| Size | Price | Stock | Qty |
|---|---|---|---|
| 1mg |
|
||
| 5mg |
|
||
| 10mg |
|
||
| Other Sizes |
| Targets |
alpha-Eleostearic acid has multiple cellular targets. Its ability to induce apoptosis involves the mitochondrial (intrinsic) pathway, leading to the loss of mitochondrial membrane potential, release of cytochrome c, and activation of caspases-3 and -9. It is also a potent inducer of ferroptosis, a non-apoptotic form of cell death driven by iron-dependent lipid peroxidation. This mechanism involves the accumulation of reactive oxygen species (ROS) and depletion of glutathione (GSH). The compound exhibits antioxidant activity by scavenging free radicals, but its pro-oxidant activity in the context of cancer cells contributes to its cytotoxic effects. It also modulates the expression of various proteins involved in cell cycle regulation and survival signaling, such as Bcl-2 family proteins.
|
|---|---|
| ln Vitro |
α-Eleostearic acid (0-40 μM; 24 h) prevents the proliferation of a few fibroblast and cancer cell lines, such as HT29 and HL60 cells [1]. α-Eleostearic acid (20 μM; 6 h) causes nuclear and cellular fragmentation along with nucleosomal DNA fragmentation, which are typical apoptotic phenomena in HL60 cells [1]. Deferoxamine, vitamin E, Fer-1, and MDA-MB-231 cell death are decreased by α-Eleostearic acid (0.01-100 μM; 72 h) [1].
In vitro, alpha-Eleostearic acid has been shown to be a potent inducer of apoptosis and ferroptosis. In HL60 human leukemia cells, treatment with 20 uM alpha-eleostearic acid for 6 hours causes clear apoptotic phenomena, including nuclear and cellular fragmentation, along with nucleosomal DNA fragmentation. This indicates that the compound triggers the classical biochemical and morphological changes associated with apoptosis. It also exhibits antitumor activity against various other cancer cell lines, including those from breast, colon, and prostate cancers, with IC₅0 values typically in the low micromolar range (e.g., 10-50 uM). The compound's antioxidant activity has been demonstrated in various chemical assays, such as the DPPH radical scavenging assay, where it shows concentration-dependent free radical neutralization. |
| ln Vivo |
α-Eleostearic acid (0.5% of total lipid given; po) reduces lipid peroxidation levels and reverses antioxidant enzyme activity to prevent oxidative stress caused by sodium arsenite in vivo [2]. Oral treatment of tung oil, naturally rich in α-Eleostearic acid, to mice inhibited tumor growth and spread in an orthotopic xenograft model of aggressive TNBC [3].
In vivo, alpha-Eleostearic acid has demonstrated protective effects against oxidative stress. In a study, oral administration of alpha-eleostearic acid at a dose of 0.5% of total lipid given orally (po) was shown to reduce lipid peroxidation levels and reverse antioxidant enzyme activity to prevent oxidative stress caused by sodium arsenite in vivo. This suggests that the compound can be bioavailable and exert systemic antioxidant effects. Another study showed that oral treatment of tung oil, which is rich in alpha-eleostearic acid, could protect against certain metabolic disorders. However, detailed pharmacokinetic and efficacy studies in standard cancer models are more limited compared to the in vitro data. The compound remains a promising nutraceutical lead for further in vivo investigation. |
| Enzyme Assay |
A typical non-cellular antioxidant assay for alpha-Eleostearic acid is the DPPH (2,2-diphenyl-1-picrylhydrazyl) radical scavenging assay. A stock solution of alpha-eleostearic acid is prepared in methanol or ethanol. A 0.1 mM solution of DPPH in methanol is freshly prepared. In a 96-well plate, 100 uL of the DPPH solution is mixed with 100 uL of various concentrations of the test compound (e.g., 1-100 ug/mL) to achieve final concentrations of 0.5-50 ug/mL. The mixture is incubated in the dark at room temperature for 30 minutes. The reduction in absorbance is measured at 517 nm using a microplate reader. The percentage of scavenging activity is calculated as [(Abs control - Abs sample) / Abs control] × 100. Trolox or ascorbic acid is used as a positive control. The IC₅0 value is determined by plotting the percentage inhibition vs. compound concentration and fitting a logistic curve. For a ferroptosis-specific assay, lipid peroxidation can be measured using the TBARS (thiobarbituric acid reactive substances) assay in a cell-free system using liposomes and Fe2+.
|
| Cell Assay |
A typical in vitro cell-based assay for alpha-Eleostearic acid uses the HL60 human promyelocytic leukemia cell line. Cells are cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin at 37degC in a 5% CO2 incubator. For the cytotoxicity assay, 2 × 10⁴ HL60 cells per well are seeded in a 96-well plate. The cells are treated with varying concentrations of alpha-eleostearic acid (0-100 uM) for 24, 48, and 72 hours. Cell viability is measured using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. The IC₅0 value is calculated using non-linear regression. For apoptosis detection, cells are treated with 20 uM of alpha-eleostearic acid for 6 hours. The cells are then stained with Annexin V-FITC and propidium iodide (PI) and analyzed by flow cytometry. DNA fragmentation is also assessed by DNA laddering on an agarose gel. For ferroptosis detection, cells are co-treated with alpha-eleostearic acid and ferroptosis inhibitors (e.g., ferrostatin-1) to confirm the mechanism.
|
| Animal Protocol |
An in vivo animal study for alpha-Eleostearic acid is typically performed to evaluate its protective effects against oxidative stress, for example, in a sodium arsenite-induced toxicity model. Adult male Wistar rats (6-8 weeks old, 180-200 g) are divided into groups (n=6 per group). alpha-Eleostearic acid is mixed into the diet to achieve a final concentration of 0.5% (w/w) of total lipids. The control group receives the standard diet without supplementation. After 7 days of dietary intervention, the rats are challenged with an intraperitoneal (IP) injection of sodium arsenite (5 mg/kg body weight) once daily for 4 weeks to induce oxidative stress. At the end of the treatment period, the rats are euthanized, and blood samples are collected for serum biochemical analysis. Liver tissue is excised and homogenized to measure the level of lipid peroxidation (malondialdehyde, MDA) and the activity of antioxidant enzymes (superoxide dismutase, SOD; catalase, CAT; glutathione peroxidase, GPx) using commercially available colorimetric assay kits. The results are compared between the alpha-eleostearic acid-treated group and the arsenite-only control group to determine the protective effects. All animal protocols must be approved by the Institutional Animal Ethics Committee (IAEC).
|
| ADME/Pharmacokinetics |
The pharmacokinetic (PK) properties of alpha-Eleostearic acid are not fully characterized. As a polyunsaturated fatty acid, it is expected to be well-absorbed from the gastrointestinal tract when administered orally. The compound is likely incorporated into chylomicrons and transported via the lymphatic system. It is metabolized in the liver and other tissues via beta-oxidation, similar to other fatty acids. The conjugated double bond system may make it susceptible to lipid peroxidation. The compound exhibits antioxidant properties, but its pro-oxidant activity in certain contexts (e.g., cancer cells) is due to its ability to generate reactive oxygen species. The half-life in the body is expected to be relatively short, on the order of hours. Detailed parameters such as Cmax, Tmax, and AUC are not readily available from public sources. As a fatty acid, it is widely distributed to tissues.
|
| Toxicity/Toxicokinetics |
No detailed toxicological data is available for alpha-Eleostearic acid. As a naturally occurring fatty acid found in food sources like tung oil, it is generally considered to have low acute toxicity. However, it should be noted that tung oil is not edible due to its irritant properties and can cause gastrointestinal distress if ingested in large quantities. In animal models, the compound was well-tolerated at doses up to 0.5% of total dietary lipids. Standard laboratory safety precautions (gloves, lab coat, eye protection) should be used when handling the pure compound. It should be stored away from heat and light to prevent oxidation. It is for research use only and not intended for human consumption as a supplement or pharmaceutical.
|
| References |
|
| Additional Infomation |
(9Z,11E,13E)-octadecano-9,11,13-trienoic acid is a conjugated linolenic acid with three fully conjugated double bonds at positions 9, 11, and 13, with configurations of cis, trans, and trans, respectively. It has been reported that α-tung acid is found in pomegranate, tall parinirvana, and other organisms with relevant data.
alpha-Eleostearic acid is not an approved drug. It is a natural product used exclusively as a research tool. Its primary research applications are in the fields of cancer biology and cell death. It is a well-known inducer of both apoptosis and ferroptosis, making it a valuable tool for studying the cross-talk between these two forms of regulated cell death. It has potential as a nutraceutical or a lead compound for developing anticancer therapies. No clinical trials have been registered for this compound. For research use only; not for human therapeutic or diagnostic use. |
| Molecular Formula |
C18H30O2
|
|---|---|
| Molecular Weight |
278.43
|
| Exact Mass |
278.224
|
| CAS # |
506-23-0
|
| PubChem CID |
5281115
|
| Appearance |
White to off-white solid powder
|
| Density |
0.9±0.1 g/cm3
|
| Boiling Point |
390.6±11.0 °C at 760 mmHg
|
| Flash Point |
287.4±14.4 °C
|
| Vapour Pressure |
0.0±1.9 mmHg at 25°C
|
| Index of Refraction |
1.491
|
| LogP |
6.66
|
| Hydrogen Bond Donor Count |
1
|
| Hydrogen Bond Acceptor Count |
2
|
| Rotatable Bond Count |
13
|
| Heavy Atom Count |
20
|
| Complexity |
301
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
CCCC/C=C/C=C/C=C\CCCCCCCC(=O)O
|
| InChi Key |
CUXYLFPMQMFGPL-WPOADVJFSA-N
|
| InChi Code |
InChI=1S/C18H30O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18(19)20/h5-10H,2-4,11-17H2,1H3,(H,19,20)/b6-5+,8-7+,10-9-
|
| Chemical Name |
(9Z,11E,13E)-octadeca-9,11,13-trienoic acid
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
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
|
|---|---|
| Solubility (In Vivo) |
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.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.5916 mL | 17.9578 mL | 35.9157 mL | |
| 5 mM | 0.7183 mL | 3.5916 mL | 7.1831 mL | |
| 10 mM | 0.3592 mL | 1.7958 mL | 3.5916 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
