- Myristic acid targets bacterial ABC transporter BmrA (IC50 for BmrA ATPase activity: ~12 μM; IC50 for rhodamine 6G efflux inhibition: ~15 μM) [2]
- Myristic acid targets the NF-κB pathway (modulates phosphorylation of IκBα and nuclear translocation of NF-κB p65) in LPS-induced BV-2 microglial cells [4]
- Myristic acid targets the ubiquitination pathway (regulates expression of ubiquitin-like protein 1, UBQLN1) in bovine mammary epithelial cells [1]

- In bovine mammary epithelial cells, treatment with Myristic acid (50–200 μM) for 24 h dose-dependently reduced triglyceride (TG) content (by 18–42% vs. control) and downregulated UBQLN1 expression (by 25–60% at mRNA and protein levels). It also decreased phosphorylation of acetyl-CoA carboxylase α (ACCα) (by 30–55%) and reduced fatty acid synthase (FASN) expression, indicating inhibition of de novo lipogenesis [1]
- In purified bacterial BmrA protein, Myristic acid (5–50 μM) dose-dependently inhibited ATPase activity (max inhibition: ~70% at 50 μM) and blocked rhodamine 6G efflux (max inhibition: ~65% at 50 μM), suppressing BmrA-mediated multidrug resistance [2]
- In human skin fibroblasts treated with TNF-α (10 ng/mL), Myristic acid (10–40 μM) for 24 h reduced secretion of pro-inflammatory cytokines IL-6 (by 22–58%) and IL-8 (by 19–52%) via downregulating TLR4/MyD88 signaling [3]
- In LPS-induced BV-2 microglial cells, Myristic acid (10–40 μM) for 24 h decreased mRNA levels of TNF-α (by 35–72%), IL-1β (by 30–68%), and iNOS (by 28–65%), and inhibited phosphorylation of IκBα (by 40–70%) and nuclear translocation of NF-κB p65 (by 38–68%) [4]

- In DNFB-induced atopic dermatitis (AD) mouse model: Mice were treated with Myristic acid (2.5% or 5% in Vaseline) via topical application on the ears once daily for 7 days. The 5% dose reduced ear swelling (by ~45% vs. AD model group), decreased epidermal thickness (by ~38%), and lowered dermal infiltration of mast cells (by ~42%). It also improved mechanical nociception (increased paw withdrawal threshold by ~35% vs. model group) by inhibiting spinal TRPV1 expression [3]

- BmrA ATPase Activity Assay: Purified BmrA protein was incubated with Myristic acid (5–50 μM) in reaction buffer containing ATP (5 mM) at 37°C for 30 min. Released inorganic phosphate (Pi) was measured using a colorimetric assay, and ATPase activity was calculated as nmol Pi/min/mg protein. Dose-response curves were generated to determine IC50 [2]
- BmrA-Mediated Rhodamine 6G Efflux Assay: E. coli cells expressing BmrA were loaded with rhodamine 6G (10 μM) for 30 min, then treated with Myristic acid (5–50 μM) and ATP (2 mM). Fluorescence intensity of rhodamine 6G remaining in cells was measured at 525 nm every 5 min for 30 min to assess efflux inhibition [2]

- Bovine Mammary Epithelial Cell Assay: Cells were seeded in 6-well plates (1×10⁶ cells/well) and cultured to 80% confluence. They were treated with Myristic acid (50–200 μM) for 24 h. TG content was measured via a colorimetric kit after lipid extraction. UBQLN1, ACCα, and FASN expression was detected by Western blot (primary antibodies against target proteins, secondary HRP-conjugated antibodies) and qPCR (primers specific for target genes, SYBR Green detection) [1]
- Human Skin Fibroblast Assay: Cells were seeded in 24-well plates (5×10⁴ cells/well) and stimulated with TNF-α (10 ng/mL) for 2 h, then treated with Myristic acid (10–40 μM) for 24 h. Culture supernatants were collected to measure IL-6 and IL-8 levels via ELISA. TLR4 and MyD88 expression was analyzed by Western blot [3]
- BV-2 Microglial Cell Assay: Cells were seeded in 6-well plates (2×10⁵ cells/well) and stimulated with LPS (1 μg/mL) for 1 h, then treated with Myristic acid (10–40 μM) for 24 h. mRNA levels of TNF-α, IL-1β, and iNOS were detected by qPCR. Phosphorylated IκBα and nuclear NF-κB p65 were analyzed by Western blot (nuclear protein extraction for p65) and immunofluorescence (p65 staining with Alexa Fluor 488-conjugated secondary antibody, nuclear counterstaining with DAPI) [4]

- DNFB-Induced AD Mouse Protocol: Female BALB/c mice (6–8 weeks old) were divided into 4 groups (n=6/group): control, AD model, 2.5% Myristic acid, and 5% Myristic acid. AD was induced by painting 0.5% DNFB on the ears (10 μL/ear) on day 0 and day 7. From day 8 to day 14, mice in treatment groups received topical application of 2.5% or 5% Myristic acid (dissolved in Vaseline) on the ears (10 μL/ear) once daily. On day 15, ear thickness was measured with a caliper, and ears were collected for H&E staining (epidermal thickness) and toluidine blue staining (mast cell count). Mechanical nociception was assessed using a von Frey filament test on day 14 [3]

Absorption, Distribution and Excretion
In normal rats, 2 hours after palmitic acid administration, radioactivity in the heart, liver, spleen, and adrenal glands was higher than after myristic acid administration. In granulomatous cyst rats, 2 hours after palmitic acid administration, radioactivity distribution in the adrenal glands and cyst exudate was higher than in the myristic acid group. Rats given myristic acid showed higher radioactivity in the gastric cyst wall. Fatty acids derived from adipose tissue storage are either bound to serum albumin or exist in the blood as free fatty acids. Oleic acid, palmitic acid, myristic acid, and stearic acid are primarily transported via the lymphatic system, while lauric acid is transported via both the lymphatic system and the portal venous system (as free fatty acids). Metabolism/Metabolites In rats fed coconut oil, myristic acid is one of the major fatty acids in liver and adipose tissue triglycerides. Ethanol increases the proportion of myristic acid.
In addition to being metabolized via β-oxidation, myristic acid has been shown to undergo chain elongation reactions to produce palmitic acid and stearic acid, desaturation reactions to produce myristoleic acid, and incorporation into liver neutral lipids (and a small amount of phospholipids).
Myristic acid showed a lower efficiency than palmitic acid in converting saturated fatty acids to monounsaturated fatty acids in the supernatant of 9000 XG rat liver homogenate. These fatty acids only produced Δ9-monoenoic acids of the same chain length.
Myristic esters incorporating 14C-labeled acetates preferentially esterified to triglycerides, while labeled stearates were converted to phospholipids in isolated rat adipocytes.
For more complete metabolite/metabolite data on myristic acid (6 metabolites in total), please visit the HSDB record page.
Known human metabolites of tetradecanoic acid include 13-hydroxytetradecanoic acid.

In bovine mammary epithelial cells, treatment with myristic acid at concentrations up to 200 μM for 24 hours did not show any effect on cell viability (MTT assay: cell viability >90%, compared to the control group) [1]
- In BV-2 microglia, treatment with myristic acid at concentrations up to 40 μM for 24 hours did not show any cytotoxicity (CCK-8 assay: cell viability >92%, compared to the control group) [4]
- In a DNFB-induced AD mouse model, topical application of 5% myristic acid for 7 days did not show any skin irritation (no redness, edema, or erosion) or changes in body weight (weight gain was similar to the control group) [3]

[1]. Myristic acid regulates triglyceride production in bovine mammary epithelial cells through the ubiquitination pathway. Agriculture, 2023, 13(10): 1870.

[2]. Myristic Acid Inhibits the Activity of the Bacterial ABC Transporter BmrA. Int J Mol Sci. 2021 Dec 17;22(24):13565.

[3]. Myristic acid reduces skin inflammation and nociception. J Food Biochem. 2022 Jan;46(1):e14013.

[4]. Anti-inflammatory effects of myristic acid mediated by the NF-κB pathway in lipopolysaccharide-induced BV-2 microglial cells. Mol Omics. 2023 Oct 30;19(9):726-734.

Tetradecanoic acid is an oily white crystalline solid. (NTP, 1992)
Tetradecanoic acid is a straight-chain, 14-carbon long-chain saturated fatty acid, mainly found in milk fat. It is a human metabolite, an EC 3.1.1.1 (carboxylesterase) inhibitor, a Daphnia magna metabolite, and an algal metabolite. It is a long-chain fatty acid and a straight-chain saturated fatty acid, and is the conjugate acid of tetradecanoic acid.
Myristic acid is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain).
Myristic acid has been reported to exist in Calodendrum capense, Camellia sinensis, and other organisms with relevant data.
Myristic acid is a saturated long-chain fatty acid with a 14-carbon backbone. Myristic acid is naturally found in palm oil, coconut oil, and milk fat. Myristic acid is a saturated 14-carbon fatty acid found in most animal and plant fats, particularly milk fat, coconut oil, palm oil, and nutmeg oil. It is used in the synthesis of fragrances and is also an ingredient in soaps and cosmetics. (From Dorland, 28th ed.). Myristic acid is also frequently added to the penultimate N-terminus glycine residue of receptor-associated kinases to impart membrane localization to the enzyme. This is achieved through myristic acid's sufficiently high hydrophobicity, allowing it to integrate into the fatty acyl core of the phospholipid bilayer of the eukaryotic cell membrane. (Wikipedia) Myristic acid is a metabolite found or produced in Saccharomyces cerevisiae. It is a saturated 14-carbon fatty acid found in most animal and plant fats, particularly milk fat, as well as coconut oil, palm oil, and nutmeg oil. It is used in the synthesis of fragrances and is also an ingredient in soaps and cosmetics. (From Dorland, 28th ed.) See also: cod liver oil (partial); saw palmetto (partial).
Mechanism of Action
...The specific hypothesis tested was that the binding of free fatty acids to the class B scavenger receptor CD36 induces activation of endothelial nitric oxide synthase (eNOS). This study used human microvascular endothelial cell lines and transfected Chinese hamster ovary cell systems to identify which free fatty acids could stimulate eNOS activity. Surprisingly, only myristic acid, and to a lesser extent palmitic acid, stimulated eNOS activity. The stimulatory effect on eNOS was dose- and time-dependent. Competitive experiments with other free fatty acids and CD36 blocking antibodies showed that the effect of myristic acid on eNOS requires binding to CD36. Further mechanistic studies indicated that the effect of myristic acid on eNOS function was independent of PI3K, Akt kinase, or calcium ions. Pharmacological studies and dominant-negative constructs confirmed that the stimulation of eNOS activity by myristic acid/CD36 depends on AMPK activation. These data reveal an unexpected link between myristic acid, CD36, AMP kinase, and eNOS activity.

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- Myristic acid regulates triglyceride (TG) production in bovine mammary epithelial cells by targeting UBQLN1-mediated ubiquitination, which may affect lipid metabolism in dairy cows [1]
- Myristic acid inhibits BmrA (an ABC transporter involved in bacterial multidrug resistance), suggesting it may act as an adjuvant to enhance the efficacy of antibiotics against drug-resistant bacteria [2]
- Myristic acid reduces skin inflammation and nociceptive sensation in Alzheimer's disease (AD) mice, supporting its potential for treating inflammatory skin diseases [3]
- Myristic acid exerts an anti-neuroinflammatory effect in BV-2 cells by inhibiting the NF-κB pathway, suggesting its potential application in the treatment of neuroinflammatory diseases such as Alzheimer's disease [4]

C14H28O2

228.3709

228.208

544-63-8

11005

White to off-white solid powder

0.9±0.1 g/cm3

319.6±5.0 °C at 760 mmHg

52-54 °C(lit.)

144.8±12.5 °C

0.0±0.7 mmHg at 25°C

1.451

6.09

1

2

12

16

155

0

TUNFSRHWOTWDNC-UHFFFAOYSA-N

InChI=1S/C14H28O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14(15)16/h2-13H2,1H3,(H,15,16)

tetradecanoic acid

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)

DMSO : ≥ 250 mg/mL (~1094.71 mM)
Ethanol : ~100 mg/mL (~437.89 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (10.95 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (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 EtOH stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (10.95 mM) (saturation unknown) in 10% EtOH + 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 EtOH stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (9.11 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 4: ≥ 2.08 mg/mL (9.11 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 5: 10% DMSO + 90% Corn Oil

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Solubility in Formulation 6: 40 mg/mL (175.15 mM) in Cremophor EL (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)