Absorption, Distribution and Excretion
Groups of three male Sprague-Dawley rats were given a single oral dose of 4, 40, or 400 mg/kg of 2,3-(14)C-acrylic acid or 2, 20, or 200 mg/kg 2,3-(14)C-ethyl acrylate in 0.5% aqueous methylcellulose (25 uCi/kg) at a volume of 10 mL/kg ... Urine, feces, and expired carbon dioxide were collected at various intervals up to 72 hours after dosing, and the animals were then killed. Acrylic acid and ethyl acrylate were eliminated rapidly, primarily in expired carbon dioxide (44% to 65%). 35% to 60% of the acrylic acid and approximately 60% of the ethyl acrylate was eliminated within 8 hours. Urinary excretion of radioactive metabolites was greater with ethyl acrylate. Within 72 hours, 90% to 76% of the radioactivity was recovered from the animals dosed with 4 and 400 mg/kg acrylic acid; 19% to 25% was recovered in the tissues, with most being found in adipose tissue, (9% to 15%). With ethyl acrylate, 108% to 73% of the dose was recovered with 2 to 200 mg/kg; 13% to 10% was found in the tissues, with the most generally being found in muscle tissue (5.6% to 5%), and 28% to 8% was excreted in the urine.
Three fasted male Sprague-Dawley rats were given 400 mg/kg 1,2,3-(13)C3-acrylic acid coadministered with 2,3-(14)C-acrylic acid (40 to 46 uCi/kg) in distilled water by gavage ... Urine, feces, and expired air were collected for 72 hours, and the animals were then killed. Total recovery was 98%. The majority of the radioactivity, 78%, was recovered in expired carbon dioxide. Approximately 13% of the radioactivity was recovered in the tissues, with almost 5% of the dose found in the muscle, 3% found in the liver, 2% found in the skin, and 1% found in adipose tissue. The tissue-to-blood radioactivity concentration ratios were 11.1, 3.2, 2.6, 2.4, 2.1, and 2.0 for the liver, kidneys, adipose tissue, stomach, spleen, and large intestine, respectively. Approximately 6% of the dose was eliminated in the urine and 1% was eliminated in the feces. Nuclear magnetic resonance spectroscopy did not detect unchanged acrylic acid in the urine.
The disposition of (14)C-acrylic acid was determined in vitro using clipped dorsal skin from male rats ... One percent (v/v) (14)C-Acrylic Acid, 95 uL, was applied to the exposed epidermal surface (1.77 sq cm), and an evaporation trap was fitted over the skin. Over a 6-hour period, 23.9% +/- 5.4% of the dose was absorbed in the effluent or was found in the skin and at least 60% of the dose was evaporated. Total recovery of the applied dose was approximately 85%.
Acrylic acid is rapidly absorbed in rats and mice after oral or inhalation administration. A hybrid computational fluid dynamics and physiologically-based pharmacokinetics inhalation dosimetry model was constructed for interspecies (rat-human) extrapolation of acrylic acid tissue dose in the olfactory region of the nasal cavity. The model simulations indicate that under similar exposure conditions human olfactory epithelium is exposed with acrylic acid to 2-3 fold lower than rat olfactory epithelium. After dermal administration some acrylic acid is evaporated, the remainder undergoes rapid absorption in these animals. Dermal absorption is strongly dependent on the vehicle and the pH value of the solution.
For more Absorption, Distribution and Excretion (Complete) data for Acrylic acid (11 total), please visit the HSDB record page.
... Absorption or accumulation in eye tissues can presumably be excluded due to the high molecular weight of polyacrylic acid (4 mio D).
... The ADE studies following a single oral dose of a crosslinked, high-molecular-weight polyacrylate polymer (PA) indicate that the majority of dosed PA (91.9%) was excreted in the feces. As expected, a small percentage (approximately 3.5%) was absorbed, possibly metabolized, and excreted. ...

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Metabolism / Metabolites
Acrylic acid is rapidly metabolized by oxidative pathways to CO2. The main metabolic pathway of acrylic acid seems to be a secondary, non-vitamin-B12 dependent pathway of propionic acid metabolism consisting in reactions similar to fatty acid beta-oxidation. In urine poorly characterized substances of a higher polarity than those of acrylic acid are detected. Unmetabolized acrylic acid could not be detected in urine, however small amounts of 3-hydroxypropionic acid were found. Epoxide intermediates were not detected. In vitro (stomach tissue) and in vivo acrylic acid reacts with glutathione and non-protein sulfhydryls to a very low extent. High dosages of acrylic acid leading to tissue damage cause the formation of small amounts of mercapturic acid derivates.
After oral administration of 4, 40, or 400 mg/kg bw [2,3-(14)C]-acrylic acid in a 0.5% aqueous methylcellulose solution to rats, within 72 hr 44-65% of the radioactivity had been eliminated via expired air and 2.9-4.3% remained in the urine. The HPLC profile of metabolites observed in the urine of rats indicated two major metabolites. One of the major metabolites co-eluted was 3-hydroxypropionic acid. Radioactivity could not be detected at the retention times corresponding to that of 2,3-epoxypropionic acid or N-acetyl-S-(2-carboxy-2-hydroxyethyl)cysteine. One hour following an oral dose of acrylic acid (4, 40, 400, or 1,000 mg/kg) in rats a significant depletion of /Non-protein sulfhydryls/ (NPSH) in the glandular stomach was reported at doses above 4 mg/kg. In the forestomach NPSH depletion occurred at a dose of 1,000 mg/kg. No significant effect of acrylic acid on NPSH in the blood or liver was observed
... The metabolites of acrylic acid and propionic acid /were compared/ using (13)C-NMR analysis of the urine of rats after gavage of single doses (400 mg/kg bw). 3-Hydroxypropionic acid, N-acetyl-S-(2-carboxyethyl)cysteine and N-acetyl-S-(2-carboxyethyl)cysteine-S-oxide were identified as metabolites of acrylic acid. No unchanged acrylic acid was detected. In contrast, the spectra of urine from a propionic acid-treated rat revealed only a few minor (13)C-enriched signals that were assigned to methylmalonic acid. These metabolites (CO2 and methylmalonic acid) are consistent with the known major vitamin B12-dependent pathway of propionate metabolism in mammals. An alternative pathway involves beta-oxidation. Acrylyl-CoA forms 3-hydroxypropionic acid that can then be oxidized to malonic semialdehyde. Further catabolism yields acetyl-CoA and CO2. It is conceivable that excretion and detection of the mercapturates are a consequence of the high dose used in this experiment.
Following single doses (40 or 150 mg/kg) of [1-(14)C]-acrylic acid to rats urinary metabolites and tissues were analyzed by HPLC. A major polar metabolite which could not be identified accounted for approximately 2 to 3% of the dose. A metabolite that coeluted with 3-hydroxypropionic acid was also detected. Small amounts of several other metabolites were detected. Plasma and liver from orally dosed rats were also analyzed for acrylic acid and metabolites by HPLC. One hour after dosing, a metabolite in plasma that co-eluted with 3-hydroxypropionic acid accounted for about 0.5% of the dose after 40 mg/kg bw. This metabolite was also detected in plasma after application of the higher dose. Neither acrylic acid nor metabolites were detected in plasma or liver at times later than 1 hr. They were not detected in kidney at any time after administration ... In other experiments, livers from mice dosed by gavage following a similar dosing regime were analyzed for acrylic acid and metabolites by HPLC. Several metabolites of higher polarity than those of acrylic acid including 3-hydroxypropionic acid were detected 1 hr after administration, but not at times later than 1 hr. Acrylic acid was not detected in livers from mice at any time after cutaneous administration of 40 mg/kg bw. After cutaneous dosing in rats, a peak that coeluted with acrylic acid was detected in urine along with the major metabolite found after oral dosing. A trace amount of another metabolite was detected in urine from the 40 mg/kg bw cutaneous dose group but not after dosing 10 mg/kg bw.
For more Metabolism/Metabolites (Complete) data for Acrylic acid (13 total), please visit the HSDB record page.

Toxicity Summary
IDENTIFICATION AND USE: Acrylic acid is a volatile colorless liquid. It is used in the manufacture of plastics, molding powder for signs, construction units, decorative emblems and insignias, polymer solutions for coatings applications, emulsion polymers, paints formulations, leather finishing, and paper coatings; also used in medicine and dentistry for dental plates, artificial teeth, and orthopedic cement. Commercial glacial acrylic acid contains polymer formation inhibitor hydroquinone monomethyl ether (200 ppm). HUMAN STUDIES: Regardless of the route of exposure, acrylic acid is rapidly absorbed and metabolized. Owing to its rapid metabolism and elimination, the half-life of acrylic acid is short (minutes) and therefore it has no potential for bioaccumulation. The substance is corrosive to the eyes, skin and respiratory tract, and also upon ingestion. Inhalation of the substance may cause lung edema. The symptoms of lung edema often do not become manifest until a few hours have passed, and they are aggravated by physical effort. ANIMAL STUDIES: Although a wide range of LD50 values has been reported, most data indicate that acrylic acid is of low to moderate acute toxicity by the oral route and moderate acute toxicity by the inhalation or dermal route. Acrylic acid is corrosive or irritating to skin and eyes, and is a strong irritant to the respiratory tract. Skin sensitization have been reported. Available reproduction studies indicate that acrylic acid is not teratogenic and has no effect on reproduction. Both positive and negative results have been obtained in in vitro genotoxicity tests. No experimental data relevant to the carcinogenicity of acrylic acid were available. ECOTOXICITY STUDIES: The toxicity of acrylic acid to bacteria and soil microorganisms is low. Algae are the most sensitive group of aquatic organisms. Acrylic acid reduces or eliminates bacterial populations in penguins receiving dietary exposure.

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Toxicity Data
LC50 (rat) = 1200 ppm/4h

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Interactions
The purpose of this work was to investigate the relationship between the feed composition of 2-hydroxyethyl methacrylate (HEMA)/acrylic acid (AAc) and hydrogel material compatibility towards ocular anterior segment tissues, particularly the corneal endothelium. The monomer solutions of HEMA and AAc were mixed at varying volume ratios of 92:0, 87:5, 82:10, 77:15, and 72:20, and were subjected to UV irradiation. Then, the 7-mm-diameter membrane implants made from photopolymerized materials were placed into the ocular anterior chamber for 4 days and assessed by biomicroscopic examinations, corneal thickness measurements, and quantitative real-time reverse transcription polymerase chain reaction analyses. The poly(HEMA-co-AAc) implants prepared from the solution mixture containing 0-10 vol.% AAc displayed good biocompatibility. However, with increasing volume ratio of AAc and HEMA from 15:77 to 20:72, the enhanced inflammatory response, decreased endothelial cell density, and increased ocular score and corneal thickness were observed, probably due to the influence of surface charge of copolymer membranes. On the other hand, the ionic pump function of corneal endothelium exposed to photopolymerized membranes was examined by analyzing the Na(+),K(+)-ATPase alpha 1 subunit (ATP1A1) expression level. The presence of the implants having higher amount of AAc incorporated in the copolymers (i.e., 15.1 to 24.7umol) and zeta potential (i.e., -38.6 to -56.5mV) may lead to abnormal transmembrane transport. It is concluded that the chemical composition of HEMA/AAc has an important influence on the corneal tissue responses to polymeric biomaterials.
... Male Sprague-Dawley rats /were dosed/ orally in quadruplicate with 4, 40, 400, and 1000 mg/kg acrylic acid or 2, 20, 100, or 200 mg/kg ethyl acrylate in 0.5% methylcellulose at a volume of 5 mL/kg with and without pretreatment with the carboxylesterase inhibitor tri-o-cresyl phosphate [TOCP]. Control animals were given 2 mL/kg corn oil with and without pretreatment. The animals were killed 1 hour after dosing. A "pronounced increase" in glandular and nonglandular stomach weights, edema, and hemorrhage were observed with > 40 mg/kg acrylic acid. Acrylic acid, > 4 mg/kg, significantly depleted nonprotein sulfhydryl [NPSH] content in the glandular stomach, but no significant effect on NPSH in the blood or liver was observed. Pretreatment with TOCP did not have a significant effect on stomach weight or NPSH content. With ethyl acrylate, a significant increase in forestomach weight was observed with the 200-mg/kg dose; no significant change in glandular stomach weight was observed. Treatment with TOCP enhanced the increase in forestomach weight. A linear depletion of NPSH content of the forestomach and glandular stomach was observed 1 hour after dosing with 2 and 20 mg/kg; NPSH content did not change with doses of 100 or 200 mg/kg. No significant dose-dependent effect of ethyl acrylate on NPSH concentration in the blood and liver was seen. Pretreatment with TOCP did not affect the depletion of NPSH content in the glandular stomach or forestomach; however, 100 and 200 mg/kg ethyl acrylate did induce a significant depletion of hepatic NPSH concentration.

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Non-Human Toxicity Values
LD50 Rat oral 193 mg/kg
LD50 Rat oral 340 mg/kg
LD50 Rat oral 1500 mg/kg
LD50 Rat oral 2500 mg/kg
For more Non-Human Toxicity Values (Complete) data for Acrylic acid (27 total), please visit the HSDB record page.
LD50 Rabbit dermal >10.0g/kg /0.20% Carbomer-934/
LD50 Rat dermal > 3.0 g/kg /Carbomer-910/
LC50 Rat inhalation 1.71 mg/L air /4 hr
LD50 Rat oral 10,250 mg/kg /Carbomer 910/
For more Non-Human Toxicity Values (Complete) data for Carbomer (18 total), please visit the HSDB record page.

[1]. Enabling aqueous processing for LiNi0.80Co0.15Al0.05O2 (NCA)-based lithium-ion battery cathodes using polyacrylic acid. Electrochimica Acta. 2021 Jun 1;380: 138203.

Acrylic acid is a colorless liquid with a distinctive acrid odor. Flash point 130 °F. Boiling point 286 °F. Freezing point 53 °F. Corrosive to metals and tissue. Prolonged exposure to fire or heat can cause polymerization. If polymerization takes place in a closed container, violent rupture may occur. The inhibitor (usually hydroquinone) greatly reduces the tendency to polymerize.
Acrylic acid is a alpha,beta-unsaturated monocarboxylic acid that is ethene substituted by a carboxy group. It has a role as a metabolite. It is a conjugate acid of an acrylate.
A α,β-unsaturated monocarboxylic acid that is ethene substituted by a carboxy group.
Acrylic acid is used in the manufacture of plastics, paint formulations, and other products. Exposure occurs primarily in the workplace. It is a strong irritant to the skin, eyes, and mucous membranes in humans. No information is available on the reproductive, developmental, or carcinogenic effects of acrylic acid in humans. Animal cancer studies have reported both positive and negative results. EPA has not classified acrylic acid for carcinogenicity.
Acrylic acid has been reported in Cocos nucifera, Gynerium sagittatum, and other organisms with data available.
See also: Calcium Polycarbophil (monomer of); Polycarbophil (monomer of); Polyquaternium-53 (monomer of) ... View More ...

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Therapeutic Uses
Substitute of tear fluid for management of dry eye conditions including keratoconjunctivitis sicca, and for unstable tear film. /ViscoTears Liquid Gel with 2.0 mg/g Carbomer/
To compare the efficacy and safety of two carbomer 940 eye gels in the treatment of dry eyes: Lacrinorm (also called GelTears), a recently introduced eye gel, and Viscotears (also called Vidisic or Lacrigel), used as a reference gel. The main difference between the two gels is in the preservative, respectively benzalkonium chloride and cetrimide. A double-masked, randomized, parallel-group study was conducted in 16 centers in four European countries. A total of 179 patients suffering from aqueous-deficient dry eye were enrolled, of whom 92 were randomized to treatment with Lacrinorm and 87 to the reference gel. Gel was instilled four times a day for a period of 30 days. After 30 days of treatment, subjective symptoms (the combined scores of foreign body sensation, ocular dryness, burning or pain, and photophobia) had improved by 50% in the Lacrinorm group and by 45% in the reference gel group, and objective test results (break-up time, fluorescein test, Schirmer test, Lissamine Green test) by 35-36% in the Lacrinorm group and 25-45% in the reference group. The improvements were significant in both treatment groups (p < 0.001), with no significant differences between the treatment groups. Subjective local tolerability upon instillation on day 30 was rated 'good' or 'very good' by 91% of patients in both treatment groups. Adverse events were reported for 21 patients in the Lacrinorm group and 17 in the reference group, the most frequent being discomfort, blurred vision, hyperemia, burning and itching. The frequency and descriptions of adverse events did not differ significantly between the two treatment groups. No serious adverse events were reported. Over the period of study, Lacrinorm eye gel was as effective and safe as Viscotears/Lacrigel in the treatment of dry eye.
To compare the safety and efficacy of polyacrylic acid 0.2% (PAA) gel and polyvinylalcohol 1.4% (PVA) in the treatment of patients with dry eyes. Eighty-nine patients with dry eyes were randomly allocated to treatment with either PAA (48) or PVA (41) in a prospective, investigator-masked study in two centers. The parameters assessed were daily frequency of instillation of the study medications, ocular signs and symptoms, tear film break up time, Schirmer's test values, local tolerance and global assessment of the improvement following treatment. The two groups were similar in patient demographics and study parameters at baseline. The total score of symptoms (gritty or foreign body sensation, burning sensation, dry eye sensation, photophobia, others) and signs (conjunctival hyperemia, ciliary injection, corneal and conjunctival epithelial staining) was reduced significantly more by treatment with PAA than with PVA at both three and six weeks (p < 0.0001). The daily frequency of instillation of PAA was significantly less than that /of/ PVA on 38 of the 41 (93%) study days. Both PAA and PVA were safe and equally well-tolerated except for blurred vision, usually mild and transient, on PAA. On global assessment of the improvement in their dry eye condition, significantly more PAA patients felt better on treatment at six (p = 0.02) weeks compared with those on PVA. Polyacrylic acid gel was as safe as and more effective than polyvinylalcohol in the treatment of patients with dry eyes.
Carbomer gel is a water-soluble polymeric resin that has been reported to maintain the tear film in contact with the eye for an extended period. The efficacy and safety of this new artificial tear were assessed. A multicenter, single-masked, randomized, placebo-controlled study was carried out on 123 patients with moderate-to-severe dry eyes. The placebo was a mannitol solution with benzalkonium chloride 0.008% as preservative. Patients were observed over an 8-week period, and subjective and objective changes analyzed, compared to a baseline of no therapy, after 1 to 7 days washout period from previous medication. All primary subjective symptoms decreased significantly in the carbomer gel-treated group compared to the placebo group (ie, dryness, discomfort, and foreign body sensation). The carbomer gel also significantly improved the rose bengal staining score relative to placebo. When data for the primary subjective efficacy variables were stratified for disease severity, there was a statistically significant improvement from baseline by day 10 for severely affected patients and from day 42 for patients with moderate disease. Secondary subjective symptoms that improved significantly in the tear gel group compared to placebo were photophobia, erythema, tear breakup time, blurry-filmy, dry-sandy sensation, and physician impression. However, no significant improvements in the secondary subjective symptoms of tearing, itching, scaling, conjuctival discharge, palpebral conjunctival redness, bulbar conjuctival redness, conjunctival luster, relief of discomfort, ease of use, and overall acceptability were found in either group over the baseline score. In addition, neither carbomer gel nor placebo improved the baseline fluorescein staining score or the Schirmer test score. Two patients suffered local allergic reactions to the carbomer gel or its preservative, which settled on withdrawal of the medication. Carbomer gel was more efficacious than was placebo in improving a number of subjective and objective symptoms of moderate-to-severe dry eye syndrome. The results of this study indicate that carbomer gel was as safe as the placebo.
For more Therapeutic Uses (Complete) data for Carbomer (6 total), please visit the HSDB record page.

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Drug Warnings
In case of any additional local ocular treatment (eg glaucoma therapy) there should be an application interval of at least 5 minutes between the two medications, Viscotears Liquid Gel always should be the last medication instilled.
Contact lenses should not be worn during instillation of the drug. After instillation there should be an interval of at least 30 minutes before reinsertion.
Viscotears Liquid Gel may temporarily influence the visual acuity. Patients with blurred vision driving a vehicle or operating machines should be alerted to the possibility of impaired reactions.
Ocular hyperemia, eye swelling, eyelid edema, eye pruritis and eye pain have been reported during post-marketing experience.
The following adverse events have been occasionally reported: mild, transient eye irritation, sticky eyelid, and blurred vision after instillation of the gel.

(C3H4O2)X

~2000 (Average)

72.021

9003-01-4

25568-87-0;25584-52-5;9003-01-4;1204391-75-2;10192-85-5 (potassium salt);10604-69-0 (ammonium salt);14643-87-9 (zinc salt);15743-20-1 (aluminum salt);51366-35-9 (calcium[2:1] salt.dihydrate);55488-18-1 (iron(3+) salt);5651-26-3 (silver salt);5698-98-6 (magnesium salt);58197-53-8 (cobalt(2+) salt);6292-01-9 (calcium[2:1] salt);7446-81-3 (hydrochloride salt);9003-01-4 (Parent)

6581

Acrid liquid
Liquid
Colorless liquid
Colorless liquid or solid (below 55 degrees F)

1.09 (30% aq.)

116ºC

106ºC

61.6ºC

n20/D 1.442

0.257

1

2

1

5

55.9

0

O([H])C(C([H])=C([H])[H])=O

NIXOWILDQLNWCW-UHFFFAOYSA-N

InChI=1S/C3H4O2/c1-2-3(4)5/h2H,1H2,(H,4,5)

prop-2-enoic acid

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)

DMSO : ~12.5 mg/mL

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.)