Behenyl alcohol

326.6

326.60

211-546-6

9G1OE216XY

759235|8407

DTXSID4027286

C47498

Colorless waxy solid

D06BB11|D - Dermatologicals

29051900

20.2

10.5

Liquid; OtherSolid; OtherSolid, Liquid; PelletsLargeCrystals; PelletsLargeCrystals, OtherSolid

0.8±0.1 g/cm3

71 °C

180 °C @ Press: 0.22 Torr

142.5±5.2 °C

1.455

Insoluble

Store at or below 25 deg C (77 deg F). Protect from freezing.

6.1X10-8 mm Hg (est)

LD50 intraperitoneal in mouse: > 800mg/kg

Henry's Law constant = 1.6X10-3 atm-cu m/mol at 25 °C (est)

A long-chain, saturated fatty alcohol|Hydroxyl radical reaction rate constant = 3.2X10-11 cu cm/molec-sec at 25 °C (est)

NONH for all modes of transport

-

S24/25

JR1315000

Stable. Combustible. Incompatible with strong oxidizing agents.

P264, P270, P301+P312, P330, P501

H302

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed over-the-counter drug products, incl docosanol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

Leung DT, Sacks SL; Docosanol: A Topical Antiviral for Herpes Labialis; Expert Opin Pharmacother 5 (12): 2567-71 (2004)

|Danger|H225 (14.08%): Highly Flammable liquid and vapor [Danger Flammable liquids]|P210, P233, P240, P241, P242, P243, P261, P264, P270, P271, P273, P280, P301+P312, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P322, P330, P337+P313, P363, P370+P378, P391, P403+P233, P403+P235, P405, and P501|Aggregated GHS information provided by 502 companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

1-Docosanol emission rates from wood smoke were calculated as 0.9 ug/g, 0.2 ug/g, and 4.3 ug/g from oak, eucalyptus and pine, respectively(1). 1-Docosanol emission rate from road dust samples was 6.0 ug/g(2). 1-Docosanol emission rate from pine wood (Pinus elliottii) smoke was measured at 66 ng/g of burnt wood(3).

SEDIMENT: 1-Docosanol was reported as extractable concentrations of 296 and 438 ng/g and bonded concentrations of 152 and 175 ng/g in anoxic continental slope sediment off southwestern Taiwan(1).

URBAN/SUBURBAN: 1-Docosanol was found in California at atmospheric concentrations of 6.6 ng/cu m and 9.3 ng/cu m in Bakersfield and Fresno, respectively(1).|RURAL/REMOTE: 1-Docosanol was found at an atmospheric concentration of 0.5 ng/cu m in Kern Wildlife Refuge, California(1).

1-Docosanol emission rates from cigarettes as 6.8 ug/cigarette(1).

Symptoms of overdose include headache, abdominal pain, increased serum lipase, nausea, dyspepsia, dizziness, and hyperbilirubinemia.

-Ouabain to heart is inhibited by long-chain fatty acids and alcohols; [J. Mol Cell Cardiol 12(9) 847 (1980)] Long-chain fatty acids and alcohols inhibit specific binding of (3)H-labeled ouabain to a particulate fraction from dog heart. The magnitude of inhibition increased with chain length, reaching max with lauric acid, myristoleic acid, and decanol in a series of saturated fatty acids, unsaturated fatty acids, and alcohols, respectively, followed by a decline with longer chain members of homologous series.[KIM RS, LABELLA FS; SPECIFIC BINDING OF|... The anti-HSV activity of acyclovir (ACV) was synergistically enhanced by treatment of cells with docosanol as judged by inhibition of progeny virus production and plaque formation. This drug interaction between ACV and docosanol was observed with laboratory strains of herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), oral and genital clinical isolates of HSV, cytomegalovirus (CMV), and varicella zoster virus (VZV). Near optimal concentrations of docosanol plus ACV inhibited HSV replication >99% more than either drug alone, including emergence of ACV-resistant variants. The response was observed with African Green Monkey kidney cells, normal human foreskin cells, and normal human lung cells. Treatment of cells with docosanol also synergistically intensified the inhibition of HSV production by trifluorothymidine (TFT), adenine arabinoside (Ara-A), and ribavirin. An additive anti-HSV effect was observed with docosanol and phosphonoformate (PFA). No evidence was found for either synergistic inhibition of cellular DNA synthesis or induction of overt cellular toxicity when docosanol was combined with ACV, TFT, Ara-A, ribavirin, PFA, 8-azaguanine, or 5-fluorouracil.|Studies of the influence of fatty acids, which were the component of intestinal mucosal lipids, on the permeability of several drugs across bilayer lipid membranes generated from egg phosphatidylcholine and intestinal lipid have been pursued. The permeability coefficients of p-aminobenzoic acid, salicylic acid and p-aminosalicylic acid (anionic-charged drug) increased when fatty acids such as lauric, stearic, oleic, linoleic and linolenic acid were incorporated into the bilayer lipid membranes generated from phosphatidylcholine. In the presence of methyl linoleate and oleyl alcohol, no enhancing effect on p-aminobenzoic acid transfer was obtained. The effect of fatty acids was more marked at pH 6.5 than at pH 4.5. In contrast, upon the addition of fatty acids to intestinal lipid membranes which originally contained fatty acids, the permeability coefficient of p-aminobenzoic acid tended to decrease, though the permeability through intestinal lipid membranes was larger than that of phosphatidylcholine membranes. The permeability of p-aminobenzoic acid across bilayer lipid membranes from intestinal phospholipids was significantly decreased to about equal that of phosphatidylcholine membranes, and reverted to the value of intestinal lipid membranes when fatty acids were added to intestinal phospholipids. It seemed reasonable to assume that free fatty acids in the intestinal neutral lipid fraction could contribute to the increase in the permeability of p-aminobenzoic acid. On the basis of above results, possible mechanisms for good absorbability of weakly acidic drugs from the intestine are discussed.

LD50 Mouse sc >800 mg/kg|LD50 Mouse ip >800 mg/kg|LD50 Rat oral greater then 10,000 mg/kg

1-Docosanol emission rates from green leaf composite samples and dead leaves were 66 ug/g and 45 ug/g, respectively(1).

1-Docosanol's production and use in synthetic fibers, lubricants and as an evaporation retardant on water surfaces(1) may result in its release to the environment through various waste streams(SRC). 1-Docosanol has also been identified in wood smoke(2), green leaf composite(3), dead leaves(3), paved road dust(3), and cigarettes(3).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.5X10+5(SRC), determined from a structure estimation method(2), indicates that 1-docosanol is expected to be immobile in soil(SRC). Volatilization of 1-docosanol from moist soil surfaces may be expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.6X10-3 atm-cu m/mole(SRC), using a fragment constant estimation method(3). 1-Docosanol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.1X10-8 mm Hg(SRC), determined from a fragment constant method(4). However, adsorption to soil is expected to attenuate volatilization(SRC). 1-Docosanol is expected to biodegrade rapidly based upon estimates from the chemical structure(5).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.5X10+5(SRC), determined from a structure estimation method(2), indicates that 1-docosanol is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 1.6X10-3 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 6 hours and 7.5 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life of 1-docosanol from a model pond is 2 years if adsorption is considered(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from an estimated log Kow of 9.7(7) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is low(SRC). 1-Docosanol is expected to biodegrade rapidly based upon estimates from the chemical structure(9).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 1-docosanol, which has an estimated vapor pressure of 6.1X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase 1-docosanol is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 12 hours(SRC), calculated from its rate constant of 3.2X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase 1-docosanol may be removed from the air by wet or dry deposition(SRC).

The rate constant for the vapor-phase reaction of 1-docosanol with photochemically-produced hydroxyl radicals has been estimated as 3.2X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 12 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 1-Docosanol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2).

An estimated BCF of 3 was calculated for 1-docosanol(SRC), using an estimated log Kow of 9.7(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 1-docosanol can be estimated to be 1.5X10+5(SRC). According to a classification scheme(2),this estimated Koc value suggests that 1-docosanol is expected to be immobile in soil.

The Henry's Law constant for 1-docosanol is estimated as 1.6X10-3 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that 1-docosanol is expected to volatilize rapidly from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 6 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 7.5 days(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life of 1-docosanol from a model pond is 2 years if adsorption is considered(3). 1-Docosanol's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). 1-Docosanol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.1X10-8 mm Hg(SRC), determined from a fragment constant method(4).

SURFACE WATER: 1-Docosanol was identified, but not quantified, in water from Lake Superior (western basin)(1).

1-Docosanol was identified in roasted and boiled Chinese chestnuts (Castanea molissima)(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 1358 workers are potentially exposed to 1-docosanol in the US(1). Occupational exposure to 1-docosanol may occur through dermal contact with this compound at workplaces where 1-docosanol is produced or used(SRC). Monitoring data indicate that the general population may be exposed to 1-docosanol via inhalation of ambient air, ingestion of food and drinking water, and dermal contact with this compound and other products containing 1-docosanol(SRC).

For the topical treatment of recurrent oral-facial herpes simplex episodes (cold sores or fever blisters).|FDA Label

Topical docosanol is indicated in the treatment of recurrent oral-facial herpes simplex (fever blisters or cold sores) in adults. /Included in US product labeling/|Docosanol ... has been approved by the US FDA as a 10% ever-the-counter cream for treatment of recurrent orolabial herpes. Docosanol inhibits the in vitro replication of many lipid enveloped viruses, including HSV /(herpes simplex virus)/, at millimolar concentrations. It dose not directly inactivate HSV but appears to block fusion between the cellular and viral envelope membranes and inhibit viral entry into the cell. Topical treatment beginning within 12 hr of prodromal symptoms or lesion onset reduces healing time by about 1 day and appears to be well tolerated. Treatment initiation at papular or later stages provides no benefit. /Docosanol/|Therap cat: Antiviral (topical)

Adverse effects occurring in 2% or more of patients receiving docosanol include headache (incidence similar to placebo), application site reaction (e.g., burning, stinging) (incidence similar to placebo), and herpes simplex outside the treatment area (incidence similar to placebo).|Docosanol 10% cream is recommended only for use on cold sores/fever blisters.|FDA Pregnancy Risk Category: B /NO EVIDENCE OF RISK IN HUMANS. Adequate, well controlled studies in pregnant women have not shown increased risk of fetal abnormalities despite adverse findings in animals, or, in the absence of adequate human studies, animal studies show no fetal risk. The chance of fetal harm is remote but remains a possibility./

Docosanol is a saturated 22-carbon aliphatic alcohol which exhibits antiviral activity against many lipid enveloped viruses including herpes simplex virus (HSV). Docosanol speeds the healing of cold sores and fever blisters on the face or lips. It also relieves the accompanying symptoms, including tingling, pain, burning, and itching. Docosanol cannot, however, prevent cold sores or fever blisters from appearing.

Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. (See all compounds classified as Antiviral Agents.)

Topical absorption has been shown to be minimal under conditions reflecting normal clinical use.|Absorption of docosanol has been shown to be minimal under conditions reflecting normal clinical use. Of 209 plasma samples taken from ten subjects 24 hours after a multi-day test, only one had a docosanol level above the quantitation limits (19 nanograms/mL).|Long chain alcohols were detected in developing rat brain at their highest level of 0.0109% of the total lipids at the age of 10 days and decreased to 0.0036% at the age of 40 days. They consited mainly of hexadecanol, octadecanol, octadecenol, eicosanol, docosanol, and tetracosanol.|A mixture of cis-9[1(-14)C] octadecenol and [1(-14)C] docosanol was injected into the brains of 19-day-old rats, and incorporation of radioactivity into brain lipids was determined after 3, 12, and 24 hr. Both alcohols were metabolized by the brain but at different rates; each was oxidized to the corresponding fatty acid, but oleic acid was more readily incorporated into polar lipids. Substantial amounts of radioactivity were incorporated into 18:1 alkyl and alk-1-enyl moieties of the ethanolamine phosphoglycerides and into 18:1 alkyl moieties of the choline phosphoglycerides. Even after the disappearance of the 18:1 alcohol from the substrate mixture (12 hr), the 22:0 alcohol was not used to any measurable extent for alkyl and alk-1-enylglycerol formation.

The 22-carbon fatty alcohol, n-docosanol, exhibits in vitro antiviral activity against several lipid-enveloped viruses including herpes simplex viruses 1 and 2 by a mechanism that interferes with normal viral entry into target cells. We previously reported that mammalian cells incorporate significant quantities of radiolabeled n-docosanol. Herein, we report that cells extensively metabolize the internalized fatty alcohol. This is evidenced by incorporation of up to 60% of cell-associated radiolabel into phospholipids that copurify with phosphatidylcholine and phosphatidylethanolamine. Analysis by chemical (Vitride) reduction suggests that a significant portion of n-docosanol is oxidized to n-docosanoic acid and then incorporated as an acyl group on polar lipids. A measurable amount of radiolabel, however, is resistant to Vitride reduction, consistent with incorporation of n-docosanol into ether lipids. The rate and extent of metabolic conversion of n-docosanol vary with the cell type and surfactant used to suspend the compound. Furthermore, the anti-HSV activity of n-docosanol is quantitatively proportional to the amount of metabolism observed. These findings suggest that the anti-HSV activity of n-docosanol involves cellular uptake and metabolism of the drug.|A mixture of cis-9[1(-14)C] octadecenol and [1(-14)C] docosanol was injected into the brains of 19-day-old rats. Both alcohols were metabolized by the brain but at different rates; each was oxidized to the corresponding fatty acid. Substantial amounts of radioactivity were incorporated into 18:1 alkyl and alk-1-enyl moieties of the ethanolamine phosphoglycerides and into 18:1 alkyl moieties of the choline phosphoglycerides.

Docosanol works by inhibiting fusion between the human cell plasma membrane and the herpes simplex virus (HSV) envelope, thereby preventing viral entry into cells and subsequent viral replication. Unlike other cold-sore antivirals, docosanol does not act directly on the virus, and as such it is unlikely it will produce drug resistant mutants of HSV.|n-Docosanol-treated cells resist infection by a variety of lipid-enveloped viruses including the herpesviruses. Previous studies of the mechanism of action demonstrated that n-docosanol inhibits an event prior to the expression of intermediate early gene products but subsequent to HSV attachment. The studies reported here indicate that n-docosanol inhibits fusion of the HSV envelope with the plasma membrane. Evidence suggests that antiviral activity requires a time-dependent metabolic conversion of the compound. Cellular resistance to infection declines after removal of the drug with a t1/2 of approximately 3 h. Reduced expression of viral genes in n-docosanol-treated cells was confirmed by a 70% reduction in expression of a reporter gene regulated by a constitutive promoter inserted into the viral genome. Inhibited release in treated cells of virion-associated regulatory proteins--an immediate post entry event--was indicated by a 75% reduction in the expression of beta-galactosidase in target cells carrying a stably transfected lacZ gene under control of an HSV immediate--early promoter. Finally, the fusion-dependent dequenching of a lipophilic fluorescent probe, octadecyl rhodamine B chloride, inserted into the HSV envelope was significantly inhibited in treated cells. Inhibition of fusion between the plasma membrane and the HSV envelope, and the subsequent lack of replicative events, may be the predominant mechanism for the anti-HSV activity of n-docosanol.|Docosanol reduces viral replication and activity by effectively inhibiting the fusion between the plasma membrane and the herpes simplex virus envelope.

Due to limited transcutaneous absorption and poor oral absorption of docosanol, the potential for an adverse reaction related to an overdose is extremely low. Treatment is essentially symptomatic and supportive.|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/|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/

1-docosanol

Grade: Technical, 99%|Trade name (USA): ABREVA /From table/ /Docosanol/|... Approved by the US FDA as a 10 % over-the-counter cream /Docosanol|Topical: Cream: 10% Abreva, (GlaxoSmithKline).

All other basic organic chemical manufacturing|1-Docosanol: ACTIVE

LANOLIN WAS SAPONIFIED & EXTRACTED WITH PETROLEUM ETHER. NEUTRAL FRACTION OF LANOLIN OBTAINED (WOOL WAX ALCOHOLS) WAS TREATED WITH DIGITONIN & CHOLESTEROL WAS ISOLATED FROM DIGITONIN-POSITIVE FRACTION. AFTER TLC, 5 FRACTIONS WERE ISOLATED FROM DIGITONIN-NEGATIVE FRACTION FROM WHICH SEVERAL STEROIDAL HYDROCARBONS, ONE OF WHICH WAS BEHENYL ALCOHOL, WERE ISOLATED.|1-DOCOSANOL WAS IDENTIFIED & DETERMINED IN EXTRACTS OF PYGEUM AFRICANUM BARK BY GC ON A COLUMN OF 5% OV-7 ON ANACRON ABS WITH FLAME IONIZATION & MASS SPECTROMETRY.

EPA Safer Chemical Functional Use Classes -> Emollients|Safer Chemical Classes -> Green circle - The chemical has been verified to be of low concern|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Fatty Acyls [FA] -> Fatty alcohols [FA05]|Cosmetics -> Emollient