Absorption, Distribution and Excretion
A gentle moisturizing body wash containing stearic acid (a key component of stratum corneum lipids) and skin-moisturizing soybean oil has been marketed. This study aimed to determine the content and distribution of stearic acid in the stratum corneum after in vivo cleansing with this formula. We conducted 1-day and 5-day clinical cleansing studies using formulas containing soybean oil or petrolatum (PJ), respectively. Free stearic acid in the formula was replaced with fully deuterated stearic acid. We used liquid chromatography-mass spectrometry to determine the stearic acid content in 10 consecutive stratum corneum strips. Additionally, we performed electron paramagnetic resonance (EPR) measurements after cleansing pigskin with a soybean oil formula containing free fatty acids (whose spin probe analog is 5-doxyl stearic acid). Deuterated stearic acid was detected in all 10 consecutive layers of the stratum corneum, with a total amount of 0.33 μg/cm² after five washes with the soybean oil formula. Spin probes in cleansed skin are integrated into partially ordered hydrophobic regions similar to those in stratum corneum lipids. Probe migration increases within the temperature range where lipid disorder is expected. The estimated total amount of fatty acids delivered to the skin via cleansing is comparable to the fatty acid content in the stratum corneum. The delivered fatty acids are likely integrated into the stratum corneum lipid phase. Some researchers have noted that increasing fatty acid chain length slightly reduces their digestibility; stearic acid has the lowest absorption rate among common fatty acids. Fatty acids derived from adipose tissue storage (including stearic acid) are either bound to serum albumin or exist in the blood as free fatty acids. Oleic acid, palmitic acid, myristic acid, and stearic acid are primarily transported via the lymphatic system, while lauric acid is transported via both the lymphatic system and the portal venous system (as free fatty acids). Radioactivity has been detected in the heart, liver, lungs, spleen, kidneys, muscles, intestines, adrenal glands, blood, lymph, and in adipose, mucosal, and dental tissues after radiolabeling of oleic acid, palmitic acid, and stearic acid. Metabolism/Metabolites It has been confirmed that rat liver metabolizes stearic acid via β-oxidation, ω-oxidation, and (ω-1)-oxidation. Removal of an acetate group yields palmitic acid, and both palmitic and stearic acid undergo desaturation reactions to produce oleic acid and palmitoleic acid, respectively. After injection of 14C-labeled stearic acid into rats, approximately 50% of the liver 14C was recovered as oleic acid, indicating extensive desaturation. Desaturation was less pronounced in extrahepatic tissues but was detected in adipose tissue and mammary gland cells. Stearic acid can also be incorporated into phospholipids, diglycerides and triglycerides, cholesterol, cholesterol esters, and other sterol esters. Mechanisms of fatty acid uptake in different tissues include passive diffusion, facilitated diffusion, or a combination of both. Absorbed fatty acids can be stored as triglycerides (98% of which are stored in adipose tissue) or oxidized for energy via catabolism pathways such as β-oxidation and the tricarboxylic acid cycle.
β-oxidation of fatty acids occurs in most spinal tissues (except brain tissue). This process requires an enzyme complex to catalyze a series of oxidation and hydration reactions, ultimately cleaving the acetate group into acetyl-CoA (CoA). Complete catabolism of oleic acid requires additional isomerization reactions. Other oxidation pathways exist in the liver (ω-oxidation) and brain tissue (α-oxidation).
Fatty acid biosynthesis mainly occurs in the liver, adipose tissue, and mammary glands of higher animals, synthesized from acetyl-CoA. A series of reduction and dehydration reactions produce saturated fatty acids with carbon chain lengths not exceeding 16 carbon atoms. Stearic acid is synthesized by the condensation of palmitoyl-CoA and acetyl-CoA in the mitochondria of cells, while oleic acid is generated via a monooxygenase system in the endoplasmic reticulum. Animal cells can synthesize palmitic acid, stearic acid, and their n-9 derivatives de novo. However, de novo synthesis requires energy. Palmitic acid (C16) is a direct precursor of stearic acid (C18). In animal cells, oleic acid is generated from stearic acid by dehydrogenation (desaturation). Oleic acid further elongates and desaturates to generate a series of n-9 fatty acids. In cell culture, the energy required for the synthesis of n-9 fatty acids can be reduced by providing palmitic acid and stearic acid. Furthermore, since palmitic acid and stearic acid are saturated fatty acids, they are not peroxidized during transport to cells. Known metabolites of stearic acid include 17-hydroxystearic acid.

Toxicity Summary
Identification and Uses: Stearic acid is a solid. It is used in the coating of suppositories, enteric-coated tablets, ointments, and bitter medicines. It is also used in the manufacture of stearates of aluminum, zinc, and other metals, stearic acid soaps for liniments invented by Paracelsus, candles, records, insulators, model compounds, plaster impregnators, and contact lens creams and other cosmetics. Stearic acid is used in animal cell culture. Human Studies: The greatest danger of ingesting large amounts of stearic acid is intestinal obstruction. Skin sensitization is uncommon. Inhalation or aspiration of stearic acid may cause chemical pneumonia. Implantation of stearic acid may cause a foreign body reaction. Animal Studies: A skin lotion formulation containing 2.8% stearic acid was administered to 10 rats by gavage at a dose of 15 g/kg, resulting in the death of one rat. The remaining surviving rats behaved and appeared normal, with no obvious abnormalities. Six rabbits showed no eye irritation after treatment with commercially available stearic acid, while three out of six rabbits developed mild conjunctival erythema after treatment with commercially available triple-pressed stearic acid. Treatment with 35% stearic acid corn oil solution and 50% stearic acid petrolatum solution mainly caused mild conjunctival erythema, which subsided within 2 days. Intravenous infusion of high doses of stearic acid caused thrombosis, platelet aggregation, and acute heart failure in rats, rabbits, and dogs. After weaning mice were fed a diet containing 5% to 50% stearic acid (in the form of monoglycerides) for 3 weeks, weight gain was inhibited when the stearic acid content in the diet exceeded 10%. Death was observed only in the group with 50% stearic acid in the diet. The above effects were less pronounced in adult mice. Rats fed a high-fat diet containing 5% stearic acid for 6 weeks or a diet containing 6% stearic acid for 9 weeks both developed shortened clotting time and hyperlipidemia. Reversible lipogranulomas appeared in the adipose tissue of rats after daily feeding of 50 g/kg stearic acid for 24 weeks. After oral administration of 3000 ppm stearic acid to rats for approximately 30 weeks, no obvious pathological damage was observed, but anorexia, increased mortality, and a higher incidence of pulmonary infection were observed. In mice, a single intraperitoneal injection of stearic acid (dose range approximately 15 to 500 mg/kg) did not lead to death, but the highest dose group resulted in weight loss. In cats, low doses of stearic acid caused increased pulmonary blood pressure but decreased systemic blood pressure. Dose exceeding 5 mg caused respiratory arrest, hypotension, and seizures, ultimately leading to death. The mutagenicity of stearic acid was tested in Salmonella Typhimurium strains TA98, TA100, TA1535, TA1537, and TA1538 using the Ames test. With or without metabolic activation, the mutagenic activity of stearic acid against the tested strains was not higher than background levels.

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Toxicity Data
Acute oral toxicity (LD50): 4640 mg/kg [rat]. Acute dermal toxicity (LD50): >5000 mg/kg [rabbit].

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Interactions
Mild to moderate erythema was observed at a few sites after treatment with a 1% aqueous solution of an emulsion formulation containing 2.8% stearic acid or a bar soap formulation containing 23% stearic acid, followed by UVA irradiation. The emulsion formulation was applied to the forearm via a 24-hour occlusive patch, and the treated area was irradiated with UVA light for 15 minutes at a distance of approximately 10 cm at a dose of 4400 μW/cm². The bar soap formulation was applied to the subscapular region of the back via a 24-hour occlusive patch, and the treated area was irradiated with UVA light for 12 minutes using a xenon arc solar simulator (150W) equipped with a Schott WG345 filter. Similar results were observed at the control sites that received UVA irradiation only.
A trial involving 52 subjects, four induction patches, and one activation patch tested the photosensitivity of a face cream formulation containing 13% stearic acid. In the trial, subjects wore occlusive and open patches for 24 hours. After patch removal and 48 hours later, the treated areas were irradiated with full-spectrum xenon ultraviolet light at a dose three times the subject's predetermined minimum erythema dose (MED). Following the 24-hour activation patch test, the treated areas were irradiated with UVA light (xenon lamp source with Schott WG345 filter) for 3 minutes. No reaction was observed with either the induction or activation patch, regardless of whether the patch was occlusive or open.
A photosensitivity study involving 100 subjects tested an eyeliner formulation containing 2.66% stearic acid, and no reaction was observed. In a closed patch/repetitive stimulation patch (RIPT) trial consisting of 10 induction patches and 1 challenge patch, the skin was irradiated for 1 minute at a distance of 1 foot using a Hanovia Tanette Mark 1 UV light source after the removal of the 1st, 4th, 7th, and 10th induction patches, and after the challenge patch trial. Approximately 50% of the subjects were identified as “sensitive subjects” because they had previously experienced rashes or irritation after using facial products, or had an adverse reaction to previous facial product patch trials. The phototoxicity of two moisturizing lotion formulations containing 2.8% stearic acid was tested. Aqueous solutions at concentrations of 100%, 75%, 50%, and 25% were applied to four different sites on the backs of 10 male Hartley albino guinea pigs weighing 324–486 g and 284–452 g, respectively. These sites were then exposed to UVA. Ten control guinea pigs, weighing 268–434 g and 344–464 g respectively, received the same topical application but were not exposed to UVA. Responses at each site were assessed at 1 hour and 24 hours post-treatment. Because the irritation symptoms in the control groups were similar to those in the irradiated groups, neither formulation was considered phototoxic to guinea pigs under these conditions. In one study, one guinea pig in the control group died. Reactions in the experimental groups ranged from suspected to moderate erythema; erythema appeared at 6 sites in the 50% formulation group, while all 10 sites were erythematosus in the 75% and 100% formulation groups. No signs of phototoxicity were observed with the 25% formulation in either study. Suspicious to moderate (50–100% sites, 50–75% sites) or pronounced (100% sites) erythema were observed in the control groups in both studies. No irritation was observed at the control sites treated with the 25% formulation.
For more complete data on interactions of stearic acid (9 types), please visit the HSDB record page.

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Non-human toxicity values
Rat intravenous LD50: 22 mg/kg
Rabbit dermal LD50: >5000 mg/kg
Mouse intravenous LD50: 23 mg/kg
Rat intravenous LD50: 21,500 μg/kg

Stearic acid is a white solid with a mild odor that floats on water. (US Coast Guard, 1999)
Octadecanic acid is a C18 straight-chain saturated fatty acid and a component of many animal and plant lipids. Besides its use in the diet, it is used in hardening soaps, softening plastics, and in the manufacture of cosmetics, candles, and plastic products. It functions as a plant metabolite, a human metabolite, a Daphnia magna metabolite, and an algal metabolite. It is a long-chain fatty acid, a straight-chain saturated fatty acid, and a saturated fatty acid. It is the conjugate acid of octadecanoate. It is derived from the hydrogenation of octadecane.
Stearic acid (IUPAC system name: octadecanoic acid) is a useful saturated fatty acid found in many animal and plant oils. It is a waxy solid.
Stearic acid is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain).
Stearic acid is reportedly found in Calodendrum capense, Amaranthus hybridus, and other organisms with relevant data.
Stearic acid is a saturated long-chain fatty acid with an 18-carbon backbone. It is found in many animal and plant fats and is a major component of cocoa butter and shea butter.
Stearic acid, also known as octadecanoic acid, is a useful saturated fatty acid found in many animal and plant oils. It is a waxy solid with the chemical formula CH3(CH2)16COOH. Its name comes from the Greek word "stear," meaning tallow. Its IUPAC name is octadecanoic acid. -- Wikipedia.
See also: Magnesium stearate (active ingredient); Sodium stearate (active ingredient); Cod liver oil (one of the ingredients)... See more...
Therapeutic Uses
/EXPL THER/ Stearic acid is a potent anti-inflammatory lipid. This fatty acid has profound and diverse effects on liver metabolism. This study aimed to investigate the effect of stearic acid on hepatocyte transplantation markers in rats with acetaminophen (APAP)-induced liver injury. Wistar rats were randomly divided into 10 groups for treatment. Rats with APAP-induced liver injury were administered stearic acid. Isolated hepatocytes were intraperitoneally injected into the rats. Blood samples were collected to assess changes in serum liver enzymes, including the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP), as well as serum albumin levels. To assess hepatocyte engraftment, rats were sacrificed, and liver DNA was extracted and detected by PCR using sex-determining region Y (SRY) primers. Serum AST, ALT, and ALP levels were significantly elevated in rats with APAP-induced liver injury, returning to control levels by day 6. Compared with rats treated with APAP alone, cell therapy significantly improved APAP-induced albumin reduction. SRY PCR analysis showed that transplanted cells were present in the livers of transplanted rats. A stearic acid-rich diet combined with cell therapy accelerated the recovery of liver function in a rat model of liver injury.
/EXPL THER/ Due to reported antiviral and anti-inflammatory activities, cream formulations containing docosanool (docosanool) or stearic acid were tested for the treatment of chemical burns in mice. In this model, damage was induced by applying a phenol-chloroform solution to the abdomen of mice. Test substances were then applied topically at 0.5, 3, and 6 hours. At 8 hours, wound progression was assessed by an evaluator using a numerical score of macromorphology. Compared to untreated sites, creams containing docosanool and stearic acid significantly and reproducibly reduced the severity and progression of skin damage, with mean damage scores reduced by 76% and 57%, respectively. Untreated wounds were red and ulcerated; wounds treated with the docosanool cream showed only mild erythema.

C18H38O2

284.48

284.272

57-11-4

18639-67-3

5281

Monoclinic leaflets from alcohol
White or slightly yellow crystal masses, or white to slightly yellow powder
Colorless, wax-like solid
White amorphous solid or leaflets

0.84

361 °C(lit.)

67-72 °C(lit.)

>230 °F

1 mm Hg ( 173.7 °C)

1.4299

6.332

1

2

16

20

202

0

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

NSC-25956; NSC 25956; Stearic 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 : ≥ 14.29 mg/mL (~50.23 mM)

Solubility in Formulation 1: 2.08 mg/mL (7.31 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.08 mg/mL (7.31 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (7.31 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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