Methoxyacetic acid
(Synonyms: 甲氧基乙酸) 目录号 : GC61048
Methoxyaceticacid是一种内源性代谢产物。
Cas No.:625-45-6
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Methoxyacetic acid is an endogenous metabolite.
| Cas No. | 625-45-6 | SDF | |
| 别名 | 甲氧基乙酸 | ||
| Canonical SMILES | O=C(O)COC | ||
| 分子式 | C3H6O3 | 分子量 | 90.08 |
| 溶解度 | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 11.1012 mL | 55.5062 mL | 111.0124 mL |
| 5 mM | 2.2202 mL | 11.1012 mL | 22.2025 mL |
| 10 mM | 1.1101 mL | 5.5506 mL | 11.1012 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。
Methoxyacetic acid esters: Applications in protecting group and glycosylation chemistry
Carbohydr Res 2019 Dec 1;486:107848.PMID:31655419DOI:10.1016/j.carres.2019.107848.
The methoxyacetate (MAc) protecting group was introduced over 50 years ago and has proved useful owing to its combination of stability and its ability to be selectively removed in the presence of unactivated esters and a wide variety of other protecting groups. Glycosyl methoxyacetates have been investigated as glycosyl donors under activation by lanthanoids. In this mini-review we highlight a range of useful transformations enabled by judicious application of the methoxyacetate group.
[Determination of Methoxyacetic acid in urine by pre-column derivatization-liquid-liquid microextraction coupled with gas chromatography]
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 2021 Aug 20;39(8):602-605.PMID:34488270DOI:10.3760/cma.j.cn121094-20200603-00317.
Objective: To establish a method for determining Methoxyacetic acid in urine by pre-column derivatization-liquid-liquid microextraction coupled with gas chromatography (GC) . Methods: Phosphate buffer solution, tert-butoxyacetic acid (internal standard) and pentafluorobenzyl bromide (derivative) were added to the urine sample. After derived in a water bath at 90 ℃ for 40 min, the mixture was cooled and filtered, then the dichloromethane was used as an extractant. After being shaken and centrifuged, the lower organic phase was sucked and injected into a gas chromatograph, separated by a DB-5 capillary column, and detected by an ECD detector. Results: The linear range of the method was 0.6~60.0 mg/L with the correlation coefficients (r) above 0.999. The average recovery was76.6%~110.7%, the inter-day precision was 8.00%~8.82%, and the detection limit was 0.13 mg/L. Conclusion: The method was founded to be high sensitivity, low organic reagent usage and green. So it is suitable for the detection of Methoxyacetic acid in urine of occupational exposure to ethylene glycol monomethyl ether.
Aminomethylphosphonic acid and Methoxyacetic acid induce apoptosis in prostate cancer cells
Int J Mol Sci 2015 May 22;16(5):11750-65.PMID:26006246DOI:10.3390/ijms160511750.
Aminomethylphosphonic acid (AMPA) and its parent compound herbicide glyphosate are analogs to glycine, which have been reported to inhibit proliferation and promote apoptosis of cancer cells, but not normal cells. Methoxyacetic acid (MAA) is the active metabolite of ester phthalates widely used in industry as gelling, viscosity and stabilizer; its exposure is associated with developmental and reproductive toxicities in both rodents and humans. MAA has been reported to suppress prostate cancer cell growth by inducing growth arrest and apoptosis. However, it is unknown whether AMPA and MAA can inhibit cancer cell growth. In this study, we found that AMPA and MAA inhibited cell growth in prostate cancer cell lines (LNCaP, C4-2B, PC-3 and DU-145) through induction of apoptosis and cell cycle arrest at the G1 phase. Importantly, the AMPA-induced apoptosis was potentiated with the addition of MAA, which was due to downregulation of the anti-apoptotic gene baculoviral inhibitor of apoptosis protein repeat containing 2 (BIRC2), leading to activation of caspases 7 and 3. These results demonstrate that the combination of AMPA and MAA can promote the apoptosis of prostate cancer cells, suggesting that they can be used as potential therapeutic drugs in the treatment of prostate cancer.
Methoxyacetic acid inhibits histone deacetylase and impairs axial elongation morphogenesis of mouse gastruloids in a retinoic acid signaling-dependent manner
Birth Defects Res 2020 Aug;112(14):1043-1056.PMID:32496642DOI:10.1002/bdr2.1712.
Background: Teratogenic potential has been linked to various industrial compounds. Methoxyacetic acid (MAA) is a primary metabolite of the widely used organic solvent and plasticizer, methoxyethanol and dimethoxyethyl phthalate, respectively. Studies using model animals have shown that MAA acts as the proximate teratogen that causes various malformations in developing embryos. Nonetheless, the molecular mechanisms by which MAA exerts its teratogenic effects are not fully understood. Methods: Gastruloids of mouse P19C5 pluripotent stem cells, which recapitulate axial elongation morphogenesis of gastrulation-stage embryos, were explored as an in vitro model to investigate the teratogenic action of MAA. Morphometric parameters of gastruloids were measured to evaluate the morphogenetic effect, and transcript levels of various developmental regulator genes were examined to assess the impact on gene expression patterns. The effects of MAA on the level of retinoic acid (RA) signaling and histone deacetylase activity were also measured. Results: MAA reduced axial elongation of gastruloids at concentrations comparable to the teratogenic plasma level (5 mM) in vivo. MAA at 4 mM significantly altered the expression profiles of developmental regulator genes. In particular, it upregulated the RA signaling target genes. The concomitant suppression of RA signaling using a pharmacological agent alleviated the morphogenetic effect of MAA. MAA at 4 mM also significantly reduced the activity of purified histone deacetylase protein. Conclusions: MAA impaired axial elongation morphogenesis in a RA signaling-dependent manner in mouse gastruloids, possibly through the inhibition of histone deacetylase.
Toxicity of Methoxyacetic acid in rats
Fundam Appl Toxicol 1982 Jul-Aug;2(4):158-60.PMID:7185613DOI:10.1016/s0272-0590(82)80039-0.
Male Fischer 344 rats were given eight daily doses of 0, 30, 100 or 300 mg/kg Methoxyacetic acid by gavage. The high dose resulted in decreased body weight, severe degeneration of testicular germinal epithelium, decreased size of the thymus with depletion of thymic cortical lymphoid elements, and reductions in bone marrow cellularity resulting in depressions of red blood cell counts, hemoglobin concentration, packed cell volume, and white blood cell counts. Some of these observations were apparent to a lesser degree in rats given 100 mg/kg. The low dose produced no apparent effects during the course of the study. These toxicological properties of Methoxyacetic acid are remarkably similar to ethylene glycol monomethyl ether (EGME), and the adverse effects of EGME in rats are probably the result of in vivo bioactivation of EGME to Methoxyacetic acid.