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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

Images & Validation

Key Properties

CAS Number57-10-3
MW256.42
Purity99.87% (May vary between batches)
FormulaC16H32O2
SMILESC(CCCCCCCCCC)CCCCC(O)=O
TargetEndogenous Metabolite,HSP
Solubility10% 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.
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.
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.

Storage & Handling

StoragePowder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
Expiration Date12 months from date of receipt.
DisclaimerFor research use only

Alternative Names

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

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Key Properties

No computed properties available.

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Palmitic acid (orb1304861)

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(Recommended: An additional animal making an allowance for loss during the experiment)

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% DMSO +
%+
% Tween 80 +
%

Available Sizes

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1 ml x 10 mM (in DMSO)
$ 70.00
5 g
$ 90.00
10 g
$ 110.00
25 g
$ 140.00
50 g
$ 190.00
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