Absorption, Distribution and Excretion
A mild moisturizing body wash with stearic acid, a key component of corneum lipids, and emollient soybean oil has been introduced in the market place. The objectives of this study are to determine the amount and the location of the stearic acid in the corneum after in vivo cleansing by the formulation. Clinical cleansing studies for one and five consecutive days were carried out with the formulation containing soybean oil or petroleum jelly (PJ). The free stearic acid in it was replaced by the fully deuterated variant. The amounts of stearic acid in 10 consecutive corneum tape strips were measured by liquid chromatograph-mass spectroscopy. Separately, electron paramagnetic resonance (EPR) measurements were taken with a porcine skin after a wash by the soybean oil formulation with its free fatty acid replaced by its spin probe analogue, 5-doxyl stearic acid. Deuterated stearic acid was detected in all 10 consecutive layers of stratum corneum and the total amount after five washes with the soybean oil formulation was 0.33 ug/sq cm. The spin probe in cleanser-treated skin was incorporated in a partially ordered hydrophobic region similar to corneum lipids. The probe mobility increased in the temperature region where lipid disorder was expected. The estimated total fatty acid delivered to skin from cleansing is comparable to the amount of fatty acid in a corneum layer. The delivered fatty acid is most likely incorporated in the corneum lipid phase.
It has been noted by several investigators that increasing fatty acid chain length slightly decreased their digestibility; stearic acid was the most poorly absorbed of the common fatty acids.
Fatty acids, /including stearic acid/, originating from adipose tissue stores are either bound to serum albumin or remain unesterified in the blood.
Oleic, palmitic, myristic, and stearic acids are primarily transported via the lymphatic system, and lauric acid is transported by the lymphatic and (as a free fatty acid) portal systems.
Radioactivity has been traced to the heart, liver, lung, spleen, kidney, muscle, intestine, adrenal, blood, and lymph, and adipose, mucosal, and dental tissues after administration of radioactive oleic, palmitic, and stearic acids.

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Metabolism / Metabolites
Stearic acid metabolism via beta-oxidation, omega-oxidation, and (omega-1)-oxidation has been demonstrated in rat liver. Removal of a single acetate moiety can occur to produce palmitic acid, and both this and stearic acid may be desaturated, producing oleic and palmitoleic acids, respectively. After (l4)C stearic acid was injected into rats, about 50 percent of the liver (14)C was recovered as oleic acid, indicating that extensive desaturation occurs. Desaturation occurs only to a small extent extrahepatically but has been detected in adipose tissue and in cells of mammary tissue. Stearic acid is also incorporated into phospholipids, di- and triglycerides, cholesterol, cholesterol esters, and other sterol esters.
Proposed mechanisms for fatty acid uptake by different tissues range from passive diffusion to facilitated diffusion or a combination of both. Fatty acids taken up by the tissues can either be stored in the form of triglycerides (98% of which occurs in adipose tissue depots) or they can be oxidized for energy via the beta-oxidation and tricarboxylic acid cycle pathways of catabolism.
The beta-oxidation of fatty acids occurs in most vertebrae tissues (except the brain) using an enzyme complex for the series of oxidation and hydration reactions resulting in the cleavage of acetate groups as acetyl-CoA (coenzyme A). An additional isomerization reaction is required for the complete catabolism of oleic acid. Alternate oxidation pathways can be found in the liver (omega-oxidation) and in the brain (alpha-oxidation).
Fatty acid biosynthesis from acetyl-CoA takes place primarily in the liver, adipose tissue, and mammary glands of higher animals. Successive reduction and dehydration reactions yield saturated fatty acids up to a 16-carbon chain length. Stearic acid is synthesized by the condensation of palmitoyl-CoA and acetyl-CoA in the mitochondria, and oleic acid is formed via a mono-oxygenase system in the endoplasmic reticulum.
Animal cells can de novo synthesize palmitic and stearic fatty acid and their n-9 derivatives. However, de novo synthesis requires the utilization of energy. Palmitic acid (C16) is the immediate precursor of stearic acid (C18). In animal cells, oleic acid is created by the dehydrogenation (desaturation) of stearic acid. Oleic acid is further elongated and desaturated into a family of n-9 fatty acids. The demand for energy used to synthesize n-9 fatty acids can be reduced in cell culture by providing palmitic and stearic acids. In addition, since palmitic and stearic acid are saturated, they are not peroxidized during delivery to the cells.
Stearic Acid has known human metabolites that include 17-Hydroxystearic acid.

Toxicity Summary
IDENTIFICATION AND USE: Stearic acid is a solid. It is used in suppositories, coating enteric pills, ointments and for coating bitter remedies. It is also used in manufacturing stearates of aluminum, zinc, and other metals, stearin soap for a liniment invented by Paracelsus, candles, phonograph records, insulators, modeling compounds, impregnating plaster of Paris, in vanishing creams and other cosmetics. Stearic acid is used in animal cell culture. HUMAN STUDIES: The greatest danger from ingestion of large quantities of stearic acid is intestinal obstruction. Skin sensitization is unusual. Aspiration or inhalation of stearic acid could cause chemical pneumonitis. Implantation of stearic acid will cause foreign body reaction. ANIMAL STUDIES: Skin lotion formulations containing 2.8% stearic acid administered at doses of 15 g/kg by gavage to groups of 10 rats resulted in 1 death. Normal behavior and appearance were observed, and there were no gross alterations in surviving rats. No ocular irritation was produced in 6 rabbits by commercial grade stearic acid, whereas mild conjunctival erythema was produced in 3 of 6 rabbits by commercial grade triple-pressed stearic acid. Treatment with 35% stearic acid in corn oil and 50% stearic acid in petrolatum was primarily producing mild conjunctival erythema, which had subsided within 2 days. Intravenous infusion of large doses of stearic acid were thrombogenic in rats, rabbits, and dogs, causing blood platelet aggregation and acute heart failure. When diets containing 5 to 50% stearic acid (as the monoglyceride) were fed to weanling mice for 3 weeks, depression of weight gain was seen above the 10% dietary level. Mortality occurred only with the 50% diet. The effects were less noticeable in adult mice. Rats fed 5% stearic acid as part of a high-fat diet for 6 weeks, or 6% stearic acid for 9 weeks, showed a decreased blood clotting time and hyperlipemia. Rats fed 50 g/kg/day stearic acid for 24 weeks developed reversible lipogranulomas in adipose tissue. No significant pathological lesions were observed in rats fed 3000 ppm stearic acid orally for about 30 weeks, but anorexia, increased mortality, and a greater incidence of pulmonary infection were observed. Single intraperitoneal doses of stearic acid in mice, ranging from approximately 15 to 500 mg/kg, caused no fatalities, but at the highest dose level caused a loss of body weight. In cats, low doses of stearic acid produced elevated pulmonary but decreased systemic blood pressure. Doses greater than 5 mg caused apnea, a fall in blood pressure, and convulsions leading to death. Stearic acid was tested for mutagenicity using the Ames test with Salmonella typhimurium strains TA98, TA100, TA1535, TA1537, and TA1538. Stearic acid had no mutagenic activity over background in the strains tested with and without metabolic activation.

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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
Minimal to mild erythema was observed at a few sites after treatment with a lotion formulation containing 2.8% stearic acid or a 1% aqueous dilution of a bar soap formulation containing 23% stearic acid followed by UVA irradiation. The lotion formulation was applied via 24-hr occlusive patches to the forearm, and treatment sites were irradiated with UVA light for 15 min at a distance of approximately 10 cm, receiving a dose of 4400 uW/sq cm. The bar soap formulation was applied via 24-hr occlusive patches to the infrascapular region of the back, and treatment sites were irradiated with UVA light from Xenon Arc Solar Simulator (150W) with a Schott WG345 filter for 12 min. Similar results were observed at control sites that had received UVA irradiation alone.
A face cream formulation containing 13% stearic acid was tested for photosensitization using 52 human subjects and 4 induction patches and 1 challenge patch. Closed and open 24-hr patches were applied, and treated sites were irradiated with the full Xenon UV light spectrum at 3 times the individuals' predetermined minimal erythemal dose (MED) after removal of each patch and 48 hr later. After the 24-hr challenge patch, treated sites were irradiated with UVA light (Xenon source plus Schott WG345 filter) for 3 min. There were no reactions observed at sites under closed or open patches at either induction or challenge sites.
No reactions were observed in 100 human subjects of a photosensitization study testing an eyeliner formulation containing 2.66% stearic acid. In a 10 induction, 1 challenge occlusive patch /repeat insult patch test/ (RIPT), treated sites were irradiated with UV light from a Hanovia Tanette Mark 1 light source for 1 min at a distance of 1 foot after removal of the 1st, 4th, 7th, and 10th induction patches and after the challenge patch. Approximately 50% of the subjects were designated as "sensitive subjects" because of past experiences of rash or irritation from the use of facial products or because of reaction to a previous patch test with a facial product.
Two skin lotion formulations containing 2.8% stearic acid were tested for phototoxicity. Aqueous preparations of the formulations, 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. These sites were exposed to UVA radiation. Ten control guinea pigs weighing 268-434 and 344-464 g received the same topical applications but no UVA irradiation. Sites were evaluated 1 and 24 hr after treatment. Neither formulation was considered phototoxic to the guinea pigs under these conditions because the control group had signs of irritation that were comparable to the irradiated test group. One guinea pig in the control group of one study died. The test groups reactions ranged from questionable to moderate erythema at 6 (50% preparation) to all 10 sites (75%, 100% preparations). The 25% preparations produced no signs of phototoxicity in either study. The control groups in both studies had questionable to moderate (50-100% sites, 50-75% sites) or considerable erythema (100% site). No irritation was observed at control sites treated with the 25% preparations.
For more Interactions (Complete) data for Stearic acid (9 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat iv 22 mg/kg
LD50 Rabbit dermal >5000 mg/kg
LD50 Mouse iv 23 mg/kg
LD50 Rat iv 21,500 ug/kg

Stearic acid is a white solid with a mild odor. Floats on water. (USCG, 1999)
Octadecanoic acid is a C18 straight-chain saturated fatty acid component of many animal and vegetable lipids. As well as in the diet, it is used in hardening soaps, softening plastics and in making cosmetics, candles and plastics. It has a role 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 a conjugate acid of an octadecanoate. It derives from a hydride of an octadecane.
Stearic acid (IUPAC systematic name: octadecanoic acid) is one of the useful types of saturated fatty acids that comes from many animal and vegetable fats and oils. It is a waxy solid.
Stearic acid is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
Stearic Acid has been reported in Calodendrum capense, Amaranthus hybridus, and other organisms with data available.
Stearic Acid is a saturated long-chain fatty acid with an 18-carbon backbone. Stearic acid is found in various animal and plant fats, and is a major component of cocoa butter and shea butter.
Stearic acid, also called octadecanoic acid, is one of the useful types of saturated fatty acids that comes from many animal and vegetable fats and oils. It is a waxy solid, and its chemical formula is CH3(CH2)16COOH. Its name comes from the Greek word stear, which means tallow. Its IUPAC name is octadecanoic acid. -- Wikipedia.
See also: Magnesium Stearate (active moiety of); Sodium Stearate (is active moiety of); Cod Liver Oil (part of) ... View More ...

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Therapeutic Uses
/EXPL THER/ Stearic acid is known as a potent anti-inflammatory lipid. This fatty acid has profound and diverse effects on liver metabolism. The aim of this study was to investigate the effect of stearic acid on markers of hepatocyte transplantation in rats with acetaminophen (APAP)-induced liver damage. Wistar rats were randomly assigned to 10-day treatment. Stearic acid was administered to the rats with APAP-induced liver damage. The isolated liver cells were infused intraperitoneally into rats. Blood samples were obtained to evaluate the changes in the serum liver enzymes, including activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) and the level of serum albumin. To assess the engraftment of infused hepatocytes, rats were euthanized, and the liver DNA was used for PCR using sex-determining region Y (SRY) primers. The levels of AST, ALT and ALP in the serum of rats with APAP-induced liver injury were significantly increased and returned to the levels in control group by day six. The APAP-induced decrease in albumin was significantly improved in rats through cell therapy, when compared with that in the APAP-alone treated rats. SRY PCR analysis showed the presence of the transplanted cells in the liver of transplanted rats. Stearic acid-rich diet in combination with cell therapy accelerates the recovering of hepatic dysfunction in a rat model of liver injury.
/EXPL THER/ Because of their reported antiviral and anti-inflammatory activities, cream formulations containing n-docosanol (docosanol) or stearic acid were tested for effects on chemically-induced burns in mice. In this model, injury was induced by painting the abdomens of mice with a chloroform solution of phenol. This was followed by the topical application of test substances 0.5, 3, and 6 hr later. Progression of the wounds was assessed by a single evaluator after 8 hr, using a numerical score of gross morphology. Docosanol- and stearic acid-containing creams substantially and reproducibly lessened the severity and progression of skin lesions compared to untreated sites with a 76% and 57% reduction in mean lesion scores, respectively. Untreated wounds appeared red and ulcerated; docosanol cream-treated wounds showed only slight 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.)