Absorption, Distribution and Excretion
In rats fed a diet containing 25% spirulina, the heptadecane content in the adipose tissue of male and female rats was 80.2 and 272 mg/g, respectively, while the content in the lungs and muscles was approximately 10-20 mg/kg, respectively. After oral administration of 1 g of heptadecane to rats, the concentrations of heptadecane in the intestinal wall, liver, intestinal contents, and feces were 0.7%, 1.4%, 1.2%, and 0.2%, respectively. /Milk/ Pigs fed a diet containing 52 ppm of heptadecane for 12 months showed the excretion of small amounts of heptadecane in their lactating milk. The partition coefficients (PCs) of octane, nonane, decane, undecane, and dodecane (n-C8 to n-C12 n-alkanes) in rat tissue/air and blood/air were determined using the vial balance method. The blood/air PC values for n-C8 to n-C12 were 3.1, 5.8, 8.1, 20.4, and 24.6, respectively. The lipid solubility of n-alkanes increases with increasing carbon chain length, indicating that lipid solubility is a crucial factor determining the blood/air PC value of n-alkanes. The PC values for muscle/blood, liver/blood, brain/blood, and fat/blood were: octane (1.0, 1.9, 1.4, and 247), nonane (0.8, 1.9, 3.8, and 274), decane (0.9, 2.0, 4.8, and 328), undecane (0.7, 1.5, 1.7, and 529), and dodecane (1.2, 1.9, 19.8, and 671). The tissue/blood PC value was highest in fat and lowest in muscle. The brain/air PC value for undecane was inconsistent with the PC values of other n-alkanes. Using the measured partition coefficients of n-alkanes, linear regression was employed to predict the tissue (excluding brain tissue) and blood/air partition coefficients of longer-chain n-alkanes (tetane, tetradecane, pentadecane, hexadecane, and heptadecane, i.e., n-C13 to n-C17). The measured tissue/air and blood/air partition coefficients for n-C8 to n-Cl2 showed good agreement with the predicted values, enhancing our confidence in the prediction of long-chain n-alkane partition coefficients. For more complete data on the absorption, distribution, and excretion of heptadecanes (6 in total), please visit the HSDB record page.

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Metabolism / Metabolites
This study investigated the in vitro metabolism of n-heptadecane using liver microsomes from Hubbard chickens, New Zealand rabbits, Westa rats, and rainbow trout. After 1 hour of incubation with 14C-labeled alkanes, differences in oxidation rates were observed among the species; the oxidation rate in chickens (per mg of protein) was approximately 20 times that of rainbow trout and approximately 10 times that of rats and rabbits. Based on cytochrome P-450 content, the heptadecane metabolism rate in chickens was approximately 20 times that of other species. Furthermore, a λmax Soray band of the reduced cytochrome P-450-CO complex at a wavelength of 452 nm was observed in chickens. The correlation between heptadecane metabolism rate and in vivo storage levels was also discussed.

Toxicity Summary
Identification and Uses: Heptadecane is a higher n-alkane containing 17 carbon atoms (C17). It can be used as a feedstock in hydrocracking processes. It is also used in oxidation and chlorination reactions. Human Exposure and Toxicity: No relevant data are currently available. Animal Studies: A series of homologues of n-alkanes with n-C12 to n-C31 carbon atoms have been found in the liver, heart, kidneys, muscle, and adipose tissue of cattle.

Hexagonal leaves. (NTP, 1992)
Heptadecane is a straight-chain alkane containing 17 carbon atoms. It is a component of the essential oils of plants such as cactus (Opuntia littoralis) and custard apple (Annona squamosa). It is both a volatile oil component and a plant metabolite.
Heptadecane has also been reported to be found in tea tree (Camellia sinensis), Madagascar vanilla (Vanilla madagascariensis), and other organisms with relevant data.

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Mechanism of Action
Heptadecane, a volatile component of Spirulina platensis, can inhibit de novo fatty acid synthesis and improve various oxidative stress-related diseases. Under redox conditions disrupted by oxidative stress, multiple kinases activate NF-κB, leading to upregulation of pro-inflammatory gene expression. Therefore, identifying and regulating novel substances that can modulate NF-κB is currently a research hotspot. This study investigated the ability of heptadecane to inhibit redox-related NIK/IKK and MAPK pathway-mediated inflammatory NF-κB activation in aged rats. In the first part of the study, 9-month-old and 20-month-old Fischer 344 rats were administered heptadecane at an average dose of approximately 20 or 40 mg/kg body weight for 10 consecutive days. This study explored the anti-inflammatory activity of heptadecane by examining its ability to inhibit COX-2 and iNOS (both NF-κB-related genes) gene expression and reactive oxygen species (RS) generation in senescent kidney tissue. The second part of the study explored the molecular mechanism of heptadecane's anti-inflammatory effect using YPEN-1 cells (an endothelial cell line), specifically by examining its regulatory role in NF-κB and its signaling pathway. Results showed that heptadecane possesses significant antioxidant activity, protecting YPEN-1 cells from tert-butyl hydroperoxide-induced oxidative stress damage. Further molecular studies revealed that heptadecane attenuates RS-induced NF-κB activity in YPEN-1 cells and senescent kidney tissue through the NIK/IKK and MAPK pathways. Based on these results, we conclude that heptadecane inhibits age-related increases in pro-inflammatory gene expression by upregulating RS-induced NIK/IKK and MAPK pathways and reducing NF-κB activity. These findings provide new insights into the molecular mechanism by which heptadecane exerts its anti-inflammatory effect in aged kidney tissue.

C17H36

240.47

240.282

629-78-7

12398

Hexagonal leaflets Leaflets Colorless liquid

0.777 g/mL at 25 °C(lit.)

302 °C(lit.)

72 °F (NTP, 1992) ; 21.97 °C

300 °F

1 mm Hg ( 115 °C)

n20/D 1.436(lit.)

6.878

0

14

17

103

0

CCCCCCCCCCCCCCCCC

NDJKXXJCMXVBJW-UHFFFAOYSA-N

InChI=1S/C17H36/c1-3-5-7-9-11-13-15-17-16-14-12-10-8-6-4-2/h3-17H2,1-2H3

heptadecane

Heptadecane

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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