N,N-Diethylacetamide
Based on 1 Customer Validation
N,N-Diethylacetamide is a polar solvent widely used in film and fiber manufacturing, as well as in laboratories as a carrier for water-insoluble chemicals. N,N-Diethylacetamide exerts potent anti-inflammatory effects by inhibiting the NF-κB pathway, suppressing the expression of NO and iNOS, and downregulating key inflammatory cytokines such as TNF-α and IL-6, without affecting the MAPK pathway. N,N-Diethylacetamide can be used to study inflammatory preterm birth.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 685-91-6
- 分子式: C6H13NO
- 分子量:115.17
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保管条件:
Store at room temperature 3 years.
In solvent -80°C, 2 years , -20°C, 1 year
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
製品説明
IC50 & Target
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NF-κB |
IL-1β |
IL-6 |
IL-8 |
CYP2B1 |
CYP2B2 |
体外実験
N,N-Diethylacetamide (10 mM; 26 h) inhibits LPS (HY-D1056)-stimulated NO secretion in RAW 264.7 cells[1].
N,N-Diethylacetamide (10 mM; 8 h) reduces LPS-induced iNOS expression in RAW 264.7 cells[1].
N,N-Diethylacetamide (0.1-10 mM; 26 h) inhibits LPS-stimulated IL-6, IL-8, and MCP-1 secretion in HTR-8/SVneo cells[1].
N,N-Diethylacetamide (10 mM; 26 h) suppresses LPS-stimulated TNF-α, IL-6, IL-1β, GM-CSF, MCP-1, and IL-10 secretion in RAW 264.7 cells[1].
N,N-Diethylacetamide (0.1-10 mM; 22 h) inhibits LPS-stimulated cytokine and chemokine secretion in human placental explants[1].
N,N-Diethylacetamide (10 mM; 2.25 h) prevents LPS-induced IkB-α degradation in RAW 264.7 cells[1].
N,N-Diethylacetamide (10 mM; 26 h) does not alter LPS-stimulated MAPK pathway protein expression in RAW 264.7 cells[1].
N,N-Diethylacetamide (10 mM; 26 h) inhibits LPS-stimulated NF-κB transcriptional activity in HEK 293 cells overexpressing TLR4, without affecting AP-1 or C/EBP activity[1].
N,N-Diethylacetamide (0.5-10 mM; 50 min) was catalyzed for deethylation by purified P4502B1 with a Km of 3.5 mM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HTR-8/SVneo, RAW 264.7, HEK 293
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Concentration:up to 10 mM
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Incubation Time:2 h (pre-treatment); 24 h (LPS treatment)
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Result:Did not significantly affect the viability of HTR-8/SVneo, RAW 264.7, or HEK 293 cells compared to untreated controls.
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Cell Line:RAW 264.7
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Concentration:0.1, 1, 10 mM
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Incubation Time:2 h (pre-treatment); 6 h (LPS treatment)
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Result:Significantly inhibited LPS-induced iNOS expression in RAW 264.7 cells at 10 mM (P < 0.001) compared to LPS control.
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Cell Line:HTR-8/SVneo
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Concentration:0.1, 1, 10 mM
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Incubation Time:2 h (pre-treatment); 24 h (LPS treatment)
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Result:Significantly suppressed LPS-stimulated IL-6 secretion at 10 mM (more effectively than BAY 11-7082), caused a 90% reduction in IL-8 secretion at 10 mM (more effective than BAY 11-7082), and significantly inhibited MCP-1 secretion at 1 and 10 mM.
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Cell Line:RAW 264.7
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Concentration:0.1, 1, 10 mM
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Incubation Time:2 h (pre-treatment); 24 h (LPS treatment)
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Result:Significantly reduced TNF-α (P < 0.0001), IL-6, IL-1β, GM-CSF (>90% reduction), MCP-1, and IL-10 (P < 0.0001) secretion from LPS-stimulated RAW 264.7 cells at 10 mM.
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Cell Line:RAW 264.7
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Concentration:0.1, 1, 10 mM
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Incubation Time:2 h (pre-treatment); 15 min (LPS treatment)
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Result:Significantly inhibited LPS-induced IkB-α degradation in RAW 264.7 cells at 10 mM (P < 0.01) compared to LPS control.\nDid not affect LPS-stimulated expression of native or phosphorylated JNK1, ERK1/2, or p38 MAPK in RAW 264.7 cells at any concentration.
体内実験
N,N-Diethylacetamide (150-500 mg/kg; i.p.; daily; 3 days) administration to rats induces P4502B1/2 and alters hepatic drug-metabolizing enzyme activities in a dose-dependent manner, with higher doses causing hepatotoxicity[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57Bl/6 (timed pregnant, weight 27–36 g)[1]
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Dosage:375 mg/kg; 750 mg/kg
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Administration:i.p.; two doses (T=-15 min and T=10 h)
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Result:Prevented delivery in all 6 mice treated with 750 mg/kg by 25 h post-LPS injection.
Delayed mean delivery time by approximately two hours and prevented delivery in 2/8 mice treated with 375 mg/kg by 25 h post-LPS injection.
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Animal Model:Sprague-Dawley (male, 5-6 weeks old)[2]
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Dosage:150, 300 mg/kg; 400-500 mg/kg
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Administration:i.p.; daily; 3 days
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Result:Significantly induced the enzymatic activities related to CYP2B1/2 (such as PROD, 16β-testosterone hydroxylation), and enhanced its own metabolism (DEAC deethylase activity).
Increased the expression of CYP2B1/2 protein, while inhibiting the expression of CYP2C11.
化学情報
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CAS 番号 685-91-6
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性状 Liquid (Density: 0.925 g/cm3)
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分子量 115.17
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分子式 C6H13NO
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Color Colorless to light yellow
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SMILES
CCN(C(C)=O)CC
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Store at room temperature 3 years
In solvent -80°C 2 years -20°C 1 year
プロトコル
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
純度とドキュメンテーション
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取扱説明書 (2659 KB)
参考文献
[1]. Gorasiya S, et al. N,N-Diethylacetamide and N,N-Dipropylacetamide inhibit the NF-kB pathway in in vitro, ex vivo and in vivo models of inflammation-induced preterm birth. Sci Rep. 2025;15(1):29861. Published 2025 Aug 14. [Content Brief]
[2]. Silvia M, et al. Microsomal metabolism of N,N-diethylacetamide and N,N-dimethylacetamide and their effects on drug-metabolizing enzymes of rat liver. Biochem Pharmacol. 1994;48(4):717-726. [Content Brief]
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
N,N-Diethylacetamide 関連分類
HY-W008829 関連分類
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