Myristyl nicotinate
(Synonyms: 肉豆蔻醇烟酸酯,Tetradecyl nicotinate) 目录号 : GC38822
Myristyl nicotinate (Tetradecyl nicotinate) 是一种酯前药和 Nicotinic acid 的亲脂衍生物。Myristyl nicotinate 被开发用于将烟酸输送到皮肤中，以防止光化性角化病及其发展为皮肤癌。Myristyl nicotinate 显示刺激光损伤的皮肤中的表皮分化，增加皮肤 NAD 含量并增强人皮肤屏障。
Cas No.:273203-62-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Myristyl nicotinate (Tetradecyl nicotinate) is an ester prodrug and a lipophilic derivative of Nicotinic acid. Myristyl nicotinate is being developed for delivery of Nicotinic acid into the skin for prevention of actinic keratosis and its progression to skin cancer. Myristyl nicotinate shows to stimulate epidermal differentiation in photodamaged skin, increasing skin NAD content and strengthening the skin barrier[1][2].
Myristyl nicotinate (Tetradecyl nicotinate) is used for treatment and prevention of conditions that involve skin barrier impairment such as chronic photodamage and atopic dermatitis or for mitigating skin barrier impairment that results from therapy such as retinoids or steroids[2].
[1]. Catz P, et al. Simultaneous determination of myristyl nicotinate, nicotinic acid, and nicotinamide in rabbit plasma by liquid chromatography-tandem mass spectrometry using methyl ethyl ketone as a deproteinization solvent. J Chromatogr B Analyt Technol Biomed Life Sci. 2005 Dec 27;829(1-2):123-35. [2]. Jacobson MK, et al. Effect of myristyl nicotinate on retinoic acid therapy for facial photodamage. Exp Dermatol. 2007 Nov;16(11):927-35.
| Cas No. | 273203-62-6 | SDF | |
| 别名 | 肉豆蔻醇烟酸酯,Tetradecyl nicotinate | ||
| Canonical SMILES | O=C(C1=CC=CN=C1)OCCCCCCCCCCCCCC | ||
| 分子式 | C20H33NO2 | 分子量 | 319.48 |
| 溶解度 | DMSO: 9.62 mg/mL (30.11 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.1301 mL | 15.6504 mL | 31.3009 mL |
| 5 mM | 0.626 mL | 3.1301 mL | 6.2602 mL |
| 10 mM | 0.313 mL | 1.565 mL | 3.1301 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Hydrolysis kinetics of the prodrug Myristyl nicotinate
Pharm Dev Technol 2022 Dec;27(10):1083-1092.PMID:36440492DOI:10.1080/10837450.2022.2152460.
Myristyl nicotinate is a prodrug of nicotinic acid. In this research, the kinetics of hydrolysis for Myristyl nicotinate was studied in an aqueous phosphate buffer solution within a 5-10 pH range and constant ionic strength at a high temperature which was 80 °C to perform accelerated hydrolysis experiments. The effect of temperature, ionic strength, buffer concentrations, and buffer type was studied. The degradation was monitored using a validated HPLC method. The kinetics of hydrolysis of Myristyl nicotinate was also studied in skin and liver homogenates. The hydrolysis was found to follow pseudo-first-order kinetics. The rate constant was calculated from the slope of a linear plot of Ln transformation (Ln) of the remaining parent prodrug concentration versus time. The hydrolysis was found pH- dependent, and a pH rate profile was constructed. Moreover, the hydrolysis rate of the prodrug was found to be buffer species dependent. Carbonate buffer has the most catalytic effect over borate and phosphate buffers. The effect of temperature on the kinetics of hydrolysis of Myristyl nicotinate in phosphate buffer at pH 9 at 343, 348, 353, and 358°K was studied. The hydrolysis was found to follow the Arrhenius equation. From the Arrhenius plot, the half-life at 25 °C, and the activation energy were calculated and were found to be 466.5 days and 24.57 kcal mol-1, respectively. The hydrolysis of the prodrug was faster in liver and skin homogenates than those in aqueous buffer solutions. The pseudo-first-order rate constants were found to be 0.012, 0.028 min-1 for Myristyl nicotinate in the liver, and skin homogenates, respectively.
Analysis and stability study of Myristyl nicotinate in dermatological preparations by high-performance liquid chromatography
J Pharm Biomed Anal 2007 Feb 19;43(3):893-9.PMID:17049429DOI:10.1016/j.jpba.2006.09.007.
Myristyl nicotinate is an ester prodrug under development for delivery of nicotinic acid to skin for treatment and prevention of conditions that involve skin barrier impairment such as chronic photodamage and atopic dermatitis or for mitigating skin barrier impairment that results from therapy such as retinoids or steroids. The formulation stability of Myristyl nicotinate is crucial because even small amounts of free nicotinic acid cause skin flushing, an effect that is not harmful but would severely limit tolerability. We report here reversed-phase HPLC methods for the rapid analysis of Myristyl nicotinate and nicotinic acid in dermatological preparations. Because of the large differences in polarity, Myristyl nicotinate and nicotinic acid were analyzed by different chromatographic conditions, but they can be rapidly extracted from cream formulations using HPLC mobile phase as a solvent followed by HPLC analysis in less than 10 min. The methods were validated in terms of linearity, precision and accuracy and mean recovery of Myristyl nicotinate from topical creams ranged from 97.0-101.2%. Nicotinic acid at levels of 0.01% in the formulations could be quantified. Stability studies show that Myristyl nicotinate formulations are stable at room temperature for 3 years with less than 0.05% conversion to nicotinic acid. These methods will be effective for routine analysis of Myristyl nicotinate stability in dermatological formulations.
Simultaneous determination of Myristyl nicotinate, nicotinic acid, and nicotinamide in rabbit plasma by liquid chromatography-tandem mass spectrometry using methyl ethyl ketone as a deproteinization solvent
J Chromatogr B Analyt Technol Biomed Life Sci 2005 Dec 27;829(1-2):123-35.PMID:16275131DOI:10.1016/j.jchromb.2005.10.003.
Myristyl nicotinate (Nia-114) is an ester prodrug being developed for delivery of nicotinic acid (NIC) into the skin for prevention of actinic keratosis and its progression to skin cancer. To facilitate dermal studies of Nia-114, a novel liquid chromatography-tandem mass spectrometry (LC-MS/MS) method using methyl ethyl ketone (MEK) as a deproteinization solvent was developed and validated for the simultaneous determination of Nia-114, NIC, and nicotinamide (NAM) in rabbit plasma. NAM is the principal metabolite of NIC, which is also expected to have chemopreventive properties. The analytes were chromatographically separated using a Spherisorb Cyano column under isocratic conditions, and detected by multiple reaction monitoring (MRM) in positive-ion electrospray ionization mode with a run time of 9 min. The method utilized a plasma sample volume of 0.2 ml and isotope-labeled D4 forms of each analyte as internal standards. The method was linear over the concentration range of 2-1000, 8-1000, and 75-1000 ng/ml, for Nia-114, NIC, and NAM, respectively. The intra- and inter-day assay accuracy and precision were within +/-15% for all analytes at low, medium, and high quality control standard levels. The relatively high value for the lower limit of quantitation (LLOQ) of NAM was demonstrated to be due to the high level of endogenous NAM in the rabbit plasma (about 350 ng/ml). Endogenous levels of NIC and NAM in human, dog, rat, and mouse plasma were also determined, and mean values ranged from <2 ng/ml NIC and 38.3 ng/ml NAM in human, to 233 ng/ml NIC and 622 ng/ml NAM in mouse. Nia-114 was generally unstable in rabbit plasma, as evidenced by loss of 44-50% at room temperature by 2 h, and loss of 64-70% upon storage at -20 degrees C for 1 week, whereas it was stable (<7% loss) upon storage at -80 degrees C for 1 month.
Formulation compatibility of Myristyl nicotinate with drugs used to treat dermatological conditions involving an impaired skin barrier
Drug Dev Ind Pharm 2007 Nov;33(11):1176-82.PMID:18058313DOI:10.1080/03639040701199274.
A number of dermatology conditions including skin photodamage, atopic dermatitis, and rosacea involve skin barrier impairment and first line therapies for these conditions including retinoids and steroids further impair skin barrier function. We have evaluated the compatibility of Myristyl nicotinate, an agent that enhances skin barrier function, with drugs used to treat conditions where skin barrier impairment is present including photodamage (retinoic acid), atopic dermatitis (hydrocortisone, triamcinolone acetonide), rosacea (metronidazole), and seborrheic dermatitis (ketoconazole). Myristyl nicotinate was found to be compatible with each of the drugs examined when formulated together and also was shown to be photocompatible with retinoic acid. Our results suggest that the combination of Myristyl nicotinate with these drugs is a feasible therapeutic development strategy.
Effect of Myristyl nicotinate on retinoic acid therapy for facial photodamage
Exp Dermatol 2007 Nov;16(11):927-35.PMID:17927576DOI:10.1111/j.1600-0625.2007.00616.x.
Based on the hypothesis that skin barrier impairment is a contributor to side-effects associated with retinoic acid therapy, a double-blind, placebo-controlled pilot study examined the combined use of retinoic acid with Myristyl nicotinate (MN), a lipophilic derivative of niacin that enhances skin barrier function, in female subjects with mild to moderate facial photodamage. The study involved a 1-month run-in period with placebo or MN prior to initiation of retinoic acid therapy for 3 months. Analysis of skin biopsies revealed that retinoic acid therapy resulted in stratum corneum thinning of approximately 25% (P = 0.006 versus baseline) that was ameliorated by MN use (P < 0.005). Therapy resulted in an increased rate of transepidermal water loss (TEWL) of approximately 45% (P = 0.001 versus baseline) and use of MN protected against the increase in TEWL with the strongest protection provided by prior use of MN (P = 0.056 versus placebo). MN use reduced the incidence of side-effects of the therapy and again prior use provided the greatest reduction of side-effects. Subjects showed statistically significant clinical improvement (P < 0.05 versus baseline) during the study. MN use did not interfere with any clinical improvement parameters and improved effects on temple laxity (P = 0.01 versus placebo). Analysis of changes in epidermal thickness, Ki67-positive cells and intensity of loricrin staining demonstrated that MN either improved or did not interfere with retinoic acid efficacy. These results show that prior and concurrent use of MN can mitigate barrier impairment and improve the tolerability of retinoic acid therapy for facial photodamage without interfering with efficacy.