Benzyl alcohol targets membrane lipids in intact renal epithelial cells (MDCK), decreasing lipid order (increasing fluidity) [1]. It modulates the adenylate cyclase-cAMP system, likely affecting the inhibitory GTP-binding protein Ni (Gi) and possibly the coupling of Ns with the catalytic subunit [1].
In APAP hepatotoxicity models, benzyl alcohol inhibits cytochrome P450 enzymes (Cyp1A2 and Cyp2E1) responsible for APAP metabolic activation [2]. The protective effect against APAP liver injury is dependent on Toll-like receptor 4 (TLR4) signaling, specifically on myeloid cells [3].

In MDCK cells, benzyl alcohol (10-80 mM) induced a dose-dependent decrease in membrane lipid order as measured by steady-state fluorescence anisotropy using TMA-DPH and propionyl-DPH probes. At 10 mM, it significantly increased PGE2- and glucagon-stimulated cAMP synthesis by 23% and 33% respectively, but did not affect basal or vasopressin-stimulated cAMP in the presence of indomethacin. At 40 mM, it decreased vasopressin- and PGE2-stimulated cAMP by 51% and 37% respectively, but not glucagon-stimulated. At 80 mM, it inhibited cAMP under all stimulated conditions. The inhibitory effect of 40 mM benzyl alcohol on vasopressin- and forskolin-stimulated cAMP was reversed by 1 mM Mn2+ (which blocks Ni) [1].
In primary mouse hepatocytes, co-treatment with benzyl alcohol (4.8, 9.6, 19.2 mM) dose-dependently protected against APAP (5 mM)-induced cell death (LDH release) measured at 16 h. APAP alone caused 70±4% LDH release; benzyl alcohol at 9.6 mM reduced LDH release to approximately 40% and at 19.2 mM to about 20%. Benzyl alcohol also reduced APAP-protein adduct formation at 4.5 h (9.6 mM reduced adducts by ~60% compared to APAP alone). However, benzyl alcohol alone caused mitochondrial membrane potential loss at 4.5 h (JC-1 assay, red/green fluorescence ratio decreased dose-dependently) and significant cell death at 46 mM at 16 h (LDH release ~60%) [2].
In primary human hepatocytes, benzyl alcohol (4.8, 9.6, 19.2 mM) did not prevent APAP (10 mM)-induced ALT release at 48 h, and benzyl alcohol alone at 19.2 mM and 46 mM caused toxicity (ALT release increased) [2].
In primary mouse hepatocytes (C57BL/6), APAP (5 mM) increased ROS production (DCF fluorescence) and JNK phosphorylation; benzyl alcohol (1 mg/mL, approx. 9.2 mM) limited both. APAP-induced cell death (trypan blue exclusion) at 8 h was limited by benzyl alcohol [3].

In mice (C57BL/6J) treated with APAP (400 mg/kg i.p.), co-administration of benzyl alcohol (270 mg/kg i.p.) significantly attenuated plasma ALT elevations and centrilobular necrosis at 6 h and 24 h post-APAP. Benzyl alcohol also reduced APAP-protein adducts in total liver and mitochondria at 2 h and 6 h, delayed hepatic GSH depletion (at 0.5 h and 2 h), and reduced GSSG levels and GSSG/GSH ratio at 6 h and 24 h. It reduced mitochondrial Bax translocation, cytosolic release of Smac and AIF at 6 h, and preserved mitochondrial respiratory control ratio at 3 h. Benzyl alcohol reduced plasma mtDNA levels at 6 h (from 15.7±6.1 ng/mL to 5.4±3.6 ng/mL) [2]. However, when administered 2 h after APAP, benzyl alcohol did not significantly protect (ALT: APAP 2573±162 U/L vs APAP+BA 2358±335 U/L at 6 h) [2].
In C57BL/6 mice, benzyl alcohol (270 μg/g i.p., co-administered with APAP 400 mg/kg) reduced serum ALT at 3 h (from ~2000 to ~500 U/L) and 6 h (from ~6000 to ~1500 U/L). Histology showed less necrosis. Benzyl alcohol was protective at doses 135-540 μg/g (135, 270, 540 μg/g all significantly reduced ALT compared to APAP alone), but 810 μg/g with APAP caused death of all mice within 6 h. Benzyl alcohol given as pretreatment (1-24 h before APAP) or post-treatment (1-2 h after APAP, but not 3 h after) reduced ALT at 6 h. Benzyl alcohol reduced APAP-induced serum IL-6, KC, IP-10, HMGB1 (western blot), IL-1β, and IL-18 levels, and reduced caspase-1 cleavage in liver tissues. The protective effect of benzyl alcohol was lost in TLR4 global knockout mice and myeloid-specific TLR4 knockout mice (LyzCre-tlr4-/-), but preserved in hepatocyte-specific (Alb-tlr4-/-), DC-specific (CD11c-tlr4-/-), and adipose-specific TLR4 knockouts. Benzyl alcohol also limited APAP-induced GSH oxidation (GSSG/GSH ratio: APAP 2.7±0.41% vs APAP+BA 1.74±0.3% at 6 h), JNK phosphorylation, and mitochondrial dysfunction (respiratory control ratio) [3].

Cytochrome P450 activity was measured using the 7-ethoxy-4-trifluoromethylcoumarin (7EFC) deethylase assay. Liver homogenates (14,000 × g supernatant) from mice were incubated with 7EFC substrate and varying concentrations of benzyl alcohol (1-10 mM) or DMSO (1-10%) as positive control. The deethylation product was monitored by fluorescence. Benzyl alcohol dose-dependently inhibited P450 activities, causing >30% inhibition at 2.5 mM and >80% inhibition at 10 mM [2].

For cAMP measurements, confluent MDCK cells (grown in serum-free or serum-supplemented medium) were washed, preincubated for 15 min in Hanks‘ balanced salt solution with 20 mM HEPES, 1 mg/mL bovine serum albumin, and 0.5 mM IBMX, then incubated for 5 min with hormones and benzyl alcohol (10-80 mM) in the same buffer. Indomethacin (10 μM) was added during both preincubation and incubation when used. The reaction was stopped with ice-cold ethanol/formic acid (85:15 v/v), extracts evaporated, and cAMP measured by RIA after acetylation [1].
For primary mouse hepatocyte isolation, a two-step collagenase perfusion technique was used. Cells (viability >90%, purity >95%) were plated on collagen I-coated plates (6×10^5 cells/well) in Williams E medium with 100 U/mL penicillin/streptomycin, 10^-7 M insulin, and 10% fetal bovine serum. Cells were co-treated with APAP (5 or 10 mM) and benzyl alcohol (0-46 mM), or each alone. Cell death was assessed by LDH release or ALT activity at 16 h or 48 h. APAP-protein adducts were measured at 4.5 h. Mitochondrial membrane potential was assessed using JC-1 dye (red/green fluorescence ratio) at 4.5 h [2].
In primary mouse hepatocytes, reactive oxygen species (ROS) production was measured using 5- and 6-chloromethyl-2‘,7’-dichlorodihydrofluorescein diacetate (CM-H2DCFDA). Cells were loaded with 1 μM CM-H2DCFDA for 30 min, and fluorescence intensity was measured at 37°C with excitation 490 nm and emission 530 nm. JNK phosphorylation was assessed by western blotting. Cell death was quantified by trypan blue exclusion [3].

Male C57BL/6J mice (8-12 weeks old) were fasted overnight then treated intraperitoneally (i.p.) with APAP (400 mg/kg) dissolved in warm saline. Benzyl alcohol (270 mg/kg) dissolved in saline or saline alone (20 mL/kg) was co-administered i.p. or given 2 h after APAP. Mice were euthanized at 0.5, 2, 6, or 24 h post-APAP. Blood and livers were collected for ALT, GSH, GSSG, protein adducts, western blotting, histology (H&E staining), and mitochondrial isolation [2].
For mitochondrial function, fresh whole-liver homogenates were used to measure oxygen consumption with a Clark-type electrode in the presence of succinate (state 4) and ADP (state 3). Respiratory control ratio (RCR) was calculated as state 3/state 4 [2].
Male C57BL/6 mice (8-12 weeks old, 20-30 g) were fasted 15-16 h then given APAP (400 mg/kg i.p.) in warm saline. Benzyl alcohol was administered i.p. at 270 μg/g body weight (unless otherwise specified) concurrently, as pretreatment (1-24 h before APAP), or as post-treatment (1-3 h after APAP). Doses tested: 135, 270, 540, 810 μg/g. Mice were euthanized at 1-24 h; blood and liver harvested. Serum ALT was measured, and liver sections stained with H&E for necrosis assessment. Cytokines (IL-6, KC, IP-10) were measured by MAGPIX multiplex assay, IL-18 by ELISA, and HMGB1, caspase-1 by western blot. TLR4 knockout mice (global and cell-type-specific: Alb-tlr4-/-, LyzCre-tlr4-/-, CD11c-tlr4-/-, adipose-tlr4-/-) were used to assess mechanism [3].

Absorption, Distribution and Excretion
Transdermal absorption was determined in rhesus monkeys. High absorption rates (56-80%) were observed over 24 hours via closed skin. No correlation was observed between skin permeability and the octanol-water partition coefficient. Under non-closed conditions, skin permeability decreased (32%) due to compound evaporation. High concentrations of benzyl alcohol (5-500 ug/10 mL plasma) were detected in uremic patients undergoing hemodialysis; benzyl alcohol was not detected in normal controls. Rabbits receiving a subcutaneous injection of 1 g of benzyl alcohol excreted 300-400 mg of hippuric acid over the following 24 hours. Rabbits receiving an oral dose of 0.40 g/kg body weight of benzyl alcohol excreted 6.7% of the dose as hippuric acid in urine within 6 hours. In humans and animals, benzyl alcohol is readily absorbed from the gastrointestinal tract. High transdermal absorption rates are observed after topical administration. In rhesus monkeys, 56-80% of the dose was absorbed within 24 hours of topical administration under closed conditions; under open conditions, absorption was lower due to evaporation. In rats, benzyl alcohol was rapidly eliminated at the injection site after intramuscular injection; its disappearance half-life was estimated to be less than 10 minutes. ...
For more complete data on the absorption, distribution, and excretion of benzyl alcohol (6 types), please visit the HSDB record page.

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Metabolism/Metabolites
Benzyl alcohol is normally rapidly oxidized to benzoic acid, which binds to glycine in the liver and is excreted as hippuric acid. However, this metabolic pathway may be underdeveloped in premature infants. Therefore, benzyl alcohol may be metabolized to benzoic acid, which the immature liver cannot bind, leading to benzoic acid accumulation and metabolic acidosis….
Benzyl alcohol is metabolized to benzoic acid via simple oxidation. Therefore, relevant data relate to benzoic acid and sodium benzoate.
Benzyl alcohol is an intermediate in the benzyl acetate metabolic pathway; subsequent metabolism is the same as benzyl alcohol. In adults, benzyl alcohol is oxidized to benzoic acid, which binds with glycine in the liver and is excreted in urine as hippuric acid. Infants have immature metabolic capabilities and therefore a weaker ability to metabolize and excrete benzyl alcohol. Premature infants metabolize benzyl alcohol to benzoic acid more readily than full-term infants, but due to glycine deficiency, they cannot convert benzoic acid to hippuric acid. This leads to the accumulation of benzoic acid. For more complete data on the metabolism/metabolites of benzyl alcohol (a total of 8 metabolites), please visit the HSDB record page. Benzyl alcohol is a known metabolite of toluene in humans.

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Biological Half-Life
In dogs, the plasma half-life of benzyl alcohol prepared in 2.5% saline after intravenous injection at doses of 52 and 105 mg/kg is approximately 1.5 hours. In rats, after intramuscular injection, benzyl alcohol rapidly disappears from the injection site; its disappearance half-life is estimated to be less than 10 minutes.

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Toxicity Summary
Identification: Benzyl alcohol is an aromatic organic alcohol, water-white in color, with a slightly aromatic odor and a pungent, burning taste; it is a preservative, solvent, and local anesthetic. Benzyl alcohol is widely used in various products, including color film developers; dyes for nylon filaments, textiles, and plastic sheets; solvents for dyes, cellulose esters, casein, and waxes; heat-sealing agents for polyethylene films; intermediates for parabens and anisoles; antibacterial agents; cosmetics, ointments, and lotions; ballpoint pen ink; and stencil inks. Human Exposure and Toxicity: Studies have found that benzyl alcohol at concentrations of 3% or higher can irritate the skin. A patch test with 0.65% benzyl alcohol did not cause skin irritation. Benzyl alcohol poisoning can lead to neonatal wheezing syndrome. The course of these infants' illness is characterized by a typical progressive neurological deterioration, severe metabolic acidosis, sudden onset of wheezing respiration, thrombocytopenia, liver and kidney failure, hypotension, cardiovascular failure, and death. Unmetabolized benzyl alcohol was detected in the urine of all infants. Hypersensitivity reactions may occur after parenteral or skin contact with benzyl alcohol. Acute reactions include urticaria, erythema, palpable edema, fatigue, nausea, diffuse angioedema, maculopapular rash, and fever. In the same patient, a delayed-type hypersensitivity reaction characterized by erythema, edema, and vesicles may occur 2 to 3 days after an immediate-type hypersensitivity reaction following a single exposure to benzyl alcohol. Neuromuscular blocking agents containing benzyl alcohol have been reported as contraindicated. Intraditional use of these drugs in newborns or epidural spaces is not recommended. Intravitreal injection of triamcinolone acetonide (TA) at a clinically relevant concentration of 0.225 mg/mL of benzyl alcohol can cause ultrastructural damage and impair function of human retinal pigment epithelial cells within 2 hours. A commercially available TA suspension at a concentration of 9.0 mg/mL can produce toxicity within 5 minutes. Animal studies: In a preliminary irritation study, no irritation was observed when a 10% benzyl alcohol solution was applied as a occlusive patch to the backs of eight male albino rabbits for 24 hours. Undiluted benzyl alcohol was applied to the skin of guinea pigs after hair removal for 24 hours, and a moderate irritation reaction was observed. Acute intravenous toxicity of benzyl alcohol was determined in mice. All strains of mice developed clinical symptoms within 24 hours, including convulsions, dyspnea, and decreased activity. Body weight decreased slightly in the first week after treatment, returning to normal in the second week. Microscopic examination showed local neurodegeneration when 5% benzyl alcohol was injected into the face of cats; while 10% benzyl alcohol produced local anesthesia. In another experiment, rats were orally administered 50, 100, 200, 400, and 800 mg/kg of benzyl alcohol for 13 consecutive weeks. High-dose groups showed clinical symptoms of neurotoxicity, including unsteady gait, dyspnea, and lethargy. Male rats in the 800 mg/kg dose group and female rats in the 200 mg/kg and above dose groups showed reduced body weight gain. Animals in the high-dose groups also showed perioral and nasal hemorrhage, as well as histological lesions in the brain, thymus, skeletal muscle, and kidneys. Fifty pregnant mice were administered benzyl alcohol solution by gavage at a dose of 750 mg/kg/day from days 6 to 13 of gestation and allowed to give birth. Decreased birth weight and weight gain were observed in the pups, but the chemical was not toxic to the mothers and had no effect on pup survival. Genotoxicity tests of benzyl alcohol were performed on five Salmonella Typhimurium strains (TA1535, TA1537, TA97, TA98, and TA100) with and without metabolic activation. The highest ineffective dose at which no toxicity was observed was 5.0 mg/plate for all Salmonella Typhimurium strains. At a concentration of 6.666 mg/plate, a slight inhibition of background colonies was observed in the cultures, but the results were not significant. In mammalian cell genotoxicity assays using CHO cells, benzyl alcohol was negative without metabolic activation and positive after metabolic activation.

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Toxicity Data
LCLo (rat) = 1,000 ppm/8h
Interactions
Acetaminophen (APAP) poisoning is the most common cause of acute liver failure in industrialized countries. Understanding the mechanisms of APAP-induced liver injury, as well as other forms of aseptic liver injury, is crucial for improving patient treatment. Recent studies have shown that danger signals and inflammasome activation play a role in APAP-induced injury. The aim of these studies was to verify whether benzyl alcohol (BA) is a therapeutic agent that protects the liver from APAP-induced liver injury by modulating danger signals. APAP-induced liver injury is partly dependent on the Toll-like receptor (TLR) 9 and the receptor for advanced glycation end products (RAGE) signaling pathway. BA reduced liver injury within a dose range of 135–540 μg/g body weight, or before, during, or after APAP treatment. Furthermore, BA also inhibited APAP-induced release of cytokines and chemokines, as well as high-mobility group box 1 (HMGB1). Furthermore, BA can inhibit the APAP-induced inflammasome signaling pathway, as evidenced by the cleavage of interleukin (IL)-1β, IL-18, and caspase-1 in liver tissue. Interestingly, the protective effect of BA in reducing liver injury and inflammasome activation depends on the TLR4 signaling pathway, rather than TLR2 or CD14. Researchers further explored the protective mechanism of BA using a TLR4 cell type-specific knockout model. These studies found that specific expression of TLR4 in myeloid cells (LyzCre-tlr4-/-) is essential for BA to exert its protective effect. Benzyl alcohol (BA) can protect the liver from acute liver injury induced by acetaminophen (APAP) through a TLR4-dependent pathway and reduce inflammasome activation. BA may be helpful in the adjuvant treatment of APAP and other types of aseptic liver injury.

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Non-human toxicity values
Mouse subcutaneous injection LD50: 950 mg/kg body weight
Rat subcutaneous injection LD50: 1700 mg/kg body weight
Guinea pig intraperitoneal injection LD50: > 400-800 mg/kg body weight
Rat intraperitoneal injection LD50: > 400-800 mg/kg body weight
For more non-human toxicity values (complete data) for benzyl alcohol (20 items in total), please visit the HSDB record page.

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In MDCK cells, 80 mM benzyl alcohol strongly inhibited ligand-stimulated cAMP accumulation, returning to unstimulated values [1].
In primary mouse hepatocytes, benzyl alcohol alone at 46 mM caused significant loss of mitochondrial membrane potential at 4.5 h (JC-1 red/green ratio decreased from ~1.0 to ~0.4) and caused LDH release of approximately 60% at 16 h. At 19.2 mM, LDH release was approximately 20% [2].
In primary human hepatocytes, benzyl alcohol alone at 19.2 mM and 46 mM caused ALT release at 48 h (ALT increased from ~10 U/L (control) to ~30 U/L at 19.2 mM and ~60 U/L at 46 mM) [2].
In mice, co-administration of benzyl alcohol at 810 μg/g (i.p.) with APAP (400 mg/kg) resulted in death of all mice (3/3) within 6 h. Benzyl alcohol alone at 810 μg/g without APAP caused no mortality within 6 h [3].
High doses of benzyl alcohol have known toxicities including respiratory failure, vasodilation, hypotension, convulsions, and paralysis [3].

[1]. Benzyl alcohol increases membrane fluidity and modulates cyclic AMP synthesis in intact renal epithelial cells. Biochim Biophys Acta. 1987 Oct 2;903(2):341-8.

[2]. Benzyl alcohol protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes but causes mitochondrial dysfunction and cell death at higher doses. Food Chem Toxicol. 2015 Dec;86:253-61.

[3]. Benzyl alcohol attenuates acetaminophen-induced acute liver injury in a Toll-like receptor-4-dependent pattern in mice. Hepatology. 2014 Sep;60(3):990-1002.

Benzyl alcohol is a colorless, transparent liquid with a pleasant odor. Its density is slightly greater than water. Its flash point is 90°C (194°F). Its boiling point is 204°C (401°F). Contact may irritate skin, eyes, and mucous membranes. Ingestion may be slightly toxic. It is used in the manufacture of other chemicals. Benzyl alcohol is an aromatic alcohol consisting of a benzene ring with a hydroxymethyl substituent. It is used as a solvent, metabolite, antioxidant, and fragrance. Benzyl alcohol is a metabolite found or produced in Escherichia coli (K12, MG1655 strains). Benzyl alcohol is a liceicide. Benzyl alcohol has been reported in tea trees, water lilies, and other organisms with relevant data. Benzyl alcohol is a metabolite found or produced in Saccharomyces cerevisiae. It is a colorless liquid with a strong burning taste and a slight odor. It is used as a local anesthetic and to relieve pain caused by lidocaine injections. Additionally, it is used in the manufacture of other benzyl compounds, as a pharmaceutical adjuvant, and in fragrances and flavorings. See also: benzyl alcohol; zinc chloride (ingredient); benzyl alcohol; lidocaine hydrochloride (ingredient); benzyl alcohol; camphor (synthetic); menthol (ingredient)... See more...

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Drug Indications
Ulesfia (benzyl alcohol) emulsion is indicated for the topical treatment of head lice infestations in patients 6 months and older. Ulesfia emulsion does not have ovicidal activity.
FDA Label

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Mechanism of Action
Benzyl alcohol inhibits the closure of respiratory pores in lice, causing the drug to block the pores, leading to suffocation and death of the lice.

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Therapeutic Use
Local anesthetic; pharmaceutical excipient
/On April 9, 2009, the U.S. Food and Drug Administration approved a new prescription drug for the treatment of head lice (Pediculosis capitis) infestation. 5% benzyl alcohol emulsion has been approved for marketing as a prescription drug for patients 6 months and older. 5% benzyl alcohol emulsion is the first FDA-approved head lice treatment product with benzyl alcohol as the active pharmaceutical ingredient. Two studies enrolled a total of 628 patients with active head lice infestation for 6 months or more, demonstrating the safety and efficacy of 5% benzyl alcohol emulsion. Subjects received two treatments, each lasting 10 minutes, using either benzyl alcohol emulsion or a local placebo, with a one-week interval between treatments. Fourteen days after the last treatment, over 75% of subjects in the 5% benzyl alcohol emulsion treatment group were lice-free. In two double-blind studies, 25 patients with early progressive idiopathic cataracts (subcapsular or cortical) received one drop of saline solution containing 0.07% benzyl alcohol every 8 hours. Eyelids were kept open for at least 2 minutes. Treatment lasted 22 months. In one study, the control group received a placebo; in the other, the control group received anti-cataract medication. Clinical outcomes were recorded every 30 days for the first 14 months, followed by follow-up for up to 18 and 22 months. Compared with patients receiving placebo or medication, patients treated with benzyl alcohol showed significantly improved visual acuity (VA) at 30 and 60 days (p < .01). Compared with patients receiving placebo and medication, 19 and 17 patients, respectively, treated with benzyl alcohol showed significantly reduced lens opacity (p < .01). During the study, the number of cataract surgeries was significantly increased in patients not treated with benzyl alcohol. One patient treated with benzyl alcohol required surgery after 22 months, compared to 38 patients receiving placebo or medication. Benzyl alcohol was well tolerated except for two patients (4%), one patient tolerated it moderately, and another tolerated it poorly. For more complete data on the therapeutic uses of benzyl alcohol (12 types), please visit the HSDB record page.

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Drug Warnings
Common side effects of 5% benzyl alcohol emulsion include skin, scalp, and eye irritation, as well as numbness at the application site. As with all medications, always use 5% benzyl alcohol as directed on the label to maximize efficacy and minimize risk. This product should only be applied to the scalp or hair attached to the scalp. This product is not approved for use in children under six months of age. Use of this product in preterm infants may result in serious respiratory, cardiac, or brain-related adverse events, such as seizures, coma, or death. Furthermore, because benzyl alcohol molecules are small, they can cross the placental barrier easily, similar to crossing the blood-brain barrier, into immature fetal tissues. Therefore, as a precaution, pregnant women should avoid using products containing benzyl alcohol. Preterm infants in the neonatal intensive care unit may require multiple medications, some of which may contain benzyl alcohol. Since there may not be a safe lower dose of benzyl alcohol for these patients, multi-dose vials containing benzyl alcohol should be avoided whenever alternatives are available. Benzyl alcohol is believed to be associated with increased intraventricular hemorrhage and mortality in very low birth weight infants (VLBW, weighing <1000g) who receive benzyl alcohol-containing flushing solutions. An increased incidence of developmental delay and cerebral palsy was also observed in the same extremely low birth weight infant population, suggesting that benzyl alcohol may have secondary damaging effects. For more complete data on benzyl alcohol (6 in total), please visit the HSDB records page.

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Benzyl alcohol increases membrane fluidity, which can modulate hormone responses in renal tubular cells. The effect on cAMP synthesis depends on the ligand: it enhances PGE2 and glucagon stimulation at low concentrations but inhibits vasopressin and PGE2 at higher concentrations, suggesting different lipid environments for receptor complexes [1].
In APAP hepatotoxicity, benzyl alcohol protects by inhibiting cytochrome P450-mediated metabolic activation of APAP (reducing NAPQI formation and protein adducts) rather than primarily through anti-inflammatory effects. The protection is lost in primary human hepatocytes, indicating species differences. Benzyl alcohol itself causes mitochondrial dysfunction and cell death at high doses, limiting its clinical utility [2].
Benzyl alcohol has been approved by the FDA for treatment of head lice (5% formulation). It is metabolized in the liver by oxidation to benzoic acid, then conjugated with glycine to form hippuric acid for excretion. In APAP overdose models, benzyl alcohol’s protective effect depends on TLR4 expression on myeloid cells and involves reduction of inflammasome activation (caspase-1, IL-1β, IL-18) [3].

C7H8O

108.1378

108.057

100-51-6

27134-46-9

244

Colorless to light yellow liquid

1.0±0.1 g/cm3

204.7±0.0 °C at 760 mmHg

-15 °C

93.9±0.0 °C

0.2±0.4 mmHg at 25°C

1.546

1.03

1

1

1

8

55.4

0

O([H])C([H])([H])C1C([H])=C([H])C([H])=C([H])C=1[H]

WVDDGKGOMKODPV-UHFFFAOYSA-N

InChI=1S/C7H8O/c8-6-7-4-2-1-3-5-7/h1-5,8H,6H2

phenylmethanol

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)

Ethanol :≥ 100 mg/mL (~924.73 mM)
H2O : ~20 mg/mL (~184.95 mM)
DMSO : ≥ 1.8 mg/mL (~16.65 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (23.12 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (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 25.0 mg/mL clear EtOH 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: ≥ 2.5 mg/mL (23.12 mM) (saturation unknown) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (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 25.0 mg/mL clear EtOH 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: ≥ 2.5 mg/mL (23.12 mM) (saturation unknown) in 10% EtOH + 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 25.0 mg/mL clear EtOH stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 33.33 mg/mL (308.21 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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