1. NF-κB Immunology/Inflammation Apoptosis Metabolic Enzyme/Protease
  2. NF-κB NO Synthase Interleukin Related TNF Receptor Cytochrome P450
  3. N,N-Diethylacetamide

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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N,N-Diethylacetamide

N,N-Diethylacetamide Chemical Structure

CAS No. : 685-91-6

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Description

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.

IC50 & Target

NF-κB

 

IL-1β

 

IL-6

 

IL-8

 

CYP2B1

 

CYP2B2

 

In Vitro

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.

Cell Viability Assay[1]

Cell Line: HTR-8/SVneo, RAW 264.7, HEK 293
Concentration: up to 10 mM
Incubation Time: 2 h (pre-treatment); 24 h (LPS treatment)
Result: Did not significantly affect the viability of HTR-8/SVneo, RAW 264.7, or HEK 293 cells compared to untreated controls.

Western Blot Analysis[1]

Cell Line: RAW 264.7
Concentration: 0.1, 1, 10 mM
Incubation Time: 2 h (pre-treatment); 6 h (LPS treatment)
Result: Significantly inhibited LPS-induced iNOS expression in RAW 264.7 cells at 10 mM (P < 0.001) compared to LPS control.

ELISA Assay[1]

Cell Line: HTR-8/SVneo
Concentration: 0.1, 1, 10 mM
Incubation Time: 2 h (pre-treatment); 24 h (LPS treatment)
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.

ELISA Assay[1]

Cell Line: RAW 264.7
Concentration: 0.1, 1, 10 mM
Incubation Time: 2 h (pre-treatment); 24 h (LPS treatment)
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.

Western Blot Analysis[1]

Cell Line: RAW 264.7
Concentration: 0.1, 1, 10 mM
Incubation Time: 2 h (pre-treatment); 15 min (LPS treatment)
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.
In Vivo

N,N-Diethylacetamide (375-750 mg/kg; i.p.; two doses) delays LPS-induced preterm birth in a dose-dependent manner, with 750 mg/kg completely preventing delivery for at least 25 h[1].
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.

Animal Model: C57Bl/6 (timed pregnant, weight 27–36 g)[1]
Dosage: 375 mg/kg; 750 mg/kg
Administration: i.p.; two doses (T=-15 min and T=10 h)
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.
Animal Model: Sprague-Dawley (male, 5-6 weeks old)[2]
Dosage: 150, 300 mg/kg; 400-500 mg/kg
Administration: i.p.; daily; 3 days
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.
Molecular Weight

115.17

Formula

C6H13NO

CAS No.
Appearance

Liquid (Density: 0.925 g/cm3)

Color

Colorless to light yellow

SMILES

CCN(C(C)=O)CC

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Store at room temperature 3 years

In solvent -80°C 2 years
-20°C 1 year
Purity & Documentation
References
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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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N,N-Diethylacetamide
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