Hentriacontane (1, 5, 10 μM, 1h) can reduce inflammatory parameters such as TNF-a, IL-6 and IL-1b in RAW 264.7 cells[1]. Hentriacontane

Hentriacontane (1, 2, 5 mg/kg, oral, single dose) can effectively inhibit inflammatory factors in the LPS-induced mouse inflammation model[1].

Western Blot Analysis[1]
Cell Types: RAW 264.7
Tested Concentrations: 1, 5, 10 μM
Incubation Duration: 1 h
Experimental Results: Increased the phosphorylation of NF-kB p65.

Animal/Disease Models: LPS-induced mice inflammation model[1]
Doses: 1, 2, 5 mg/kg
Route of Administration: p.o.
Experimental Results: Inhibited TNFa、IL-6 and IL-1b.

Absorption, Distribution and Excretion
Samples were collected from the liver, heart, kidneys, muscle, and adipose tissue (perirhinal and subcutaneous) of six cattle for hydrocarbon composition analysis. Qualitative and quantitative analyses were performed using gas chromatography and gas chromatography-mass spectrometry. Despite varying proportions, a range of homologous n-alkanes with carbon chain lengths ranging from n-C12 to n-C31 were found in all samples. Additionally, isoprene hydrocarbons phytane and phyene (phyene-1 and phyene-2) were identified. (These findings are relevant to human health from consuming hydrocarbon-contaminated meat.) /n-Alkanes/ This report describes a novel human disease characterized by the accumulation of long-chain n-alkanes from plants in the viscera of human patients. Lipid analysis of tissue from an adult male who died suddenly (with diffuse visceral granuloma containing lipophilic crystalline material) revealed the presence of anomalous compounds, identified as long-chain n-alkanes with carbon numbers of 29 (n-nonacosane), 31 (n-hexadecane), and 33 (n-trisane). Studies of the distribution of n-alkanes in the patient's tissues showed that these compounds mainly accumulated in the lumbar aortic lymph nodes, adrenal glands, lungs (highest concentration in pulmonary granulomas), and liver; significantly lower concentrations were found in the myocardium and kidneys, while they were not detected in brain tissue. Based on the structural composition and tissue distribution of these accumulated n-alkanes, this article explores their dietary (plant) sources and their pathophysiological mechanisms in tissues.

Toxicity Summary
Identification and Uses: Heptane is a higher n-alkane containing 31 carbon atoms (C31). It is used as a conventional medicine and in experimental therapies. Human Exposure and Toxicity: A case report describes a human disease characterized by the accumulation of long-chain n-alkanes from plants in the internal organs. Diffuse visceral granulomas contained lipophilic crystalline substances, indicating the presence of long-chain n-alkanes, including heptane. Studies of the distribution of n-alkanes in patient tissues showed significant accumulation in the lumbar aortic lymph nodes, adrenal glands, lungs, and liver; significantly lower levels were detected in the myocardium and kidneys, while no levels were detected in brain tissue. Animal Studies: Heptane can cause "paraffin liver" in cattle. The abnormal substance was found in very high levels in the bovine liver, indicating low toxicity and clearly the result of long-term accumulation.

[1].Khajuria V, Gupta S, Sharma N, Kumar A, Lone NA, Khullar M, Dutt P, Sharma PR, Bhagat A, Ahmed Z. Anti-inflammatory potential of hentriacontane in LPS stimulated RAW 264.7 cells and mice model. Biomed Pharmacother. 2017 Aug;92:175-186. doi: 10.1016/j.biopha.2017.05.063. Epub 2017 May 23. PMID: 28549290.

Heptane is a long-chain alkane with anti-tuberculosis activity. It has been reported to be found in plants of the genus Euphorbia piscatoria, Vanilla madagascariensis, and other organisms with relevant data. Oldenlandia diffusa (OD) has long been used as a natural medicine for treating cancer in Asia, particularly in Korea. However, the anti-inflammatory mechanism of OD is not fully understood. This study aimed to investigate the effects of OD and one of its components, heptane, on lipopolysaccharide (LPS)-induced inflammatory responses in mouse peritoneal macrophages. The results showed that OD inhibited the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and prostaglandin E2 (PGE2). OD also inhibited LPS-induced increases in cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) levels. Studies have shown that the anti-inflammatory effect of OD is achieved by regulating the activation of nuclear factor (NF)-κB and caspase-1. Furthermore, hexadecane can also improve the expression of inflammatory mediators (TNF-α, IL-6, PGE2, COX-2, and iNOS) and the activation of NF-κB and caspase-1 in LPS-stimulated peritoneal macrophages. These results provide new insights into the pharmacological effects of OD, making it a potential candidate drug for developing new drugs to treat inflammatory diseases. Ulcerative colitis (UC) is an inflammatory bowel disease, belonging to the category of chronic gastrointestinal diseases. Oldenlandia diffusa (OD), as a traditional Chinese medicine, has long been used to treat inflammation. However, the regulatory role of OD in intestinal inflammation and its molecular mechanisms remain unclear. This study investigated the protective effect of OD against dextran sulfate sodium (DSS)-induced colitis. Mice treated with DSS exhibited significant clinical symptoms, including weight loss and shortened colon length. Administration of OD alleviated these symptoms and significantly inhibited the levels of interleukin (IL)-6, IL-1β, and cyclooxygenase-2 expression in DSS-treated colonic tissue. OD also reduced the transcriptional activity of nuclear factor-κB p65 in DSS-treated colonic tissue. One of the components of OD, hexadecane, alleviated DSS-induced weight loss, colonic shortening, and elevated IL-6 levels. In summary, the experimental results suggest that OD may be a useful therapeutic agent for patients with ulcerative colitis (UC). One treatment method for diabetes is to reduce postprandial hyperglycemia by inhibiting major carbohydrate hydrolases. This study used enzyme inhibition assays (α-amylase, α-glucosidase, and dipeptidyl peptidase-IV) to test the antidiabetic potential of crude extracts of the seaweed Turbinaria ornata. Among the tested extracts, the methanol and acetone extracts showed significant inhibitory effects on α-amylase (IC50 250.9 μg/mL), α-glucosidase (535.6 μg/mL), and dipeptidyl peptidase-4 (55.2 μg/mL), respectively. The free radical scavenging activity (65%) of these extracts was analyzed using the DPPH assay. In vitro toxicity tests of the extracts were performed using DNA fragmentation, hemolysis, and MTT assays. None of the extracts showed toxicity in the test models. Furthermore, GC-MS analysis revealed the presence of hexadecane, Z,Z-6,28-heptatriendien-2-one, 8-heptadecene, and 1-heptadecanool in the major extracts. Our results suggest that Turbinaria ornata may serve as a potential source for further in vivo studies to investigate its role in controlling hyperglycemia.
A substance that can kill or inhibit the growth of Mycobacterium tuberculosis, used for the treatment of tuberculosis.

C31H64

436.84

436.501

630-04-6

12410

White to off-white solid powder

0.808g/cm3

180 °C / 4mmHg

67-69 °C

313.1ºC

1.451

12.339

0

0

28

31

254

0

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])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]

IUJAMGNYPWYUPM-UHFFFAOYSA-N

InChI=1S/C31H64/c1-3-5-7-9-11-13-15-17-19-21-23-25-27-29-31-30-28-26-24-22-20-18-16-14-12-10-8-6-4-2/h3-31H2,1-2H3

hentriacontane

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)

Typically soluble in DMSO (e.g. 10 mM)

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.)