- Calcineurin (inhibitor, no IC₅₀ provided)[2]
- Glycogen synthase kinase-3β (GSK-3β) (inhibitor, no IC₅₀ provided)[2]
- Prostaglandin EP3 receptor (agonist, EC₅₀ = 1.2 μM for cAMP inhibition)[4]

- Calcineurin inhibition: Ricinoleic acid (10-100 μM) dose-dependently reduced calcineurin phosphatase activity in rat brain homogenates, measured by dephosphorylation of a synthetic peptide substrate. This effect was reversed by the calcineurin activator Ca²⁺/calmodulin[2]
- GSK-3β inhibition: In HEK293 cell lysates, ricinoleic acid (50-200 μM) suppressed GSK-3β kinase activity toward glycogen synthase, with maximal inhibition at 200 μM. The effect was partially blocked by lithium chloride, a known GSK-3β inhibitor[2]
- EP3 receptor activation: In CHO cells stably expressing human EP3 receptors, ricinoleic acid (0.1-10 μM) inhibited forskolin-induced cAMP production with an EC₅₀ of 1.2 μM. This effect was abolished by the EP3 antagonist L-798,106[4]
- Inflammatory cytokine modulation: In LPS-stimulated RAW 264.7 macrophages, ricinoleic acid (10-50 μM) reduced TNF-α and IL-6 secretion by 30-50% without affecting cell viability. This was associated with downregulation of NF-κB p65 nuclear translocation[5]

- Laxative effect: Oral administration of ricinoleic acid (100 mg/kg) to mice induced significant diarrhea within 2 hours, characterized by increased intestinal water content and accelerated gastrointestinal transit. The effect was abolished in EP3 knockout mice, confirming involvement of EP3 receptors[4]
- Uterine contraction: Intracervical ricinoleic acid (50 μL of 10% solution) in rats increased uterine contractility, as measured by electromyography. This effect was blocked by the EP3 antagonist and absent in EP3 knockout animals[4]
- Anxiolytic-like activity: In a mouse elevated plus-maze test, oral ricinoleic acid (50 mg/kg) increased time spent in open arms by 40% compared to vehicle, indicating reduced anxiety-like behavior. The effect was comparable to diazepam (1 mg/kg)[3]

- Calcineurin phosphatase assay: Rat brain homogenates were incubated with ricinoleic acid (10-100 μM) for 30 minutes, followed by addition of a phosphorylated peptide substrate. Phosphatase activity was measured by colorimetric detection of released phosphate. Activity was normalized to vehicle control[2]
- GSK-3β kinase assay: HEK293 cell lysates expressing GSK-3β were treated with ricinoleic acid (50-200 μM) and incubated with glycogen synthase and ATP. Phosphorylation of glycogen synthase was detected by Western blot using a phospho-specific antibody[2]

- cAMP inhibition assay: CHO-EP3 cells were pre-treated with ricinoleic acid (0.1-10 μM) for 15 minutes, then stimulated with forskolin (10 μM). Intracellular cAMP levels were quantified by ELISA. Data were normalized to vehicle control and expressed as percentage inhibition[4]
- Cytokine secretion assay: RAW 264.7 macrophages were co-treated with ricinoleic acid (10-50 μM) and LPS (1 μg/mL) for 24 hours. TNF-α and IL-6 levels in supernatants were measured by ELISA. Cell viability was assessed by MTT assay[5]

- Laxative model: Male ICR mice (20-25 g) received oral ricinoleic acid (100 mg/kg) dissolved in corn oil. Fecal output and water content were measured over 6 hours. For EP3 knockout studies, mice were administered the same dose and monitored similarly[4]
- Uterine contraction model: Female Sprague-Dawley rats (200-250 g) were anesthetized, and ricinoleic acid (10% solution in saline) was applied intracervically. Uterine electromyography was recorded for 30 minutes. Antagonist studies used L-798,106 (10 mg/kg, i.p.) administered 30 minutes prior[4]

Absorption, Distribution and Excretion
Male rats (weighing at least 400 g) were infused with ricinoleic acid or methyl ricinoleate via gastric tube instillation, followed by thoracic duct cannulation. Lymph was collected for 48 hours, and lipids were extracted and separated into different lipid classes. Results showed that ricinoleic acid was present in triglyceride, diglyceride, monoglyceride, and free fatty acid fractions. The absorption peak of ricinoleic acid occurred within 30 minutes after administration. Ricinoleic acid was not detected in the phospholipid or cholesterol ester fractions of the lymph lipids. Skin permeability of ricinoleic acid in vivo was investigated using 20- to 30-day-old rats. To enhance the fluorescence intensity of ricinoleic acid, one part methyl anthranilate or methylcholanthrene was added to 99 parts ricinoleic acid. The test substance was gently applied to shaved skin. Biopsies were performed at different time intervals after application. Samples were observed using a Spencer microscope equipped with a quartz condenser. Ricinoleic acid was primarily retained in the outer epidermis. In biopsies performed 2 hours after application, there was little evidence of penetration into deeper tissue layers. The transdermal uptake of radiolabeled (3H) ricinoleic acid (specific activity = 20.0 mCi/mmol) mixtures was evaluated in a Brownau flow-through diffusion cell system using porcine skin membranes or silicone (polydimethylsiloxane) membranes. [3H] ricinoleic acid (5%) mixtures were dissolved in water containing 5% mineral oil or 5% PEG 200, respectively. Other [3H] ricinoleic acid mixtures were supplemented with three commonly used cutting fluid additives: triazine, linear alkylbenzene sulfonate, and triethanolamine. Eight hours after local exposure, the uptake of ricinoleic acid (based on the amount recovered in the recipient fluid) ranged from 1% to 13% in silicone membranes and from 0.1% to 0.3% in porcine skin membranes. Peak uptake of ricinoleic acid occurred within 3 hours for most mixtures. In both membranes, the control mixture containing PEG showed the highest peak concentration of ricinoleic acid. Researchers investigated the accumulation of hydroxy acids in the adipose tissue of rats after feeding them ricinoleic acid in two experiments. In the first experiment, adult male rats (number, strain, and weight not specified) were fed ricinoleic acid (5% emulsion, 20 mL) for 7 consecutive days. In the second experiment, the animals were fed for 27 days. Lipids were extracted from the adipose tissue and then hydrolyzed to obtain a mixture of fatty acids. Gas-liquid chromatography revealed a large number of hydroxy fatty acids with chain lengths shorter than ricinoleic acid, namely: 10-hydroxyhexadecenoic acid (Experiment 1: 0.60% of total fatty acids; Experiment 2: 0.33% of total fatty acids), 8-hydroxytetradecenoic acid (Experiment 1: 0.03% of total fatty acids; Experiment 2: 0.08% of total fatty acids), and 6-hydroxydodecenoic acid (Experiment 2: 0.03% of total fatty acids). In Experiment 1, ricinoleic acid accounted for 0.51% of total fatty acids, and in Experiment 2, it accounted for 3.85% of total fatty acids.
For more data on the absorption, distribution, and excretion (complete) of ricinoleic acid (9 in total), please visit the HSDB record page.

---

Metabolism/Metabolites
Three healthy subjects were given castor oil orally (10 to 15 mL). Urine was collected 2 to 8 hours after administration. The following three epoxydicarboxylic acids were excreted in the urine: 3,6-epoxyoctanoic acid; 3,6-epoxysepaidanoic acid; and 3,6-epoxydodecanoic acid. These three ricinoleic acid metabolites were also detected in rat urine…

---

-Absorption: Rapidly absorbed after oral administration, with peak plasma concentrations (Cmax) of 5–10 μM in rats within 1 hour [4]
-Metabolism: Extensively metabolized in the liver by β-oxidation to 12-hydroxyoctadecanoic acid and other derivatives [4]
-Excretion: Approximately 60% was excreted in the urine as metabolites within 24 hours; approximately 20% was excreted in the feces [4]

Acute toxicity: Mouse LD₅₀ >2000 mg/kg (oral). Common adverse reactions include diarrhea, vomiting and transient hypotension [4,5]
- Plasma protein binding: Approximately 95% bound to plasma proteins in human serum [4]

---

Toxicity summary
Cosmetic ingredient review results: Safe at the current methods of use and concentrations. Ingredient, concentration and usage information is available at: https://cir-reports.cir-safety.org

---

Interactions
Castoroleic acid (RA) is a potential skin irritant, as is found in many machine tool cutting fluids and other industrial formulations, but little is known about its skin permeability. 3H-ricinoleic acid was formulated into a mixture with three commonly used cutting fluid additives; specifically, triazine (TRI), linear alkylbenzene sulfonate (LAS) and triethanolamine (TEA) were applied topically to inert silicone membranes and in vitro porcine skin in the form of aqueous mineral oil (MO) or polyethylene glycol (PEG) mixtures. These additives significantly reduced the partitioning of ricinoleic acid from the formulation to the stratum corneum (SC) in the PEG-based mixture. All additives except LAS made the formulation alkaline (pH = 9.3–10.3). In both silica gel membranes and porcine skin, the addition of ricinoleic acid, alone or in combination, significantly reduced its permeability. The distribution trends of ricinoleic acid in both membranes suggest that the interactions of the mixtures are inherently more physicochemical and may not be related to changes in biofilm chemistry caused by local contact with potentially irritating agents. PMID:14700524

---

Antidote and Emergency Treatment
/SRP:/ Immediately take first aid measures: Ensure adequate decontamination has been performed. If the patient stops breathing, begin artificial respiration immediately, preferably using a ventilator on demand, bag-valve-mask, or simple breathing mask, and follow the training instructions. Perform cardiopulmonary resuscitation if necessary. Immediately flush contaminated eyes with running water. Do not induce vomiting. If vomiting occurs, lean the patient forward or place them in the left lateral decubitus position (head down if possible) to maintain an open airway and prevent aspiration. Keep the patient calm and maintain normal body temperature. Seek medical attention. /Class A and B Poisons/
/SRP:/ Basic Treatment: Establish a patent airway (using an oropharyngeal or nasopharyngeal airway if necessary). Suction if necessary. Observe for signs of respiratory failure and provide assisted ventilation if necessary. Administer oxygen using a non-invasive breathing mask at a flow rate of 10 to 15 liters per minute. Monitor for pulmonary edema and treat as necessary… Monitor for shock and treat as necessary… Anticipate seizures and treat as necessary… If eyes are contaminated, flush with water immediately. During transport, continuously flush each eye with 0.9% normal saline (NS)… Do not use emetics. If swallowed, rinse mouth and dilute with 5 ml/kg body weight to 200 ml of water, provided the patient is able to swallow, has a strong gag reflex, and does not drool… After decontamination, cover burns with a dry, sterile dressing… /Class A and B Poisons/
/SRP:/ Advanced Treatment: For patients with impaired consciousness, severe pulmonary edema, or severe respiratory distress, consider oropharyngeal or nasopharyngeal endotracheal intubation to control the airway. Positive pressure ventilation with a bag-valve-mask may be effective. Consider medical treatment for pulmonary edema… Consider the use of a beta-agonist (such as salbutamol) for severe bronchospasm… Monitor heart rhythm and treat arrhythmias as needed… Initiate intravenous infusion of 5% glucose solution (D5W) /SRP: “Keep patent,” minimum flow rate/. If signs of hypovolemia appear, use 0.9% normal saline (NS) or lactated Ringer's solution. Administer fluids with caution in cases of hypotension accompanied by signs of hypovolemia. Be alert for signs of fluid overload… Use diazepam or lorazepam to treat seizures… Use promecaine hydrochloride to assist eye irrigation… /Toxins A and B/

---

Human Toxicity Excerpt
/Human Exposure Studies/ Between January 1996 and December 1999, a Singapore clinic specializing in contact and occupational dermatitis treated 202 consecutive patients with eczematous cheilitis (182 women and 20 men) with patch testing. The mean age of the female patients was 31.1 years, and that of the male patients was 28.8 years. Patch testing was performed according to the recommendations of the International Contact Dermatitis Study Group (ICDRG). 29 patients (2 men and 27 women) showed a positive reaction to ricinoleic acid. Of the 29 reactions, 22 were considered relevant positive results.
/Human Exposure Studies/ Perfusion studies in healthy volunteers showed that ricinoleic acid caused significant fluid secretion and simultaneously inhibited the absorption of all tested solutes, including glucose, xylose, L-leucine, L-lysine, folic acid, and 2-monoleic glycerides. Its mechanism may be related to mucosal damage and altered mucosal permeability. /Signs and Symptoms/ Castor oil is known for its laxative effect and can be used to induce labor. Both castor oil and ricinoleic acid are approved for use in food. Its laxative mechanism may involve the disruptive effect on cell membranes similar to detergent molecules (such as sodium ricinoleate, a type of "soap"). These effects have been shown to be dose-related, and there is a threshold in both animals and humans below which no obvious laxative response occurs. PMID:16831502 /Signs and Symptoms/ The lowest dose that can cause death after accidental ingestion is 5000 mg/kg. /Non-human Toxicity Excerpt/ Experimental Animals: Acute Exposure/ Clearance to Specific Pathogens (SPF) Significant changes occurred in the proximal small intestinal mucosa after a single dose of ricinoleic acid (the active ingredient in castor oil) was administered to mice by gavage. Two hours after administration, duodenal villi were significantly shortened, and a large number of columnar and goblet cells were shed. This disruption of the mucosal barrier leads to the formation of continuity between the intestinal lumen and the lamina propria of the villi. Due to the disruption of the mucosal barrier, bacteria of the gut microbiota migrate from the gastrointestinal lumen to the mesenteric lymph nodes, spleen, and liver…PMID: 2942438
/Experimental Animals: Acute Exposure/ It is known that the major autoxidation products of polyunsaturated fatty acids can stimulate DNA synthesis and induce the activity of ornithine decarboxylase in the colonic mucosa. …This study…determined the structural features of oxidized fatty acids required to stimulate these two components of mitosis. The compounds were dissolved in aqueous or mineral oil carriers and administered rectally. After 3 hours (ornithine decarboxylase activity) or 12 hours (tritium-labeled thymidine incorporation), animals were sacrificed and colonic mucosa was collected for measuring two parameters of cell proliferation. Hydroperoxides and hydroxy fatty acids derived from oleic acid and stearic acid were investigated. This study also examined ricinoleic acid and α,β-unsaturated ketones derived from oleic acid. The minimum requirement for stimulating cell proliferation is the presence of an oxidized functional group adjacent to the carbon-carbon double bond. The active compounds in all studies were roughly equivalent in potency, suggesting the possible existence of common mediators. These results indicate that, in addition to bile steroids, the autoxidation products of unsaturated fatty acids may play a role in promoting tumorigenesis at high dietary fat levels. Furthermore, the data suggest a possible mechanism of action for these active compounds. PMID:3349456/Experimental Animals: Acute Exposure/ A single dose of 0.1 mL ricinoleic acid (100 mg/mL) was administered by gavage to fasted, specific pathogen-free mice (CD-1 strain, number not specified). This dose of ricinoleic acid, calculated based on body weight, is roughly equivalent to the therapeutic dose in humans. Mice were sacrificed at different time intervals, and structural changes were identified using optical microscopy, transmission electron microscopy, and scanning electron microscopy. Two hours after administration, duodenal villi were significantly shortened compared to the control group. This widespread villus erosion throughout the duodenum resulted in the extensive shedding of columnar and goblet cells, filling the intestinal lumen with cellular debris and mucus. Disruption of the mucosal barrier led to communication between the intestinal lumen and the lamina propria of the villi, resulting in the leakage of hemocytes and lamina propria components into the intestinal lumen. Four hours after administration, mucosal damage was more localized, and villus erosion was largely repaired. Repair was complete six hours after administration. /Experimental Animals: Acute Exposure/...This study used six male albino Duncan-Hartley guinea pigs to evaluate the pro-inflammatory and anti-inflammatory effects of ricinoleic acid (concentration not specified). Ricinoleic acid (0.1 mL, dissolved in peanut oil) was applied topically to the entire eyelid surface. Eyelid thickness was measured in millimeters using ophthalmic miniature calipers. Topical application of ricinoleic acid (10, 30, or 100 mg/guinea pig) resulted in eyelid redness and edema. The report showed moderate, dose-dependent eyelid edema following ricinoleic acid administration, specifically: 0.12 ± 0.05 mm (10 mg ricinoleic acid), 0.18 ± 0.02 mm (30 mg), and 0.23 ± 0.1 mm (100 mg). Maximum edema was reached 2 hours after administration. The use of ricinoleic acid as an excipient did not cause any significant edema. Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of Castor Seed Oil, Hydrogenated Castor Oil, Glyceryl Ricinate, Glyceryl Ricinate SE, Ricinolic Acid, Potassium Ricinate, Sodium Ricinate, Zinc Ricinate, Cetyl Ricinate, Ethyl Ricinate, Glycol Ricinate, Isopropyl Ricinate, Methyl Ricinate, and Octyl Dodecyl Ricinate; International Journal of Toxicology 26(3 Supplement): 31-77 (2007).

---

Ecological Information
Environmental Fate/Exposure Overview
The production and use of ricinoleic acid in the manufacture of cosmetics, coatings, lubricants, and chemicals may result in its release into the environment through various waste streams. Ricinoleic acid is primarily found in the oil of castor (Euphorbiaceae) seeds. This compound accounts for approximately 90% of the triglyceride fatty acids in castor oil and about 40% of the triglyceride fatty acids in ergot oil. Ricinoleic acid is found in the seed oils of castor beans (Euphorbiaceae), Mexican poppies (Papaveraceae), Indian rosewood (Fabaceae), and corn (Poaceae). If released into the air, its vapor pressure at 25°C is estimated at 4.49 × 10⁻³ mmHg, indicating that ricinoleic acid exists only as a vapor in the atmosphere. Gaseous ricinoleic acid degrades in the atmosphere by reacting with photochemically generated hydroxyl radicals; the half-life of this reaction in the air is estimated at 4.6 hours. Gaseous ricinoleic acid also degrades in the atmosphere by reacting with ozone; the half-life of this reaction in the air is estimated at 2.1 hours. If released into soil, based on an estimated Koc value of 900, the mobility of ricinoleic acid is expected to be low. The estimated pKa value of ricinoleic acid is 4.74, indicating that the compound exists almost entirely in anionic form in the environment, and anions are generally not more readily adsorbed into soils containing organic carbon and clay than their corresponding neutral ions. Because this acid exists in anionic form, and anions are not easily volatile, it is not expected to volatilize from moist soil. If released into water, ricinoleic acid is expected to adsorb onto suspended solids and sediments based on the estimated Koc value. Using activated sludge, 29.7% of the theoretical oxygen demand was achieved within 24 hours, indicating that biodegradation is an important environmental fate process. The estimated pKa value indicates that ricinoleic acid exists almost entirely in anionic form at pH 5 to 9, therefore its volatilization from the water surface is not expected to be an important fate process. The estimated bioaccumulation factor (BCF) is 56, indicating a moderate bioaccumulation potential in aquatic organisms. Hydrolysis is not expected to be an important environmental fate process because the compound lacks functional groups that can be hydrolyzed under environmental conditions. Occupational exposure to this compound may occur through skin contact at sites where ricinoleic acid is produced or used. Use data indicate that the general population may be exposed to ricinoleic acid through skin contact, especially when using cosmetics or personal care products containing ricinoleic acid. (SRC)

[1]. Identification of genes associated with ricinoleic acid accumulation in Hiptage benghalensis via transcriptome analysis. Biotechnol Biofuels. 2019 Jan 21;12:16.
[2]. Inhibition of Calcineurin and Glycogen Synthase Kinase-3β by Ricinoleic Acid Derived from Castor Oil. Lipids. 2020 Mar;55(2):89-99.
[3]. Indulging Curiosity: Preliminary Evidence of an Anxiolytic-like Effect of Castor Oil and Ricinoleic Acid. Nutrients. 2024 May 18;16(10):1527.
[4]. Castor oil induces laxation and uterus contraction via ricinoleic acid activating prostaglandin EP3 receptors. Proc Natl Acad Sci U S A. 2012 Jun 5;109(23):9179-84.
[5]. Pro- and anti-inflammatory actions of ricinoleic acid: similarities and differences with capsaicin. Naunyn Schmiedebergs Arch Pharmacol. 2001 Aug;364(2):87-95.

Ricinoleic acid is a (9Z)-12-hydroxyoctadec-9-enoic acid, wherein the 12-hydroxy group has an R configuration. It is the conjugate acid of ricinoleate. Ricinoleic acid has been reported to be found in clover (Claviceps paspali), jackfruit (Artocarpus integer) and other organisms with relevant data. See also: polyglycerol-6 polyricinoleate (monomer); polyglycerol-4 polyricinoleate (monomer); polyglycerol-5 polyricinoleate (monomer)...

---

- Mechanism of action: exerts laxative and uterine effects through EP3 receptor activation; neuroprotective effects are associated with calcineurin/GSK-3β inhibition; anti-inflammatory activity involves NF-κB inhibition [2,4,5] - Therapeutic use: approved for use as a laxative; research use in anxiety disorders and uterine atony [3,4] - FDA status: listed as a generally recognized safe (GRAS) laxative [4]

C18H34O3

298.46

298.25

C, 72.44; H, 11.48; O, 16.08

141-22-0

Ricinoleic acid (purity≥99%);141-22-0

643684

Colorless to yellow viscous liquid

1.0±0.1 g/cm3

416.4±20.0 °C at 760 mmHg

〈10ºC

219.8±18.3 °C

0.0±2.2 mmHg at 25°C

1.480

5.7

2

3

15

21

261

1

CCCCCC[C@@H](O)C/C=C\CCCCCCCC(O)=O

WBHHMMIMDMUBKC-QJWNTBNXSA-N

InChI=1S/C18H34O3/c1-2-3-4-11-14-17(19)15-12-9-7-5-6-8-10-13-16-18(20)21/h9,12,17,19H,2-8,10-11,13-16H2,1H3,(H,20,21)/b12-9-/t17-/m1/s1

(Z,12R)-12-hydroxyoctadec-9-enoic acid

Acide ricinoleique; Castor oil acid; Ricinoleic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~335.05 mM)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

---

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.)