Absorption, Distribution and Excretion
Three male Sprague-Dawley rats were randomly divided into four groups and administered 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 of ethyl 2,3-(14)C-acrylate (dissolved in 0.5% methylcellulose aqueous solution (25 μCi/kg)), with an oral volume of 10 mL/kg. Urine, feces, and exhaled carbon dioxide were collected at different time intervals within 72 hours after administration, and the animals were subsequently sacrificed. Acrylic acid and ethyl acrylate were rapidly excreted, primarily via exhaled carbon dioxide (44% to 65%). 35% to 60% of acrylic acid and approximately 60% of ethyl acrylate were excreted within 8 hours. The ethyl acrylate group had higher urinary excretion of radioactive metabolites. Within 72 hours, 90% to 76% of the radioactive material was recovered in animals given 4 and 400 mg/kg acrylic acid, respectively; 19% to 25% of the radioactive material was recovered in tissues, with the majority found in adipose tissue (9% to 15%). In animals given 2 to 200 mg/kg ethyl acrylate, the recovery rate was 108% to 73%. 13% to 10% of the radioactive material was detected in tissues, with the highest concentration in muscle tissue (5.6% to 5%), and 28% to 8% was excreted in urine. Three fasted male Sprague-Dawley rats were administered 400 mg/kg of 1,2,3-(13)C3-acrylic acid and 2,3-(14)C-acrylic acid (40 to 46 μCi/kg), dissolved in distilled water… Urine, feces, and exhaled gases were collected, and the animals were sacrificed 72 hours later. The overall recovery rate was 98%. Most of the radioactive material (78%) was found in exhaled carbon dioxide. Approximately 13% of the radioactive material was recovered into tissues, with nearly 5% in muscle, 3% in liver, 2% in skin, and 1% in adipose tissue. The tissue-to-blood radioactivity ratios for liver, kidney, adipose tissue, stomach, spleen, and large intestine were 11.1, 3.2, 2.6, 2.4, 2.1, and 2.0, respectively. Approximately 6% of the dose was excreted in urine, and 1% in feces. Unmetabolized acrylic acid was not detected in urine by nuclear magnetic resonance spectroscopy. The distribution of 14C-acrylic acid was determined in vitro using dorsal skin tissue from male rats… 95 μL of 1% (v/v) 14C-acrylic acid was applied to an exposed epidermal surface (1.77 cm²), and an evaporation collector was attached to the skin. Within 6 hours, 23.9% ± 5.4% of the dose was absorbed into the effluent or remained in the skin, and at least 60% evaporated. The overall recovery was approximately 85%.
Acrylic acid is rapidly absorbed after oral or inhalation administration in rats and mice. This study constructed a hybrid computational fluid dynamics and physiological pharmacokinetic inhalation dosing model to extrapolate the tissue dose of acrylic acid in the nasal olfactory region across species (rat-human). Model simulation results indicate that, under similar exposure conditions, the dose of acrylic acid exposed to the human olfactory epithelium is 2–3 times lower than that of the rat olfactory epithelium. After transdermal administration, some acrylic acid evaporates, while the remainder is rapidly absorbed by these animals. Skin absorption is strongly dependent on the pH of the carrier and solution.
For more complete data on the absorption, distribution, and excretion of acrylic acids (11 in total), please visit the HSDB record page.
…Due to the high molecular weight of polyacrylic acid (4 million Daltons), it can be inferred that it will not be absorbed or accumulate in ocular tissues.
...An ADE study following a single oral administration of cross-linked high molecular weight polyacrylate (PA) polymer showed that the majority of the administered PA (91.9%) was excreted in feces. As expected, a small portion (approximately 3.5%) was absorbed, likely metabolized, and then excreted. ...

---

Metabolism/Metabolites
Acrylic acid is rapidly metabolized to CO2 via an oxidative pathway. The primary metabolic pathway of acrylic acid appears to be a secondary pathway of propionic acid metabolism, independent of vitamin B12, and its reaction is similar to fatty acid β-oxidation. Some substances with higher polarity than acrylic acid but of unknown nature were detected in urine. Unmetabolized acrylic acid was not detected in urine, but trace amounts of 3-hydroxypropionic acid were detected. Epoxide intermediates were not detected. In vitro (gastric tissue) and in vivo experiments showed that acrylic acid reacts very little with glutathione and non-protein thiol groups. High doses of acrylic acid can cause tissue damage and produce small amounts of thiouric acid derivatives.
After rats were orally administered 4, 40, or 400 mg/kg body weight of [2,3-(14)C]-acrylic acid (dissolved in 0.5% methylcellulose aqueous solution), 44-65% of the radioactive material was exhaled within 72 hours, with 2.9-4.3% remaining in the urine. High-performance liquid chromatography analysis of the metabolites in rat urine revealed the presence of two major metabolites. One of the major metabolites co-eluted with 3-hydroxypropionic acid. No radioactivity was detected at the positions corresponding to the retention times of 2,3-epoxypropionic acid or N-acetyl-S-(2-carboxy-2-hydroxyethyl)cysteine. One hour after oral administration of acrylic acid (4, 40, 400, or 1000 mg/kg), the content of non-protein thiol (NPSH) in the proventriculus was significantly reduced, especially at doses above 4 mg/kg. The reduction in NPSH content in the forestomach occurred at a dose of 1000 mg/kg. No significant effect of acrylic acid on NPSH in blood or liver was observed. ...Using 13C-NMR analysis, the urine of rats administered a single dose (400 mg/kg body weight) of acrylic acid and propionic acid by gavage was analyzed to compare their metabolites. The results showed that 3-hydroxypropionic acid, N-acetyl-S-(2-carboxyethyl)cysteine, and N-acetyl-S-(2-carboxyethyl)cysteine-S-oxide were metabolites of acrylic acid. Unmetabolized acrylic acid was not detected. In contrast, the urine spectra of propionic acid-treated rats showed only a small amount of weak 13C enrichment signals, which were attributed to methylmalonic acid. These metabolites (CO2 and methylmalonic acid) are consistent with the known major vitamin B12-dependent propionic acid metabolic pathway in mammals. Another pathway involves β-oxidation. Acrylyl-CoA generates 3-hydroxypropionic acid, which can be oxidized to malonyl hemialdehyde. Further catabolism produces acetyl-CoA and CO2. It can be inferred that the excretion and detection of thiourate are due to the high dose used in this experiment. Following a single injection of [1-14C]-acrylic acid (40 or 150 mg/kg) into rats, urinary metabolites and tissue samples were analyzed by high-performance liquid chromatography (HPLC). An unidentifiable major polar metabolite comprised approximately 2% to 3% of the dose. A metabolite co-eluted with 3-hydroxypropionic acid was detected. Several other metabolites were also detected in small amounts. The levels of acrylic acid and its metabolites in the plasma and liver of orally administered rats were analyzed by HPLC. One hour after administration, the metabolite co-eluted with 3-hydroxypropionic acid in plasma comprised approximately 0.5% of the administered dose at a dose of 40 mg/kg body weight. This metabolite was also detected in plasma after higher doses. One hour after administration, acrylic acid and its metabolites were not detected in plasma or liver. They were not detected in the kidneys at any time point after administration… In other experiments, acrylic acid and its metabolites were also analyzed by high-performance liquid chromatography (HPLC) in the livers of mice administered via gavage using a similar dosing regimen. Several metabolites with higher polarity than acrylic acid, including 3-hydroxypropionic acid, were detected 1 hour after administration, but were not detected 1 hour after administration. Acrylic acid was not detected in the livers of mice after transdermal administration of 40 mg/kg body weight. In rats, a peak co-eluted with acrylic acid was detected in the urine after transdermal administration, as well as the major metabolite found after oral administration. Trace amounts of other metabolites were detected in the urine of the 40 mg/kg body weight transdermal administration group, but were not detected in the 10 mg/kg body weight administration group.
For more complete metabolite/metabolite data on acrylic acid (13 metabolites in total), please visit the HSDB record page.

Toxicity Summary
Identification and Uses: Acrylic acid is a volatile, colorless liquid. It is used in the manufacture of plastics, signage molding powders, building components, decorative badges and signs, polymer solutions for coatings, emulsion polymers, paint formulations, leather finishing agents, and paper coatings; it is also used in medicine and dentistry, such as dentures, dentures, and orthodontic cement. Commercially available icy acrylic acid contains the polymer formation inhibitor hydroquinone monomethyl ether (200 ppm). Human Studies: Acrylic acid is rapidly absorbed and metabolized regardless of the route of exposure. Due to its rapid metabolism and elimination, acrylic acid has a short half-life (minutes), thus there is no possibility of bioaccumulation. This substance is corrosive to the eyes, skin, and respiratory tract, and is also corrosive after ingestion. Inhalation of this substance may cause pulmonary edema. Symptoms of pulmonary edema usually appear several hours later and are exacerbated by physical activity. Animal Studies: Although the reported LD50 values range widely, most data indicate that acrylic acid has low to moderate acute toxicity via oral route and moderate acute toxicity via inhalation or skin route. Acrylic acid is corrosive or irritating to the skin and eyes, and strongly irritating to the respiratory tract. Skin sensitization has been reported. Existing reproductive studies indicate that acrylic acid is not teratogenic and has no effect on reproduction. In vitro genotoxicity tests have yielded both positive and negative results. Currently, there is no experimental data related to the carcinogenicity of acrylic acid. Ecotoxicity studies: Acrylic acid has low toxicity to bacteria and soil microorganisms. Algae are the most sensitive group among aquatic organisms. Acrylic acid can reduce or eliminate the number of bacteria in the bodies of penguins after ingestion.

---

Toxicity Data
LC50 (Rat) = 1200 ppm/4h
Interactions
This study aims to investigate the relationship between the 2-hydroxyethyl methacrylate (HEMA)/acrylic acid (AAc) dietary composition and the compatibility of the hydrogel material with anterior segment ocular tissues (particularly the corneal endothelium). Monomer solutions of HEMA and AAc were mixed at different volume ratios of 92:0, 87:5, 82:10, 77:15, and 72:20 and irradiated with ultraviolet light. Implants with a diameter of 7 mm made from the photopolymer material were then placed in the anterior chamber of the eye for 4 days and evaluated by biomicroscopy, corneal thickness measurement, and quantitative real-time reverse transcription polymerase chain reaction analysis. The poly(HEMA-co-AAc) implants prepared from mixed solutions containing 0–10 vol.% AAc exhibited good biocompatibility. However, as the volume ratio of AAc to HEMA increased from 15:77 to 20:72, enhanced inflammation, decreased endothelial cell density, increased ocular score, and increased corneal thickness were observed, possibly due to the influence of the surface charge of the copolymer membrane. On the other hand, the ion pump function of the corneal endothelium exposed to the photopolymer membrane was investigated by analyzing the expression level of the Na(+),K(+)-ATPase α1 subunit (ATP1A1). Implants with high AAc content (15.1 to 24.7 μmol) and high zeta potential (-38.6 to -56.5 mV) in the copolymer may lead to abnormal transmembrane transport. The conclusion is that the chemical composition of HEMA/AAc has a significant impact on the response of corneal tissue to polymeric biomaterials. Male Sprague-Dawley rats were administered four-fold oral doses of acrylic acid (4, 40, 400, and 1000 mg/kg) or ethyl acrylate (2, 20, 100, or 200 mg/kg, dissolved in 0.5% methylcellulose at a volume of 5 mL/kg), with some groups pre-administered the carboxylesterase inhibitor tricresyl phosphate (TOCP). Control animals were given 2 mL/kg of corn oil, with some groups pre-administered TOCP. Animals were sacrificed one hour after administration. When the acrylic acid dose exceeded 40 mg/kg, significant increases in glandular and non-glandular gastric weight, edema, and hemorrhage were observed. Acrylic acid (dose > 4 mg/kg) significantly reduced the content of non-protein thiol (NPSH) in the proventriculus, but no significant effect on NPSH content in blood or liver was observed. TOCP pretreatment had no significant effect on gastric weight or NPSH content. Ethyl acrylate at a dose of 200 mg/kg significantly increased forestomach weight; proventriculus weight did not change significantly. TOCP treatment enhanced the increase in forestomach weight. One hour after administration of 2 mg/kg and 20 mg/kg, a linear decrease in NPSH content was observed in both the forestomach and proventriculus; no change was observed at doses of 100 mg/kg and 200 mg/kg. No significant dose-dependent effect of ethyl acrylate on NPSH concentrations in blood or liver was observed. TOCP pretreatment did not affect the decrease in NPSH content in the proventriculus or forestomach. However, ethyl acrylate at doses of 100 and 200 mg/kg did result in a significant decrease in liver NPSH concentration.

---

Non-human toxicity values
Oral LD50 in rats: 193 mg/kg
Oral LD50 in rats: 340 mg/kg
Oral LD50 in rats: 1500 mg/kg
Oral LD50 in rats: 2500 mg/kg
For more complete non-human toxicity data for acrylic acid (27 items in total), please visit the HSDB record page.
Rabbit skin LD50: >10.0 g/kg / 0.20% Carbomer-934 /
Rabbit skin LD50: >3.0 g/kg / Carbomer-910 /
Rabbit inhalation LC50: 1.71 mg/L air / 4 hours
Oral LD50 in rats: 10,250 mg/kg / Carbomer-910 /
For more complete non-human toxicity data for carbomers (18 items in 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 pungent odor. Flash point: 130°F (54°C). Boiling point: 286°F (140°C). Freezing point: 53°F (12°C). It is corrosive to metals and tissues. Prolonged exposure to fire or high temperatures will cause polymerization. If polymerization occurs in a closed container, violent breakage may occur. Inhibitors (usually hydroquinone) can significantly reduce the tendency to polymerize.
Acrylic acid is an α,β-unsaturated monocarboxylic acid, formed by replacing ethylene with a carboxyl group. It is a metabolite and the conjugate acid of acrylates.
Acrylic acid is used in the manufacture of plastics, paint formulations, and other products. Exposure primarily occurs in the workplace. It is a strong irritant to human skin, eyes, and mucous membranes. Currently, there is no information regarding the effects of acrylic acid on human reproduction, development, or carcinogenicity. Animal carcinogenicity studies have yielded both positive and negative results. The U.S. Environmental Protection Agency (EPA) has not classified acrylic acid as a carcinogen.
According to reports, acrylic acid is found in coconut (Cocos nucifera), arrow-leaf tree (Gynerium sagittatum), and several other organisms with relevant data.
See also: Polycarbofi calcium (monomer); Polycarbofi (monomer); Polyquaternium-53 (monomer)...See more...

---

Therapeutic Uses
Used as a tear film substitute for the treatment of dry eye, including dry keratoconjunctivitis and conditions of tear film instability. /ViscoTears liquid gel containing 2.0 mg/g carbomer/
This study aimed to compare the efficacy and safety of two carbomer 940 ophthalmic gels for the treatment of dry eye: one is the newly marketed ophthalmic gel Lacrinorm (also known as GelTears), and the other is Viscotears (also known as Vidisic or Lacrigel) as a control gel. The main difference between the two gels lies in the preservatives, benzalkonium chloride and cetyltrimethylammonium bromide, respectively. This was a double-blind, randomized, parallel-group study conducted at 16 centers in four European countries. A total of 179 patients with aqueous-deficient dry eye were included, with 92 randomly assigned to the Lacrinorm group and 87 to the control gel group. The gel was administered four times daily for 30 days. After 30 days of treatment, subjective symptoms (combined scores of foreign body sensation, dry eye, burning or pain, and photophobia) improved by 50% in the Lacrinorm group and by 45% in the control gel group. Objective test results (tear film breakup time, fluorescein test, Schirmer test, and erythromycin green test) improved by 35-36% in the Lacrinorm group and by 25-45% in the control gel group. Both improvements were statistically significant (p < 0.001), and there was no statistically significant difference between the groups. On day 30, 91% of patients in both groups rated local tolerability as "good" or "very good." Adverse events were reported in 21 patients in the Lacrinorm group and 17 in the control gel group. The most common adverse events included discomfort, blurred vision, congestion, burning, and itching. There were no significant differences in the frequency and description of adverse events between the two treatment groups. No serious adverse events were reported. During the study period, Lacrinorm ocular gel was comparable to Viscotears/Lacrigel in efficacy and safety for the treatment of dry eye. This study aimed to compare the safety and efficacy of 0.2% polyacrylic acid (PAA) gel and 1.4% polyvinyl alcohol (PVA) gel in the treatment of patients with dry eye. In a prospective, investigator-blinded study, 89 patients with dry eye were randomly assigned to either the PAA group (48 patients) or the PVA group (41 patients) at two centers. Parameters assessed included daily drop frequency of the study drug, ocular signs and symptoms, tear film breakup time, Schirmer test value, local tolerability, and assessment of overall improvement after treatment. The two groups were similar in patient demographics and study parameters at baseline. At 3 and 6 weeks of treatment, the total symptom scores (foreign body sensation, burning sensation, dry eye sensation, photophobia, etc.) and total sign scores (conjunctival hyperemia, ciliary hyperemia, corneal and conjunctival epithelial staining) in the PAA treatment group were significantly lower than those in the PVA treatment group (p < 0.0001). During the 41 study days, the daily drop frequency of PAA was significantly lower than that of PVA for 38 days (93%). Except for mild and transient blurred vision that may occur in the PAA group, both PAA and PVA were safe and well-tolerated. In the overall assessment of improvement in dry eye symptoms, the proportion of patients experiencing improvement at 6 weeks of treatment was significantly higher in the PAA group compared to the PVA group (p = 0.02). In treating dry eye patients, polyacrylic acid gel is as safe and effective as polyvinyl alcohol, and even more effective. Carbomer gel is a water-soluble polymer resin that has been reported to maintain longer contact between the tear film and the eyeball. This study evaluated the efficacy and safety of this novel artificial tear. A multicenter, single-blind, randomized, placebo-controlled study enrolled 123 patients with moderate to severe dry eye. The placebo was a mannitol solution containing 0.008% benzalkonium chloride as a preservative. Patients were observed for 8 weeks, and subjective and objective changes were analyzed 1 to 7 days after discontinuation of the previous medication and compared with a treatment-free baseline. Compared with the placebo group, the carbomer gel treatment group showed significant reductions in all major subjective symptoms (i.e., dryness, discomfort, and foreign body sensation). The carbomer gel treatment group also showed significantly better rose-red staining scores than the placebo group. When data on the major subjective efficacy variables were stratified according to disease severity, patients with severe symptoms showed statistically significant improvement from baseline on day 10, and patients with moderate symptoms showed statistically significant improvement from baseline on day 42. Secondary subjective symptoms that showed significant improvement compared with the placebo group in the tear gel group included photophobia, erythema, tear film breakup time, blurred vision/film sensation, dryness/gritty sensation, and physician impression. However, no significant improvement from baseline scores was observed in either group of patients in secondary subjective symptoms such as tearing, itching, desquamation, conjunctival discharge, palpebral conjunctival hyperemia, bulbar conjunctival hyperemia, conjunctival gloss, discomfort relief, ease of use, and overall acceptability. Furthermore, neither carbomer gel nor placebo improved baseline fluorescein staining scores or Schirmer test scores. Two patients experienced local allergic reactions to carbomer gel or its preservatives; symptoms resolved upon discontinuation. Carbomer gel was more effective than placebo in improving a variety of subjective and objective symptoms of moderate to severe dry eye. These results indicate that carbomer gel is as safe as placebo.
For more complete data on the therapeutic uses of carbomer (6 types), please visit the HSDB record page.
Drug Warnings
If any other topical ocular treatment (e.g., glaucoma treatment) is required, at least 5 minutes should be allowed between any two medications. Viscotears liquid gel should always be used as the last medication.
Do not wear contact lenses while using this medication. After applying the drops, wait at least 30 minutes before wearing them again. Viscotears liquid gel may temporarily impair vision. Patients with blurred vision should be aware that their reaction time may be impaired when driving or operating machinery. Post-marketing surveillance data has reported cases of eye congestion, eye swelling, eyelid edema, eye itching, and eye pain. Occasional reported adverse events include mild, transient eye irritation, eyelid adhesion, and blurred vision after applying 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.

---

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).

View More

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)

---

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).

View More

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

---

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.

---

 (Please use freshly prepared in vivo formulations for optimal results.)