| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
The primary target of 2-Fluoropalmitic acid is long-chain acyl-CoA synthetase (ACSL), an enzyme that catalyzes the formation of acyl-CoA from fatty acids, ATP, and CoA. It also inhibits sphingosine biosynthesis, thereby affecting cellular lipid metabolism. By inhibiting ACSL, the compound disrupts the activation of long-chain fatty acids, a critical step in their subsequent metabolic processing. This enzyme is essential for lipid homeostasis, and its inhibition can lead to altered energy metabolism in cells. The compound's specificity for different ACSL isoforms is determined by the fatty acid's carbon chain length, with palmitic acid derivatives showing high affinity for long-chain ACSLs.
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| ln Vitro |
In vitro studies demonstrate that 2-Fluoropalmitic acid effectively inhibits glioma stem cell (GSC) viability and the stem-like phenotype at concentrations ranging from 12.5 to 50 ug/ml. It suppresses the expression of phospho-ERK, CD133, and SOX-2, while also reducing MMP-2 activity and increasing MGMT promoter methylation. The compound exhibits significant cytotoxicity against human leukemia cell lines (e.g., MOLT-4) but shows minimal toxicity to normal human dermal fibroblasts (HDF), indicating selectivity for cancer cells. Additionally, it inhibits long-chain acyl-CoA synthetase activity with an IC₅0 of 0.2 mM, as measured by palmitoyl-CoA formation in Balb/c 3T3 cell lysates. The compound is also incorporated into membrane lipids, including phosphatidylcholine and sphingomyelin, without modification.
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| ln Vivo |
In vivo studies have indicated that 2-Fluoropalmitic acid possesses antitumor activity. Palmitic acid, a related compound, has shown in vivo antitumor effects in mouse models, and 2-Fluoropalmitic acid is expected to exhibit similar activity. The compound is being explored as a potential anti-glioma agent, with physiological studies required to further examine its efficacy in vivo against glioblastoma. It inhibits sphingosine biosynthesis and long-chain acyl-CoA synthetase, with an IC₅0 of 0.2 mM, and is considered a candidate for anti-glioma research. However, comprehensive in vivo pharmacokinetic and efficacy data are still needed to fully establish its therapeutic potential in animal models.
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| Enzyme Assay |
Standard in vitro enzyme inhibition assays for acyl-CoA synthetase activity are conducted using cell lysates or purified enzyme preparations. The reaction mixture typically contains the enzyme source, substrate (e.g., palmitic acid), CoA, ATP, and magnesium ions. After incubation at 37degC for a specified time (e.g., 30-60 minutes), the formation of palmitoyl-CoA is quantified by HPLC or a coupled enzyme assay. For 2-Fluoropalmitic acid, inhibition is measured by pre-incubating the enzyme with various concentrations of the compound (e.g., 0-1 mM) before adding the substrate. The IC₅0 is determined by fitting a dose-response curve to the inhibition data. Sphingosine biosynthesis inhibition can be assessed using radiolabeled substrates and measuring labeled sphingolipid products.
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| Cell Assay |
Cellular activity is typically evaluated using cancer cell lines such as MOLT-4 (leukemia) or various glioma stem cell (GSC) lines. Cells are seeded in 96-well plates and treated with increasing concentrations of 2-Fluoropalmitic acid (e.g., 12.5-50 ug/ml) for 48-72 hours. Cell viability is assessed using standard assays such as MTT or CellTiter-Glo. Apoptosis is detected using Annexin V-FITC/PI staining followed by flow cytometry. For mechanism studies, cells are lysed and analyzed by Western blot for target proteins including ERK, CD133, and SOX-2. The compound is typically dissolved in DMSO and diluted in culture medium (final DMSO concentration ≤0.1%).
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| Animal Protocol |
In vivo efficacy studies commonly utilize xenograft mouse models of glioblastoma. Tumor-bearing mice are administered 2-Fluoropalmitic acid via intraperitoneal (i.p.) or oral (p.o.) routes at doses determined from pilot toxicity studies (e.g., 10-50 mg/kg). Treatment is typically given daily or every other day for 2-4 weeks. Tumor volume is measured every 2-3 days using calipers, and body weight is monitored as an indicator of toxicity. At study endpoint, tumors are excised for histopathological analysis and biomarker evaluation. For pharmacokinetic analysis, blood samples are collected at various time points post-dose to determine plasma concentrations of the compound and its metabolites.
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| ADME/Pharmacokinetics |
Detailed pharmacokinetic data for 2-Fluoropalmitic acid are limited. However, based on its structural properties as a fluorinated fatty acid, it is expected to have high plasma protein binding, extensive tissue distribution, and a long terminal half-life due to its resistance to beta-oxidation. The fluorine substitution likely reduces metabolic clearance via beta-oxidation and may enhance oral bioavailability. Similar fluorinated fatty acids have shown slow elimination from tissues. The compound's lipophilic nature suggests it readily crosses cell membranes and partitions into lipid bilayers. Comprehensive PK studies are needed to determine parameters such as Cmax, Tmax, AUC, and bioavailability.
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| Toxicity/Toxicokinetics |
Available toxicological data suggest that 2-Fluoropalmitic acid has a favorable safety profile. Concentrations of 12.5-50 ug/ml show significant cytotoxicity against human leukemia cell lines (e.g., MOLT-4) but have no obvious toxicity to normal fibroblasts (HDF cells), indicating a degree of selectivity for cancer cells. In bacterial reverse mutation tests, the compound is considered non-mutagenic at concentrations up to 5000 ug/plate. Further in vivo toxicity studies are required to assess potential organ-specific toxicities and to determine the maximum tolerated dose (MTD) in animals. Long-term toxicity and genotoxicity profiles remain to be fully characterized in preclinical models.
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| References | |
| Additional Infomation |
2-Fluorohexadecanoic acid is a long-chain fatty acid and also a fluorinated fatty acid.
2-Fluoropalmitic acid serves as a valuable research tool for studying fatty acid metabolism, particularly the role of ACSL and sphingolipid biosynthesis in cancer progression. Its resistance to beta-oxidation makes it useful in metabolic flux analyses. The compound is not currently approved for clinical use but is classified as a biochemical tool for research purposes. It is available with high purity (typically ≥98%) and has a molecular weight of 274.41 g/mol with formula C1₆H31FO2. Storage recommendations include maintaining the powder at -20degC, with solutions prepared in DMSO for cell-based assays. As an acyl-CoA synthetase inhibitor, it enables researchers to better understand metabolic disorders such as obesity, diabetes, and cardiovascular diseases. |
| Molecular Formula |
C16H31O2F
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| Molecular Weight |
274.41454
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| Exact Mass |
274.23
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| CAS # |
16518-94-8
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| PubChem CID |
1560
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| Appearance |
White to off-white solid powder
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| Density |
0.9±0.1 g/cm3
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| Boiling Point |
376.1±12.0 °C at 760 mmHg
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| Flash Point |
181.3±19.6 °C
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| Vapour Pressure |
0.0±1.8 mmHg at 25°C
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| Index of Refraction |
1.444
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| LogP |
7.03
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
14
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| Heavy Atom Count |
19
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| Complexity |
207
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
JGRIJJOLCNCSNX-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C16H31FO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15(17)16(18)19/h15H,2-14H2,1H3,(H,18,19)
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| Chemical Name |
2-fluorohexadecanoic acid
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| HS Tariff Code |
2934.99.9001
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| 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)
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| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~364.42 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (9.11 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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.6442 mL | 18.2209 mL | 36.4418 mL | |
| 5 mM | 0.7288 mL | 3.6442 mL | 7.2884 mL | |
| 10 mM | 0.3644 mL | 1.8221 mL | 3.6442 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.
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