzymes, including CYP2D6, 2C19, 1A2, 1A1, and 2E1. (L528, A197, L529, A198)

Toxicity Summary
Identification and Uses: p-Cresol is a crystalline solid below 95°F (35°C). It has been used in industries such as explosives, petroleum, photography, paints, and agriculture, in the manufacture of synthetic resins; in disinfectants and fumigants; and as an industrial solvent. p-Cresol is used in the formulation of antioxidants. p-Cresol has wide applications in the fragrance and dye industries. It is also found in synthetic food flavorings. In veterinary medicine, it is used as a topical antiseptic, antiparasitic agent, and disinfectant. Human Exposure and Toxicity: p-Cresol is the final product of aromatic amino acids, produced by intestinal bacteria from food proteins, and can be detected in blood, urine, and feces. p-Cresol may cause atherosclerosis and thrombosis in patients with uremia. Elevated serum p-cresol levels in patients with chronic kidney disease are associated with increased cardiovascular mortality. p-Cresol can reduce the spontaneous contraction rate of cardiomyocytes and cause irregular cardiomyocyte beating. In cases of acute p-cresol poisoning and prolonged exposure (e.g., in patients with severe uremia), p-cresol may inhibit thrombosis by suppressing platelet aggregation and lead to hemorrhagic disorders. P-cresol may play a role in immunodeficiency in uremia patients. Studies inducing unplanned DNA synthesis have shown that p-cresol responds positively to human lung fibroblasts in the presence of liver homogenate. Animal studies: P-cresol causes severe local irritation and corrosion upon skin and eye contact. In experiments, injection of 0.5–1.0% p-cresol emulsion (dissolved in physiological saline) into the anterior chamber of rabbits and monkeys induced glaucoma. Applying 0.5% p-cresol to the skin of black and spiky mice for 6 weeks resulted in permanent skin and hair depigmentation. All three p-cresol isomers, administered orally, showed higher toxicity in mice than in rats. o-cresol was the most toxic, followed by p-cresol, and then m-cresol. Their toxic effects are similar to, but less severe than, those of phenol exposure. Phenol, o-cresol, and p-cresol exhibited roughly the same toxicity in cats, while m-cresol showed slightly lower toxicity. A single intravenous injection of 180–280 mg/kg p-cresol into rabbits resulted in convulsions, coma, and death. In a 28-day study, male and female rats and mice were fed diets containing 300–30,000 ppm p-cresol. All rats survived to the end of the study; some mice died at dietary concentrations of 10,000 ppm and 30,000 ppm. Increased liver and kidney weight was observed in both animals at doses as low as 3,000 ppm. Bone marrow hyperplasia and atrophy of the uterus, ovaries, and mammary glands were observed in the 10,000 ppm and 30,000 ppm dietary concentration groups. In a 90-day study, rats were administered 50, 175, or 600 mg/kg body weight of p-cresol by gavage. The highest dose resulted in death and significantly reduced body weight and food consumption; central nervous system effects included somnolence, ataxia, coma, dyspnea, tremor, and seizures, which appeared within 15–30 minutes after administration. A detailed oral neurotoxicity study of moderate duration was conducted in rats using all three isomers of p-cresol. All three isomers were reported to produce a range of clinical signs suggestive of neurotoxicity (including decreased activity, tachypnea, dyspnea, excessive salivation, and tremor) at doses of 50 mg/kg/day or higher. Seizures occurred at doses of 450 mg/kg/day or higher. Fetal toxicity was observed at parenteral toxicity doses in two generations of rat reproduction studies. An in vitro study of cultured rat embryos showed that the effects of p-cresol on embryonic growth and structural abnormalities were dose-dependent. p-cresol prolonged the estrous cycle in rats at doses of 7500 and 30000 mg/kg; it had no effect on the estrous cycle in mice. Female mice were injected with a single dose of dimethylbenzanthracene, followed by twice-weekly injections of 25 μL of 20% p-cresol benzene solution for 12 weeks, starting one week later. P-cresol caused tumors (papilloma) in 7 out of 20 surviving mice. Dietary supplementation with p-cresol for 20 weeks increased the incidence of mild to moderate forestomach hyperplasia in hamsters. P-cresol showed no genotoxicity in vivo or in vitro. Ecotoxicity studies: 0.028 mM p-cresol in water significantly increased serum sorbitol dehydrogenase activity in rainbow trout after 96 hours of exposure. Pikeperch mortality was very high under 48-hour pulsed exposure to 8 mg/L p-cresol. Smallmouth bass showed a marked stress response; largemouth bass, while not showing a marked stress response, stopped feeding. The effects of p-cresol on benthic macroinvertebrates were studied at the EPA's outdoor experimental stream facility in Monticello, Minnesota. The main function of p-cresol is to affect the photosynthesis and respiration of aquatic plants. p-Cresol is an inhibitor of cholinesterase, or acetylcholinesterase (AChE). Cholinesterase inhibitors (or "anticholinesterases") inhibit the activity of acetylcholinesterase. Because acetylcholinesterase has important physiological functions, chemicals that interfere with its activity are potent neurotoxins; even low doses can cause excessive salivation and lacrimation, followed by muscle spasms and ultimately death. Neurotoxins and substances in many pesticides have been shown to exert their effects by binding to serine residues at the active site of acetylcholinesterase, thereby completely inhibiting the enzyme's activity. Acetylcholinesterase breaks down the neurotransmitter acetylcholine, which is released at the neuromuscular junction, causing muscle or organ relaxation. The mechanism of action of acetylcholinesterase inhibitors is to cause the accumulation and sustained action of acetylcholine, leading to continuous nerve impulse transmission and unstoppable muscle contraction. The most common acetylcholinesterase inhibitors are phosphorus-containing compounds; these compounds act by binding to the active site of the enzyme. The structural requirements are: one phosphorus atom connected to two lipophilic groups, one leaving group (e.g., a halide or thiocyanate), and one terminal oxygen atom.

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Toxicity Data
LC50 (Rat)> 710 mg/m³/1hr
LD50: 207 mg/kg (oral, rat) (T13)
LD50: 301 mg/kg (dermal, rabbit) (T13)
LD50: 25 mg/kg (intraperitoneal, mouse) (T13)

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Interactions
/Experimental Animals: Chronic Exposure or Carcinogenicity/Mice received a single transdermal application of 9,10-dimethyl-1,2-benzanthracene (DMBA, a carcinogen), followed by two applications of 20% o-cresol, p-cresol, or m-cresol benzene solution. This was repeated weekly for 12 weeks. This dose of cresol exposure has been shown to have acute toxicity, resulting in high non-tumor-related mortality. Therefore, all tumor results were based on the number of surviving mice (14–20 per group). The carcinogenic effect of cresol led to an increase in the average number of skin papillomas per mouse, and an increased proportion of exposed mice with at least one papilloma. o-cresol was the most potent isomer, while p-cresol was the least potent. No carcinogenesis was observed after cresol exposure, but the observed papillomas had the potential to develop into cancer. One issue with this study was the use of benzene (a known carcinogen) as a solvent for cresol. However, no papillomas were observed in the benzene control group in the cresol experiments, nor in the four parallel experiments (a small number of papillomas were observed in the fifth benzene control group). Therefore, the results of this study suggest that all three cresol isomers promote the development of DMBA-induced skin tumors, a conclusion that appears valid. p-cresol is a known uremic toxin and environmental toxin that may affect platelet function. This study found that p-cresol (1-5 μM) inhibited arachidonic acid (AA)-induced platelet aggregation, with inhibition rates of 47% and 82% at 2 μM and 5 μM concentrations, respectively. Under similar experimental conditions, p-cresol had almost no effect on U46619-induced platelet aggregation. Quantitative analysis of lactate dehydrogenase release revealed that p-cresol (<500 μM) had no significant cytotoxicity to platelets. The antiplatelet effect of p-cresol is related to its inhibition of thromboxane A₂ (TXA₂) and prostaglandin D₂ (PGD₂) production. P-cresol (2-100 μM) partially inhibited AA-induced platelet reactive oxygen species (ROS) production and phosphorylation of extracellular signal-regulated kinases (ERK1/2) and p38. p-Cresol further inhibited AA-induced rabbit platelet-rich plasma (PRP) aggregation (IC50 = 2 μM) and human PRP aggregation (IC50 = 13.6 μM). Intravenous injection of p-cresol (250-1000 nmol) effectively inhibited in vitro platelet aggregation in mice, while having little effect on red blood cell count, hemoglobin (HGB), hematocrit, mean corpuscular volume (MCV), mean corpuscular hemoglobin content (MCH), mean corpuscular hemoglobin concentration (MCHC), platelet count, and lymphocyte count. These results suggest that in cases of acute p-cresol poisoning and long-term exposure to p-cresol (e.g., in patients with severe uremia), p-cresol may inhibit thrombosis and lead to hemorrhagic diseases by inhibiting platelet aggregation, reactive oxygen species (ROS) generation, ERK/p38 activation, and TXA₂ formation. ...We examined the formation of DNA adducts in myeloperoxidase-containing HL-60 cells treated with the toluene metabolite p-cresol. Treatment of HL-60 cells with p-cresol and H₂O₂ yielded four DNA adducts: 1 (75.0%), 2 (9.1%), 3 (7.0%), and 4 (8.8%), with adduct levels ranging from 0.3 to 33.6 × 10⁻⁷. The level of DNA adducts formed by p-cresol depended on the concentrations of p-cresol and H₂O₂, as well as the treatment time. In vitro incubation of p-cresol with myeloperoxidase and H₂O₂ generated three DNA adducts: 1 (40.5%), 2 (28.4%), and 3 (29.7%), with a relative adduct content of 0.7 × 10⁻⁷. The quinone methyl derivative of p-cresol (PCQM) was prepared by oxidation with Ag(I)O. Calf thymus DNA reacted with PCQM to generate four adducts: 1 (18.5%), 2 (36.4%), 3 (29.0%), and 5 (16.0%), with a relative adduct content of 1.6 × 10⁻⁷. Retrieval chromatography analysis showed that DNA adducts 1–3 formed in HL-60 cells after treatment with p-cresol and activation by myeloperoxidase were similar to those generated by the reaction of DNA with PCQM. This observation indicates that p-cresol was activated to quinone methyl compounds in these activation systems. In summary, these results suggest that PCQM is the active intermediate leading to DNA adduct formation in HL-60 cells treated with p-cresol. Furthermore, the DNA adducts formed by PCQM may serve as biomarkers for assessing occupational toluene exposure.

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Non-human toxicity values
Rat dermal LD50: 750 mg/kg
Rat oral LD50: 207 mg/kg
Rat oral LD50: 1.8 g/kg
Mouse intravenous LD50: 1460 mg/kg
For more non-human toxicity values (complete data) for p-cresol (12 in total), please visit the HSDB record page.

[1]. Toxicol Sci. 2020 Feb 1;173(2):267-279.
[2]. Cells. 2022 Nov 26;11(23):3782.

p-Cresol is a colorless solid with a tarry odor. It sinks to the bottom of water and dissolves slowly. (USCG, 1999)
p-Cresol is a cresol compound formed by replacing the hydroxyl group at the 4-position of toluene. It is an aromatic amino acid metabolite produced by the intestinal flora of humans and animals. It is a uremic toxin and a metabolite of both humans and E. coli.
p-Cresol is a metabolite found or produced in E. coli (K12 strain, MG1655 strain).
p-Cresol has also been reported in Artemisia, Viburnum, and other organisms with relevant data.
p-Cresol (4-methylphenol) is a volatile, low-molecular-weight compound with a molecular weight of 108.1 Da, belonging to the phenolic class. p-Cresol is a partially lipophilic molecule that, under normal conditions, binds strongly (nearly 100%) to plasma proteins. p-Cresol is primarily metabolized through conjugation reactions, including sulfation and glucuronidation, but unconjugated p-cresol is at least partially excreted in urine. Therefore, it is not surprising that this compound, along with several other phenolic compounds, accumulates in the body during kidney failure. p-Cresol is an end product of protein breakdown; increased protein intake in healthy individuals leads to increased p-cresol production and urinary excretion. Uremic patients can reduce serum p-cresol concentrations through a low-protein diet. p-Cresol is a metabolite of the amino acid tyrosine, and to some extent, also a metabolite of phenylalanine. These metabolites are converted to 4-hydroxyphenylacetic acid by intestinal bacteria, which then decarboxylates to p-cresol (putrefaction). The main pathogens are aerobic bacteria (primarily Enterobacteriaceae), but anaerobic bacteria (primarily Clostridium perfringens) also play a role. In uremia, alterations in the gut microbiota lead to the overgrowth of specific p-cresol-producing bacteria. Antibiotic use kills p-cresol-producing bacteria, thus reducing urinary excretion. Environmental factors may also have an effect. Hepatochrome P450 metabolizes toluene into benzyl alcohol, as well as o-cresol and p-cresol. Toluene is not only widely used in industry but is also one of the most widely abused solvents by inhalation. Furthermore, p-cresol is a metabolite of mentholatum, which in turn is a metabolite of R-(+)-menthone. Mentholatum is found in extracts of peppermint (Mentha pulegium) and peppermint tea (Hedeoma pulegioides), both plants commonly known as peppermint oil and peppermint tea. These extracts are popular as unconventional herbal remedies and have been used as abortifacients, diaphoretics, emmenagogues, and hallucinogens. Peppermint oil is widely used in the fragrance industry for its pleasant minty aroma. The toxicity of peppermint oil and mentholatum is well-known. Another compound used in traditional medicine (especially in Japan) is a precursor to p-cresol—wood tar creosote oil. p-Cresol has been reported to affect a variety of biochemical, biological, and physiological functions: (i) it reduces oxygen uptake in rat cerebral cortex slices; (ii) it increases the concentration of free active drugs of warfarin and diazepam; (iii) it is associated with growth retardation in weaned piglets; (iv) it alters cell membrane permeability, at least in bacteria; (v) it induces leakage of lactate dehydrogenase (LDH) in rat liver slices; (vi) it induces auditory epilepsy; and (vii) it blocks cellular potassium channels. (A7723). p-Cresol is a uremic toxin; in hemodialysis patients, peritoneal dialysis at least partially removes p-Cresol and influences the progression of renal failure. (MID: 11169029). At concentrations encountered during uremia, p-Cresol inhibits phagocytic cell function and reduces the adhesion of leukocytes to cytokine-stimulated endothelial cells. (A3274). See also: Cresol (note moved to).

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Therapeutic Uses
Drugs (Veterinary): Topical antiseptic, antiparasitic, disinfectant; formerly used as an intestinal antiseptic.
Disinfectant

C7H8O

108.14

108.057

C, 77.75; H, 7.46; O, 14.79

106-44-5

27289-34-5;1121-70-6 (hydrochloride salt);72269-62-6 (aluminum salt)

2879

Crystalline solid [Note: A liquid above 95 degees F]

1.0±0.1 g/cm3

202.0±0.0 °C at 760 mmHg

32-34 °C(lit.)

81.0±8.2 °C

0.2±0.4 mmHg at 25°C

1.546

1.94

1

1

0

8

62.8

0

CC1=CC=C(C=C1)O

IWDCLRJOBJJRNH-UHFFFAOYSA-N

InChI=1S/C7H8O/c1-6-2-4-7(8)5-3-6/h2-5,8H,1H3

4-methylphenol

NSC-3696; NSC 3696; p-Cresol

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.)