在小鼠巨噬细胞RAW 264.7中，N,N-二甲基乙酰胺 (DMA) 以浓度依赖的方式显著抑制了脂多糖 (LPS) 刺激诱导的一氧化氮 (NO) 产生。[1]
免疫细胞化学分析显示，DMA (浓度为0.01和1 µmol/L) 抑制了LPS诱导的RAW 264.7细胞中NF-κB p65亚基的核转位。在更高浓度 (1 µmol/L) 下抑制作用更明显。[1]
MTT实验证实，在0.1至10 µmol/L浓度范围内，DMA 无论是否存在LPS刺激，均未显著影响RAW 264.7细胞的活力，表明观察到的效应并非由于细胞毒性。[1]

在LPS诱导的早产小鼠模型中，腹腔注射DMA (剂量为0.2, 0.39, 0.78, 1.56和3.1 mg/kg) 以剂量依赖的方式防止了定时怀孕C57BL/6小鼠的早产。除最低剂量 (0.2 mg/kg) 外，所有剂量均显著降低了早产小鼠的比例，最高剂量 (1.56和3.1 mg/kg) 完全防止了分娩。[1]
DMA 处理也以剂量依赖的方式挽救了因LPS触发的自然流产的幼崽。所有DMA处理组丢失的幼崽数量均显著低于仅LPS对照组，在1.56和3.1 mg/kg剂量下实现了完全挽救。[1]
胎盘组织学分析显示，DMA (1.56 mg/kg) 显著减轻了LPS诱导的炎性细胞 (主要是多形核中性粒细胞) 向胎盘迷路的强烈浸润。DMA处理小鼠的组织外观与假手术对照组相似。[1]
胎盘组织裂解液的Western印迹分析显示，与仅LPS对照组相比，DMA (1.56 mg/kg) 显著降低了促炎细胞因子IL-1β、TNF-α和IL-6的表达，并降低了基质金属蛋白酶-8 (MMP-8) 的水平。同时，DMA 显著增加了抗炎细胞因子IL-10的表达。[1]
对265只宫内暴露于DMA的幼崽进行检查，未发现先天性畸形的证据 (肢体异常、颅面部发育异常或腹壁缺陷)。[1]

为评估DMA对巨噬细胞功能的影响，将RAW 264.7细胞接种并用不同浓度的DMA处理。一小时后，用LPS (0.1 µg/mL) 刺激细胞。24小时后，收集细胞培养上清液，离心，使用Griess试剂法测定亚硝酸盐浓度来确定一氧化氮产量。在540 nm波长下读取吸光度。[1]
为评估DMA对NF-κB核转位的影响，将RAW 264.7细胞接种、贴壁，然后在存在或不存在DMA (0.01或1 µmol/L) 的情况下，用或不用LPS (100 ng/mL) 处理2小时。细胞固定、透化、封闭，并在4°C下与抗NF-κB p65一抗孵育过夜。洗涤后，细胞与荧光染料标记的二抗孵育。细胞核进行复染。通过免疫荧光显微镜评估核转位。[1]
为测试DMA对细胞活力的影响，将RAW 264.7细胞接种、贴壁，然后在存在一系列DMA浓度的情况下用LPS (1 µg/mL) 刺激24小时。加入MTT溶液并孵育2小时。溶解形成的甲瓒晶体，使用酶标仪在570 nm波长下测量吸光度。[1]

Timed-pregnant C57BL/6 mice at embryonic day 15.5 (E15.5) received an intraperitoneal (i.p.) injection of LPS (50 mg/kg dissolved in 500 µL PBS). Mice were then randomly assigned to control or treatment groups. At 0.5 hours before and 10 hours after LPS injection, mice received i.p. injections of either 0.5 mL PBS (control) or 0.1 mL of varying concentrations of DMA (corresponding to doses of 0.2, 0.39, 0.78, 1.56, and 3.1 mg/kg). A sham group received PBS instead of LPS, followed by PBS injections. Mice were observed for preterm delivery for 24 hours, after which they were autopsied to confirm pregnancy status, count retained pups, and evaluate for fetal anomalies. Placentas were harvested for histological and molecular analysis. [1]

Absorption, Distribution and Excretion
/N,N-DIMETHYLACETAMIDE/ ... READILY ABSORBED THROUGH SKIN ... .
N,N-dimethylacetamide is rapidly absorbed through biological membranes.
No correlation between personal airborne exposure and excretion of mono-methylacetamide in urine was detected during a full workshift (5 days). Most (n = 6) workers studied (n = 8) excreted about 13% of the calculated inhaled dose as metabolite in urine.
DMAC is readily absorbed in man after oral, dermal, or inhalation exposure. ... About 2% of a dose of dimethylacetamide is recovered in the urine as MMAC /N-methylacetamide/ after inhalation; 10% is recovered after inhalation plus skin exposure. Exposure to 10 ppm of DMAC results in complete excretion of MMAC with in 30 hr. Maximal concns of 45 & 100 ppm (mg/L) of MMAC in the urine are found in subjects exposed both by inhalation & skin. In workers continuously exposed to DMAC vapor (inhalation plus skin) & subjected to DMAC airborne levels of 6-22 ppm ..., about 13.5% of the estimated dose is excreted as MMAC in the urine. Some workers may excrete about 30% of a dose as MMAC.
For more Absorption, Distribution and Excretion (Complete) data for N,N-DIMETHYLACETAMIDE (7 total), please visit the HSDB record page.

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Metabolism / Metabolites
N-DEMETHYLATION OF ... DIMETHYLACETAMIDE OCCURRED IN RAT, RESPECTIVE MONOMETHYLAMIDES APPEARING IN URINE ... IN THE CASE OF DIMETHYLACETAMIDE WAS DIDEMETHYLATED PRODUCT, ACETAMIDE, ALSO FOUND.
ANALYSIS OF HUMAN URINE AFTER OCCUPATIONAL EXPOSURE TO DIMETHYLACETAMIDE SHOWS N-METHYLACETAMINE. /FROM TABLE/
Gas chromatographic analysis of the urine of rats which had received dimethylacetamide by the subcutaneous route indicated the presence of N-methyl-acetamide and acetamide. Both metabolites were also found ... in incubation mixtures of dimethylacetamide with rat liver homogenate. N-Methylacetamide was detected in the urine of human volunteers who had inhaled dimethylacetamide or absorbed dimethylacetamide vapor through the skin. Measurement of the amount of the metabolite N-methylacetamide excreted by individuals exposed to dimethylacetamide vapors with or without face masks which allowed the inhalation of air free of dimethylacetamide indicated that more dimethylacetamide was absorbed through the lung than through the skin. ... Only 2-10% of the amount of dimethylacetamide inhaled was recovered in the urine in the form of N-methylacetamide. It has been suggested that the major urinary metabolite of the analogous dimethylformamide is N-(hydroxymethyl)-N-methylformamide and not N-methylformamide, since the carbinolamide decomposes on the gas chromatography column (to N-methylformamide) but is relatively stable in aqueous solution. In analogy, it would be logical to assume that the N-methylacetamide found in the urine after exposure to dimethylacetamide really arose from chemical breakdown of N-(hydroxymethyl)-N-methylacetamide during the analytical process.
N,N-dimethylacetamide is metabolized by demethylation first to monomethyl derivatives and then to the parent acetamide.

Toxicity Data
LC50 (rat) = 2,475 ppm/1H

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Interactions
DAILY INJECTIONS OF PROGESTERONE (5 MG/HAMSTER/DAY, FOR 4 DAYS) BLOCKED ANTIFERTILITY EFFECT OF DMA (ADMIN @ NIDATION) AS DID INJECTIONS OF A LUTEOTROPIC COMPLEX (1 MG/HAMSTER/DAY PROLACTIN PLUS 5.1 IU/HAMSTER/DAY OF PREGNANT MARE SERUM GONADOTROPIN, FOR 4 DAYS.
DIMETHYLACETAMIDE LOWERED THE YIELDS AND/OR INCIDENCES OF TOTAL TUMORS, BENIGN PLAQUES, BENIGN HYPERKERATOTIC LESIONS AND ADVANCED TUMORS PROMOTED BY RETINYL ACETATE OR CROTON OIL AFTER INITIATION BY 7,12-DIMETHYLBENZ(A)ANTHRACENE.
SINGLE EXPT WITH 45 MG/KG RAT OF PYRIMETHAMINE ISETHIONATE IN 6% DIMETHYLACETAMIDE, 6% DIMETHYL SULFOXIDE OR 95% ETHANOL SHOWED THAT TERATOGENIC EFFECT WAS CUMULATIVE IN DIMETHYL SULFOXIDE OR ETHANOL BUT AFTER ADMIN IN DMA RESPONSE-DOSE RELATION FOLLOWED A PARABOLIC CURVE.
PCC4azal embryonal carcinoma tumors were grown in strain 129 mice by sc transplantation. When palpable, the tumors were treated with a combination of retinoic acid and dimethylacetamide. In vitro, this embryonal carcinoma cell line shows minimal spontaneous differentiation and is exquistely sensitive to retinoic acid and/or dimethylacetamide induction of differentiation. Ten daily 20 ul intratumor injections of a solution of 10 mg retinoic acid per ml of dimethylacetamide resulted in nearly complete induction of morphological differentiation mainly into neuropithelial and glandular derivatives. Control tumors showed minor spontaneous differentiation. Differentiation was associated with decreased tumor growth rate, decreased mitotic index, decreased extent of necrosis, and increased survival time of the hosts. In 4 of 18 cases, long-term survival of the hosts was effected by a complete differentiation of the malignant embryonal carcinoma tumors into benign teratomas. Retinoic acid: dimethylacetamide was also effective in inducing differentiation with the same dosage and schedule when admin systemically, ie, ip or sc.

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Non-Human Toxicity Values
LD50 Rat oral 5.4 ml/kg
LD50 Mouse ip 3240 mg (3.4 ml)/kg
LD50 Rat male oral 5,809 mg/kg
LD50 Rat female oral 4,390 mg/kg
For more Non-Human Toxicity Values (Complete) data for N,N-DIMETHYLACETAMIDE (16 total), please visit the HSDB record page.

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In this study, DMA at the doses used (up to 3.1 mg/kg) did not cause congenital anomalies in exposed mouse pups. [1]
The article states that DMA is used clinically as a vehicle at doses many-fold higher than those shown to be effective in this study. However, it is also noted that with prolonged exposure, DMA can cause liver injury in humans. [1]
The in vitro MTT assay indicated that DMA concentrations up to 10 µmol/L did not significantly affect RAW 264.7 cell viability over 24 hours. [1]

[1]. N,N-dimethylacetamide regulates the proinflammatory response associated with endotoxin and prevents preterm birth. Am J Pathol. 2013 Aug;183(2):422-30.

[2]. N,N-dimethylacetamide targets neuroinflammation in Alzheimer's disease in in-vitro and ex-vivo models. Sci Rep. 2023 May 1;13(1):7077.

[3]. FDA-Approved Excipient N, N-Dimethylacetamide Attenuates Inflammatory Bowel Disease in In Vitro and In Vivo Models. Fortune J Health Sci. 2022;5:499-509.

N,N-Dimethylacetamide can cause cancer according to California Labor Code. It can cause developmental toxicity and male reproductive toxicity according to an independent committee of scientific and health experts.
Dimethylacetamide appears as a clear colorless liquid with a faint odor similar to ammonia. About the same density as water. Flash point 145 °F. Vapors heavier than air. May by toxic by skin absorption. May irritate eyes and skin.
N,n-dimethyl acetamide solution (40% or less) is a colorless liquid with a slight ammonia-like odor. (USCG, 1999)
N,N-dimethylacetamide is a member of the class of acetamides that is acetamide in which the hydrogens attached to the N atom have been replaced by two methyl groups respectively. Metabolite observed in cancer metabolism. It has a role as a human metabolite. It is a member of acetamides and a monocarboxylic acid amide. It is functionally related to an acetamide.
N,N-Dimethylacetamide is a dipolar aprotic solvent and reagent that may be used in the production of fibers and pharmaceuticals, and as a non-aldehyde fixative.
Hallucinogen is any naturally-derived or synthetic substance that can induce hallucinations.

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Therapeutic Uses
Commercial solvent tested as a parenteral drug vehicle and as an antitumor agent.

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N,N-Dimethylacetamide (DMA) is described as an inexpensive, common aprotic organic solvent. The study identifies it as a novel anti-inflammatory agent capable of suppressing the proinflammatory response associated with endotoxin (LPS). [1]
The proposed mechanism involves DMA suppressing macrophage activation, inhibiting NF-κB nuclear translocation, downregulating pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), upregulating anti-inflammatory IL-10, and reducing inflammatory cell infiltration, thereby preventing inflammation-mediated preterm birth. [1]
The authors suggest that DMA represents a potential nontoxic therapy for a broad range of inflammatory disorders, although its in vivo and clinical validation for such indications requires further assessment. [1]

C4H9NO

87.1204

87.068

127-19-5

N,N-Dimethylacetamide-d9;16727-10-9;N,N-Dimethylacetamide-d6;31591-08-9;N,N-Dimethylacetamide-d3;20255-66-7

31374

Colorless to light yellow liquid

0.9±0.1 g/cm3

166.1±0.0 °C at 760 mmHg

-20 °C

70.0±0.0 °C

1.8±0.3 mmHg at 25°C

1.407

-0.75

20.31

0

1

0

6

58.6

0

O=C(C([H])([H])[H])N(C([H])([H])[H])C([H])([H])[H]

FXHOOIRPVKKKFG-UHFFFAOYSA-N

InChI=1S/C4H9NO/c1-4(6)5(2)3/h1-3H3

N,N-dimethylacetamide

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 : ≥ 100 mg/mL (~1147.84 mM)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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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));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
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；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。