- 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
Ricinoleic acid or methyl ricinoleate was administered via gastric intubation to male rats (minimum weight of 400 g) with a cannulated thoracic duct. Lymph was collected for 48 hr, and the lipids were then extracted and separated into various lipid classes. Results indicated that Ricinoleic acid was present in the triglyceride, diglyceride, monoglyceride, and free fatty acid fractions. Peak absorption of ricinoleic acid occurrred within 30 min post administration. Ricinoleic acid was not present in the phospholipid or cholesterol ester fractions of the lymph lipids.
The skin penetration of ricinoleic acid in vivo /was investigated/ using rats that were 20 to 30 days old. In order to increase the fluorescence of ricinoleic acid, either one part of methyl anthranilate or methylcholanthrene was added to 99 parts ricinoleic acid. The test substance was gently rubbed on to skin that had been clipped free of hair. Biopsies were taken at various intervals post application. The preparations were observed using a Spencer microscope with a quartz condenser. Ricinoleic acid was retained mainly in the outer strata of the epidermis. There was little evidence of deeper penetration in biopsies that were taken at 2 hr post application.
The percutaneous absorption of a radiolabeled (3H)ricinoleic acid (specific activity = 20.0 mCi/mmol) mixture was evaluated using porcine skin membranes or silastic (polydimethylsioloxane) membranes in the Bronaugh flow-through diffusion cell system. [3H]Ricinoleic acid (5%) mixtures were prepared in water containing either 5% mineral oil or 5% PEG 200. Other (3H)Ricinoleic acid mixtures were formulated with the following three commonly used cutting fluid additives: triazine, linear alkylbenzene sulfonate, and triethanolamine. At 8 hr after topical exposure, Ricinoleic acid absorption (based on amount recovered in receptor fluid) ranged from 1% to 13% in silastic membranes and 0.1% to 0.3% in porcine skin membranes. For most mixtures, peak absorption of ricinoleic acid occurred within 3 hr. The greatest ricinoleic acid peak concentrations were associated with the control mixtures containing PEG in both membranes.
/Investigators/ studied the accumulation of hydroxyl acids in depot fat after rats were fed with ricinoleic acid in two experiments. In the first experiment, adult male rats (number, strain, and weights not stated) were fed ricinoleic acid (5% emulsion, 20 mL) for 7 days. In the second experiment, the animals were fed for 27 days. Lipid extraction from the fat tissue was followed by hydrolysis to yield a fatty acid mixture. A gas-liquid chromatogram indicated appreciable amounts of the following hydroxy fatty acids with shorter chain lengths than ricinoleic acid: 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). Ricinoleic acid comprised 0.51% of total fatty acids in experiment 1 and 3.85% of total fatty acids in experiment 2.
For more Absorption, Distribution and Excretion (Complete) data for Ricinoleic acid (9 total), please visit the HSDB record page.

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Metabolism / Metabolites
Three healthy subjects /were/ administered castor oil (10 to 15 mL) orally. Urine was collected between 2 and 8 hr post dosing. The following three epoxydicarboxylic acids were excreted in the urine: 3,6-epoxyoctanedioic acid; 3,6-epoxydecanedioic acid; and 3,6-epoxydodecanedioic acid. These three ricinoleic acid metabolites were also detected in the urine of rats...

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

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

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Toxicity Summary
Cosmetic Ingredient Review Finding(s) Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

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Interactions
Ricinoleic acid (RA) like many of the ingredients in machine cutting fluids and other industrial formulations are potential dermal irritants, yet very little is known about its permeability in skin. 3H-ricinoleic acid mixtures were formulated with three commonly used cutting fluid additives; namely, triazine (TRI), linear alkylbenzene sulfonate (LAS), and triethanolamine (TEA) and topically applied to inert silastic membranes and porcine skin in vitro as aqueous mineral oil (MO) or polyethylene glycol (PEG) mixtures. These additives significantly decreased ricinoleic acid partitioning from the formulation into the stratum corneum (SC) in PEG-based mixtures. Except for LAS, all other additives produced a more basic formulation (pH = 9.3-10.3). In silastic membranes and porcine skin, individual additives or combination of additives significantly reduced ricinoleic permeability. This trend in ricinoleic acid disposition in both membranes suggests that the mixture interaction is more physicochemical in nature and probably not related to the chemical-induced changes in the biological membrane as may be assumed with topical exposures to potentially irritant formulations. PMID:14700524

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Antidote and Emergency Treatment
/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

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Human Toxicity Excerpts
/HUMAN EXPOSURE STUDIES/ 202 consecutive patients (182 females, 20 males) with eczematous cheilitis who attended a contact and occupational dermatoses clinic in Singapore between January of 1996 and December of 1999 were patch-tested. Mean ages for female and male patients were 31.1 and 28.8 years, respectively. Patch tests were conducted according to International Contact Dermatitis Research Group (ICDRG) recommendations. Twenty-nine patients (2 males, 27 females) had positive reactions to ricinoleic acid. Of the 29 reactions, 22 were considered relevant positives.
/HUMAN EXPOSURE STUDIES/ Perfusion studies...in healthy volunteers.../showed/ ricinoleic acid provoked a marked secretion of fluid & concomitantly inhibited absorption of all solutes tested, incl glucose, xylose, l-leucine, l-lysine, folic acid, & 2-monoolein. Mechanism may be related to mucosal damage & altered mucosal permeability.
/SIGNS AND SYMPTOMS/ Castor oil is known for its purgative effects and can be used to induce labor. Both castor oil and ricinoleic acid are approved for use in food. The mechanistic basis for purgative actions likely includes the membrane-disruptive effects of detergent-like molecules, such as sodium ricinoleate (a "soap"). These effects have been shown to be dose-related and to exhibit a threshold below which no laxative response was evident, in both animals and in humans. PMID:16831502
/SIGNS AND SYMPTOMS/ The lowest dose at which mortality occurred following an accidental ingestion was 5000 mg/kg.

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Non-Human Toxicity Excerpts /LABORATORY ANIMALS: Acute Exposure/ A single dose of ricinoleic acid, the active component of castor oil, administered intragastrically to specific pathogen-free mice produced significant alterations in the proximal small intestinal mucosa. Two hours after drug administration, the duodenal villi were markedly shortened with massive exfoliation of columnar and goblet cells. This disruption of the mucosal barrier resulted in continuity between the intestinal lumen and the lamina propria of the villi. Because of the loss of the mucosal barrier, bacteria of the indigenous gastrointestinal flora translocated from the gastrointestinal lumen to the mesenteric lymph nodes, spleen, and liver... PMID:2942438
/LABORATORY ANIMALS: Acute Exposure/ The primary autoxidation products of polyunsaturated fatty acids are known to stimulate DNA synthesis and induce ornithine decarboxylase activity in colonic mucosa. ... The present study ... determined the structural features of the oxidized fatty acids necessary for the stimulation of these two components of mitogenesis. Compounds were instilled intrarectally in either aqueous or mineral oil vehicles and 3 hr later (ornithine decarboxylase activity) or 12 hr later (tritiated thymidine incorporation), the animals were killed and the colonic mucosa harvested for measurement of the two parameters of cell proliferation. Hydroperoxy and hydroxy fatty acids derived from oleate and stearate were studied. Ricinoleic acid and the alpha,beta-unsaturated ketone derived from oleic acid were also investigated. The minimal requirement for stimulation of cell proliferation is the presence of an oxidized functionally adjacent to a carbon-carbon double bond. All active compounds studied were roughly equipotent, which suggests a common mediator may be involved. These results imply that, in addition to biliary steroids, the autoxidation products of unsaturated fatty acids may play a role in the enhancement of tumorigenesis by high levels of dietary fat. Furthermore, the data suggest a possible mechanism of action for the active compounds. PMID:3349456
/LABORATORY ANIMALS: Acute Exposure/ A single 0.1 mL dose of ricinoleic acid (100 mg/mL) was administered intragastrically to fasted, specific pathogen-free mice (strain CD-1, number not stated). This dosage of Ricinoleic acid was determined, on a weight basis, to be approximately the dosage that is used therapeutically in humans. Groups of mice were killed at various intervals, and light microscopy and transmission and scanning electron microscopy were used to identify structural alterations. At 2 hr post dosing, the duodenal villi were markedly shortened when compared to control duodenal villi. This erosion of the villi throughout the duodenum caused massive exfoliation of columnar and goblet cells, filling the lumen with cellular debris and mucus. Disruption of the mucosal barrier resulted in continuity between the intestinal lumen and lamina priopria of the villi, with the loss of formed blood elements and lamina propria constituents into the intestinal lumen. The mucosal damage was much more localized at 4 hr post dosing, and the erosion of the villi had been largely repaired. Repair was complete at 6 hr post dosing.
/LABORATORY ANIMALS: Acute Exposure/ ... Groups of six male albino Dunkin-Hartley guinea pigs, /were used/ in a study evaluating pro- and anti-inflammatory effects of ricinoleic acid (concentration not stated). Ricinoleic acid (0.1 mL, in peanut oil) was administered topically to the entire eyelid surface. The thickness of the eyelid was measured in mm using ophthalmic microcallipers. Topical treatment with ricinoleic acid (10, 30, or 100 mg/guinea pig) caused eyelid reddening and edema. A moderate, dose-dependent eyelid edema was reported as follows: 0.12 +/- 0.05 mm (10 mg ricinoleic acid), 0.18 +/- 0.02 mg (30 mg), and 0.23 +/- 0.1 mm (100 mg). Maximal edema was achieved at 2 hr post-application. The application of ricinoleic acid vehicle did not cause any appreciable edema. Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of Ricinus Communis (Castor) Seed Oil, Hydrogenated Castor Oil, Glyceryl Ricinoleate, Glyceryl Ricinoleate SE, Ricinoleic Acid, Potassium Ricinoleate, Sodium Ricinoleate, Zinc Ricinoleate, Cetyl Ricinoleate, Ethyl Ricinoleate, Glycol Ricinoleate, Isopropyl Ricinoleate, Methyl Ricinoleate, and Octyldodecyl Ricinoleate; International Journal of Toxicology 26 (3 Suppl): 31-77 (2007).

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Ecological Information
Environmental Fate / Exposure Summary

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Ricinoleic acid's production and use in cosmetics, coatings, lubricants, and in the manufacture of chemicals may result in its release to the environment through various waste streams. Ricinoleic acid is found primarily in oils from the seeds of Ricinus communis (Euphorbiaceae). The compound accounts for about 90% of the triglyceride fatty acids of castor oil, and up to about 40% of the glyceride fatty acids of ergot oil. Ricinoleic acid is found in the oils from the seeds of Ricinus communis (Euphorbiaceae), Argemone mexicana (Papaveraceae), Pterocarpus marsupium (Fabaceae), and in Zea mays (Poaceae). If released to air, an estimated vapor pressure of 4.49X10-3 mm Hg at 25 °C indicates ricinoleic acid will exist solely as a vapor in the atmosphere. Vapor-phase ricinoleic acid will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 4.6 hours. Vapor-phase ricinoleic acid will be degraded in the atmosphere by reaction with ozone; the half-life for this reaction in air is estimated as 2.1 hours. If released to soil, ricinoleic acid is expected to have low mobility based upon an estimated Koc of 900. The estimated pKa of ricinoleic acid is 4.74, indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts. Volatilization from moist soil is not expected because the acid exists as an anion and anions do not volatilize. If released into water, ricinoleic acid is expected to adsorb to suspended solids and sediment based upon the estimated Koc. Utilizing activated sludge, 29.7% of the theoretical oxygen demand was reached in 24 hours indicating that biodegradation is an important environmental fate process. The estimated pKa indicates ricinoleic acid will exist almost entirely in the anion form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process. An estimated BCF of 56 suggests the potential for bioconcentration in aquatic organisms is moderate. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Occupational exposure to ricinoleic acid may occur through dermal contact with this compound at workplaces where ricinoleic acid is produced or used. Use data indicate that the general population may be exposed to ricinoleic acid via dermal contact with this compound, especially when using cosmetic 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.

- Mechanism of action: Laxative and uterine effects mediated via EP3 receptor activation; neuroprotective effects linked to calcineurin/GSK-3β inhibition; anti-inflammatory activity involves NF-κB suppression[2,4,5]
- Therapeutic uses: Approved as a laxative; investigational use in anxiety disorders and uterine atony[3,4]
- FDA status: Classified as Generally Recognized As Safe (GRAS) for use as a laxative[4]

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Ricinoleic acid is a (9Z)-12-hydroxyoctadec-9-enoic acid in which the 12-hydroxy group has R-configuration.. It is a conjugate acid of a ricinoleate.
Ricinoleic acid has been reported in Claviceps paspali, Artocarpus integer, and other organisms with data available.
See also: Polyglyceryl-6 polyricinoleate (monomer of); Polyglyceryl-4 polyricinoleate (monomer of); Polyglyceryl-5 polyricinoleate (monomer of) ...

C18H34O3

298.46

298.25

C, 72.44; H, 11.48; O, 16.08

141-22-0

Ricinoleic acid (purity≥99%);141-22-0;89141-22-0

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

(E/Z)-12-hydroxyoctadec-9-enoic acid; (E,12R)-12-hydroxyoctadec-9-enoic acid

Acide ricinoleique; Castor oil acid; RICINOLEIC ACID; 141-22-0; Ricinolic acid; Ricinic acid; (9Z,12R)-12-hydroxyoctadec-9-enoic acid; Kyselina ricinolova; D-12-Hydroxyoleic acid; 12-Hydroxy-cis-9-octadecenoic 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.

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\n\nInjection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
\n*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
\n 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)
\n Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
\nExample: 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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\n 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)]
\n*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.
\n Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
\n 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)
\n Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
\n Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
\nInjection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
\n 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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\n\nOral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
\nOral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
\nExample: 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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\n\nOral Formulation 3: Dissolved in PEG400
\nOral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
\nOral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
\n\nOral Formulation 6: Mixing with food powders

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\n\n\nNote: 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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\n\n\n (Please use freshly prepared in vivo formulations for optimal results.)