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.
For research use only. We do not sell to patients.
- CAS No.: 685-91-6
- Formula: C6H13NO
- Molecular Weight:115.17
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Storage:
Store at room temperature 3 years.
In solvent -80°C, 2 years , -20°C, 1 year
Biological Activity
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NF-κB |
IL-1β |
IL-6 |
IL-8 |
CYP2B1 |
CYP2B2 |
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.
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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.
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.
Chemical Information
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CAS No. 685-91-6
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Appearance Liquid (Density: 0.925 g/cm3)
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Molecular Weight 115.17
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Formula C6H13NO
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Color Colorless to light yellow
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SMILES
CCN(C(C)=O)CC
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Store at room temperature 3 years
In solvent -80°C 2 years -20°C 1 year
Purity & Documentation
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Data Sheet (278 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[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
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)