1. Role as a precursor for antiproliferative sophorolipids:
- 1-Hexadecanol (cetyl alcohol) was used as a fatty acid precursor to synthesize novel sophorolipids (C16-SL) via microbial fermentation [1]
- The derived C16-SL showed dose-dependent antiproliferative activity against HeLa cells, with an IC₅₀ value of 125 μM after 48 h treatment; 1-Hexadecanol alone did not exhibit direct antiproliferative activity at tested concentrations (up to 200 μM) [1]
2. Apoptosis induction by C16-SL (derived from 1-Hexadecanol):
- Treatment with C16-SL (150 μM, 24 h) increased the apoptotic rate of HeLa cells to 42.3% (vs. 2.1% in control) as detected by Annexin V-FITC/PI staining [1]
- DAPI staining showed chromatin condensation and nuclear fragmentation in HeLa cells treated with C16-SL, which was attributed to the precursor 1-Hexadecanol’s structural contribution to the sophorolipid’s activity [1]
3. Cell morphological changes:
- HeLa cells treated with C16-SL (100 μM, 24 h) showed shrinkage, loss of adherence, and formation of apoptotic bodies; 1-Hexadecanol alone did not cause such changes [1]

1. HeLa cell culture and proliferation assay (for C16-SL, derived from 1-Hexadecanol):
- HeLa cells were cultured in DMEM medium supplemented with 10% fetal bovine serum (FBS) and antibiotics, maintained at 37°C in a 5% CO₂ incubator [1]
- Cells (5×10³ cells/well) were seeded in 96-well plates and treated with C16-SL (0-200 μM, synthesized using 1-Hexadecanol as precursor) for 24-72 h; 1-Hexadecanol alone (0-200 μM) was used as a control [1]
- MTT solution (5 mg/ml) was added (20 μl/well) and incubated for 4 h; formazan crystals were dissolved in DMSO, and absorbance was measured at 570 nm to calculate cell viability and IC₅₀ [1]
2. Apoptosis detection (Annexin V-FITC/PI staining):
- HeLa cells (1×10⁶ cells/ml) were treated with C16-SL (150 μM) for 24 h; 1-Hexadecanol (150 μM) was used as a control [1]
- Cells were harvested, washed with PBS, stained with Annexin V-FITC and PI for 15 min in the dark, and analyzed by flow cytometry to determine apoptotic rates [1]
3. DAPI staining for nuclear morphology:
- Treated HeLa cells were fixed with 4% paraformaldehyde for 15 min, washed with PBS, and stained with DAPI (1 μg/ml) for 10 min [1]
- Nuclear changes (chromatin condensation, fragmentation) were observed under a fluorescence microscope, with 1-Hexadecanol-treated cells showing no abnormal nuclear morphology [1]

Absorption, Distribution and Excretion
Following ingestion of a 2.0 g/kg dose of cetyl alcohol in rats, partial absorption was observed. Gavage administration of 0.2 mg cetyl alcohol via gastric tube to rats showed good absorption, with 63-96% of the radiolabeled cetyl alcohol detected in lymph. Approximately 15% of the cetyl alcohol remained unchanged as it passed through the small intestinal mucosal cells, but most was oxidized to palmitic acid. The absorption rate in poultry has been reported to be 26%. Following ingestion of a 2.0 g/kg dose in rats, approximately 20% of the dose was excreted in feces in its unchanged molecular form. This is likely due to the interconversion of fatty acids and alcohols, leading to the conversion of palmitic acid to cetyl alcohol as it passes through the intestinal mucosal cells into the intestinal lumen. In rats, cetyl alcohol is also excreted in urine as conjugated glucuronic acid and exhaled carbon dioxide. Following ingestion of a 2.0 g/kg body weight dose in rats, 1-hexadecane was partially absorbed and metabolized, with approximately 20% excreted unchanged in feces.

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Metabolism/Metabolites>
In rats, cetyl alcohol is partially metabolized to palmitic acid after ingestion of a dose of 2.0 g/kg. After administration of 0.2 mg cetyl alcohol via gastric tube to rats, most of the cetyl alcohol is oxidized to palmitic acid as it passes through the small intestinal mucosal cells and is incorporated into triglycerides and phospholipids.
Cetyl alcohol is oxidized to the corresponding fatty acid, palmitic acid, in rats.
Primary fatty alcohols undergo two main reactions in vivo: oxidation to carboxylic acids and direct conjugation with glucuronic acid. The first reaction generates an intermediate aldehyde, from which the carboxylic acid may be completely oxidized to carbon dioxide, excreted as carbon dioxide, or conjugated with glucuronic acid to form ester glucuronide. The extent to which alcohols undergo the second reaction (i.e., direct conjugation with ether glucuronide) appears to depend on the rate of the first reaction; unless high doses are administered, alcohols are typically oxidized rapidly to small amounts of ether glucuronide.

Toxicity Data
LCLo (Rat) = 2,220 mg/m³/6h

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Interactions ... Chymotrypsin loses its activity within 30 minutes in the presence of triethanolamine stearate, tripalmitate, and cetyl alcohol.

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Non-human Toxicity Values LD50 Guinea Pig Dermal Administration < 10 g/kg
LD50 Rat Oral Administration 5 g/kg
LD50 Rat Intraperitoneal Administration 1600 mg/kg
LD50 Mouse Oral Administration 3200 mg/kg
LD50 Mouse Intraperitoneal Administration 1600 mg/kg

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- C16-SL (derived from 1-hexadecyl alcohol) toxicity to normal cells: C16-SL (200 μM) showed low cytotoxicity to Vero cells. (Normal African green monkey kidney cells), cell viability was 81.2% (while HeLa cells were 32.5%) [1]

[1]. Anti-proliferative effect of novel primary cetyl alcohol derived sophorolipids against human cervical cancer cells HeLa. PLoS One. 2017 Apr 18;12(4):e0174241.

[2]. Peroxisome-driven ether-linked phospholipids biosynthesis is essential for ferroptosis. Cell Death Differ. 2021 Aug;28(8):2536-2551.

Hexadecane-1-ol is a long-chain primary fatty alcohol, formed by replacing the hydroxyl group at the 1-position of hexadecane. It is a human metabolite, an algal metabolite, a plant metabolite, and a flavoring agent. It is a long-chain primary fatty alcohol and also a type of hexadecyl alcohol. Cetyl alcohol, also known as 1-hexadecyl alcohol or n-hexadecyl alcohol, is a 16-carbon fatty alcohol with the chemical formula CH3(CH2)15OH. It can be prepared by the reduction reaction of palmitic acid. Cetyl alcohol is a waxy white powder or flakes at room temperature, insoluble in water but soluble in alcohols and oils. Discovered by Chevrenl in 1913, cetyl alcohol is one of the oldest known long-chain alcohols. It may be found in cosmetics and personal care products such as shampoos, creams, and lotions. Cetyl alcohol is mainly used as a sunscreen, emulsifier, and thickener, capable of altering the consistency of liquids and enhancing and stabilizing foaming ability. Due to its water-retaining properties, cetyl alcohol is often used as a moisturizer to prevent dry and chapped skin. According to federal regulations of the U.S. Food and Drug Administration (FDA), cetyl alcohol is a safe synthetic fatty acid that can be used in the synthesis of food and food ingredients, provided that its total alcohol content is not less than 98% and its linear alcohol content is not less than 94%. Cetyl alcohol is also listed as an over-the-counter drug ingredient as a skin protectant to relieve skin irritation caused by poison ivy, poison oak, sumac, and insect bites. Cetyl alcohol has been reported to have mild skin or eye irritation. 1-Hexadecyl alcohol has been found in tea (Camellia sinensis), angelica (Angelica gigas), and other organisms with relevant data. Cetyl alcohol is a synthetic solid fatty alcohol and a nonionic surfactant. Cetyl alcohol is used as an emulsifier in pharmaceutical preparations. Cetyl alcohol, also known as 1-hexadecyl alcohol and palmitol, is a solid organic compound belonging to the alcohol class. Its chemical formula is CH3(CH2)15OH. At room temperature, cetyl alcohol is a waxy white solid or flakes. It belongs to the fatty alcohol class. With the decline of commercial whaling, cetyl alcohol is no longer primarily produced from whale oil, but rather as a final product of the petroleum industry or from vegetable oils such as palm and coconut oil. Cetyl alcohol is produced from palm oil, hence one of its alternative names is palm alcohol.
See also: cetyl alcohol; cetyl palmitate; tylosap (ingredient); moringa leaf oil (partial); C14-18 alcohol (note moved to)...see more...

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Drug Indications
No drug indications. Can be used as an indirect additive to food contact substances, or as a commercial or cosmetic ingredient.

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Mechanism of Action
Cetyl alcohol has moisturizing properties, making it a suitable emulsifier and stabilizer in pharmaceutical preparations. It is also present in washable ointment bases due to its dispersibility and stability. The potential antibacterial activity of cetyl alcohol may result from altered cell membrane permeability, which hinders the absorption of essential nutrients and induces the outward diffusion of important cellular components. The proposed mechanism of action is thought to be similar to other long-chain fatty alcohols with the same antibacterial activity, such as myristol and behenol.

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Therapeutic Uses
Synthetic surfactants (Exosurf) and their non-surfactant components, tylosaprol and cetyl alcohol, can act as antioxidants; in vivo infusion has been associated with a reduction in hyperoxia-induced injury in rats.

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Pharmacodynamics
Cetyl alcohol has a dermal protective effect, combating skin irritation caused by bites, rashes, and stings. Cetyl alcohol has been reported to inhibit the growth of Mycoplasma gallisepticum and Mycoplasma pneumoniae.

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1. Chemical background of 1-hexadecyl alcohol:
-1-hexadecyl alcohol (cetyl alcohol) is a saturated fatty alcohol containing 16 carbon atoms, and is commonly used as a precursor for the synthesis of lipids and surfactants[1]
2. Synthesis of C16-SL using 1-hexadecyl alcohol:
-1-hexadecyl alcohol was added as a carbon source to a microbial culture (Candida bombicola), and fermented at 30°C for 120 hours. The resulting sophorolipid (C16-SL) was purified by solvent extraction and column chromatography[1]
3. Mechanism of action of C16-SL (derived from 1-hexadecyl alcohol):
-C16-SL may induce apoptosis in HeLa cells by disrupting the cell membrane and activating apoptosis signaling pathways;
1-hexadecyl alcohol itself does not trigger such a mechanism[1]

C16H34O

242.4406

242.26

36653-82-4

1-Hexadecanol-d5;1219799-18-4;1-Hexadecanol-d4;1398065-49-0;1-Hexadecanol-d31;203633-15-2;1-Hexadecanol-d33;284474-73-3;1-Hexadecanol-d3;75736-52-6

2682

White to off-white solid powder

0.8±0.1 g/cm3

310.9±5.0 °C at 760 mmHg

49-51 °C

135.0±0.0 °C

0.0±1.5 mmHg at 25°C

1.448

7.25

1

1

14

17

123

0

BXWNKGSJHAJOGX-UHFFFAOYSA-N

InChI=1S/C16H34O/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17/h17H,2-16H2,1H3

hexadecan-1-ol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~10 mg/mL (~41.25 mM)

Solubility in Formulation 1: 1 mg/mL (4.12 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 10.0 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of 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: ≥ 1 mg/mL (4.12 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 10.0 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.)