Palmitic acid

SKU: orb1304861

Description

Palmitic acid, a ubiquitous saturated fatty acid present across biological kingdoms, exhibits documented antitumor properties. It is widely utilized in biochemical research to study lipid metabolism, cancer biology, and as a key component in both in vitro cell culture studies and in vivo metabolic research models.

Research Area

Metabolism Research, Signal Transduction

Key Properties

• CAS Number: 57-10-3
• MW: 256.42
• Purity: 99.87% (May vary between batches)
• Formula: C₁₆H₃₂O₂
• SMILES: O=C(O)CCCCCCCCCCCCCCC
• Target: Endogenous Metabolite,HSP
• Solubility: 10% DMSO+40% PEG300+5% Tween 80+45% Saline:0.26 mg/mL (1.01 mM);DMSO:100 mg/mL (389.99 mM);Ethanol:40.83 mg/mL (159.23 mM)

Bioactivity

• Target IC50:
  Colo-320-DM cells:0.35 µg/mL|Caco-2 cells:0.75 µg/mL|MCF-7 cells:0.55 µg/mL|WRL-68 cells:1 µg/mL
• In Vivo:
  METHODS: To investigate the effects on adverse biological behaviors in mice, Palmitic acid (0.3-30 μmol/mouse in castor oil) was administered as a single intraperitoneal injection to C57BL/6J mice, and biological behaviors were analyzed 2-24 h later. RESULTS: In a dose-dependent manner, Palmitic acid rapidly reduced locomotor activity in mice through a mechanism dependent on fatty acid chain length. 24 h after Palmitic acid administration, mice exhibited anxiety-like behaviors, whereas there was no impairment of locomotion, food intake, depression-like behaviors, or spatial memory. METHODS: To investigate the effects on myocardial injury, Palmitic acid (5 mM in 500 μL solution) was injected intravenously into the tail of wild-type C57BL/6 (B6) and Md2-/- (KO) mice once a day for seven days. RESULTS: Palmitic acid induced myocardial inflammatory injury via TLR4 accessory protein MD2 and protected Md2 knockout mice from myocardial injury induced by Palmitic acid and high-fat diet.
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• In Vitro:
  METHODS: Mouse microglia BV2 were treated with Palmitic acid (25-200 nM) for 6-48 h, and cell viability was measured by MTT. RESULTS: Palmitic acid had concentration- and time-dependent inhibitory effects on microglia viability. METHODS: Monocyte-derived dendritic cells MoDC were treated with Palmitic acid (150 μM) for 12 h. The expression of DC co-stimulatory factors was measured by Flow Cytometry. RESULTS: Palmitic acid induced the expression of CD86 and CD83, indicating that the activation and maturation of MoDC were induced simultaneously.
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• Cell Research:
  Cell Experiment Solubilisation Formula: 1. Dissolve 1 mg of palmitic acid in 78 μL of anhydrous ethanol to obtain a 50 mM stock solution; if a higher concentration is required, dissolve 1 mg of palmitic acid in 39 μL of anhydrous ethanol to obtain a 100 mM stock solution. 2. Prepare a 10% BSA solution using culture medium (e.g., DMEM); BSA without fatty acids is preferable, with a concentration of 100 mg/mL. 3. For the solvent control group, prepare ethanol and BSA control solutions at the corresponding concentrations without lipids. 4. As an example of preparing 1 mL of a 0.25 mM working solution, mix 5 μL of 50 mM palmitic acid stock solution + 100 μL of 10% BSA solution + 895 μL of culture medium. The final solution will contain 1% BSA. The ethanol concentration should be controlled between 0.1%~0.5%. 5. Filter the working solution using a sterile filter membrane for use in cell processing.
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Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Inhibitor, inhibit, Palmitic acid, hexadecanoic acid, Hexadecoic acid, Heat shock proteins, EndogenousMetabolite, Endogenous Metabolite, HSP, Cetylic acid

Compound Identifiers

PubChem CID

985