Myristic acid   中文名称: 正十四碳酸

- 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]

- 在牛乳腺上皮细胞中，用肉豆蔻酸（50–200 μM）处理24小时，可剂量依赖性降低甘油三酯（TG）含量（较对照组降低18–42%），下调UBQLN1表达（mRNA和蛋白水平分别降低25–60%）；同时降低乙酰辅酶A羧化酶α（ACCα）的磷酸化水平（降低30–55%），减少脂肪酸合成酶（FASN）表达，表明其可抑制脂肪从头合成[1]
- 在纯化的细菌BmrA蛋白中，肉豆蔻酸（5–50 μM）剂量依赖性抑制ATP酶活性（50 μM时最大抑制率~70%），阻断罗丹明6G外排（50 μM时最大抑制率~65%），从而抑制BmrA介导的细菌多药耐药[2]
- 在TNF-α（10 ng/mL）处理的人皮肤成纤维细胞中，肉豆蔻酸（10–40 μM）处理24小时，通过下调TLR4/MyD88信号通路，减少促炎细胞因子IL-6（降低22–58%）和IL-8（降低19–52%）的分泌[3]
- 在LPS诱导的BV-2小胶质细胞中，肉豆蔻酸（10–40 μM）处理24小时，降低TNF-α（mRNA水平降低35–72%）、IL-1β（mRNA水平降低30–68%）和iNOS（mRNA水平降低28–65%）的表达，同时抑制IκBα磷酸化（降低40–70%）及NF-κB p65核转位（降低38–68%）[4]

- 在DNFB诱导的特应性皮炎（AD）小鼠模型中：小鼠耳部每日局部涂抹含肉豆蔻酸（2.5%或5%，溶于凡士林）的制剂，连续7天。5%剂量组可降低耳肿胀度（较AD模型组降低~45%），减薄表皮厚度（降低~38%），减少真皮肥大细胞浸润（降低~42%）；同时通过抑制脊髓TRPV1表达，改善机械痛感受（爪退缩阈值较模型组升高~35%）[3]

- BmrA ATP酶活性测定：将纯化的BmrA蛋白与肉豆蔻酸（5–50 μM）在含ATP（5 mM）的反应缓冲液中37°C孵育30分钟。采用比色法检测释放的无机磷酸盐（Pi），以nmol Pi/min/mg蛋白计算ATP酶活性，通过剂量-反应曲线确定IC50[2]
- BmrA介导的罗丹明6G外排测定：将表达BmrA的大肠杆菌细胞与罗丹明6G（10 μM）孵育30分钟以负载染料，随后加入肉豆蔻酸（5–50 μM）和ATP（2 mM）。在30分钟内，每5分钟检测一次细胞内罗丹明6G的荧光强度（525 nm），评估外排抑制效果[2]

- 牛乳腺上皮细胞实验：将细胞接种于6孔板（1×10⁶个细胞/孔），培养至80%融合后，用肉豆蔻酸（50–200 μM）处理24小时。脂质提取后，通过比色试剂盒检测TG含量；采用Western blot（目标蛋白一抗、HRP标记二抗）和qPCR（目标基因特异性引物、SYBR Green检测）检测UBQLN1、ACCα和FASN的表达[1]
- 人皮肤成纤维细胞实验：将细胞接种于24孔板（5×10⁴个细胞/孔），用TNF-α（10 ng/mL）刺激2小时后，加入肉豆蔻酸（10–40 μM）处理24小时。收集培养上清液，通过ELISA检测IL-6和IL-8水平；采用Western blot分析TLR4和MyD88的表达[3]
- BV-2小胶质细胞实验：将细胞接种于6孔板（2×10⁵个细胞/孔），用LPS（1 μg/mL）刺激1小时后，加入肉豆蔻酸（10–40 μM）处理24小时。通过qPCR检测TNF-α、IL-1β和iNOS的mRNA水平；采用Western blot（p65检测需提取核蛋白）和免疫荧光（p65用Alexa Fluor 488标记二抗染色，DAPI染核）分析磷酸化IκBα和NF-κB p65核转位[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

37.3

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)

配方 1 中的溶解度: ≥ 2.5 mg/mL (10.95 mM) (饱和度未知) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL 澄清 EtOH 储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL 生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (10.95 mM) (饱和度未知) in 10% EtOH + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 EtOH 储备液加入900 μL 玉米油中，混合均匀。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (9.11 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清的DMSO储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 4 中的溶解度: ≥ 2.08 mg/mL (9.11 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100μL 20.8mg/mL澄清的DMSO储备液加入到900μL 20％SBE-β-CD生理盐水中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 5 中的溶解度: 10% DMSO + 90% Corn Oil

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配方 6 中的溶解度: 40 mg/mL (175.15 mM) in Cremophor EL (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶.

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
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10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
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