C12-iE-DAP
Based on 1 publication(s) in Google Scholar
C12-iE-DAP (Lauroyl-γ-D-glutamyl-meso-diaminopimelic acid) is a highly potent and selective NOD1 agonist, with an EC50 of 0.027 nM in HEK-Blue cells expressing human NOD1. C12-iE-DAP activates the NOD1/RIPK2 signaling pathway and its downstream p38 MAPK and NF-κB, induces the expression of inflammatory mediators such as IL6 and IL8, and exerts synergistic effects with TLR4, Dectin-1 or Mincle signaling. C12-iE-DAP can be used in studies related to vascular inflammation, tumor metastasis and neuroinflammation.
For research use only. We do not sell to patients.
- CAS No.: 1269619-57-9
- Formula: C24H43N3O8
- Molecular Weight:501.61
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Publications Citing Use of MedChemExpress (MCE) C12-iE-DAP
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Biological Activity
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hNOD1 0.027 nM (EC50) |
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Cell Line
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Type | Value | Description | References |
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| HEK293 | EC50 |
0.027 nM
Compound: 16
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Agonist activity at human NOD-1 expressed in human HEK293 cells assessed as NF-kappaB induction by spectrophotometric analysis
Agonist activity at human NOD-1 expressed in human HEK293 cells assessed as NF-kappaB induction by spectrophotometric analysis
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[PMID: 21299227] |
C12-iE-DAP (compound 16) (Lauroyl-γ-D-glutamyl-meso-diaminopimelic acid) induces NF-κB/AP-1-dependent SEAP signaling in HEK-Blue cells expressing human NOD1, with an EC50 of 0.027 nM[5].
C12-iE-DAP (0.01-10 μg/mL; 18 h) acts synergistically with Curdlan or TDB to enhance NF-κB/AP-1-dependent SEAP expression in the human monocytic cell line THP1-XBlue-CD14, with activity levels exceeding the additive effect of stimulation by each agonist alone[2].
C12-iE-DAP (1-100 μg/mL; 24 h) acts synergistically with Curdlan or TDB to enhance the production of the IL-8 cytokine in the human monocyte cell line THP-1, with the production level exceeding the additive effect of stimulation by individual agonists[2].
C12-iE-DAP (10-9-10-8 M; 1 h) upregulates CD11b in granulocytes from fresh human whole blood in a dose-dependent manner, with a stronger induction effect at 10-8 M than at 10-9 M; whereas compound 27 exhibits stronger activity at both of the above concentrations[5].
C12-iE-DAP (5 μg/mL; 6 h) induces IL6 and IL8 mRNA expression in primary human brain pericytes and increases IL-8 release in cell culture supernatants[1].
C12-iE-DAP (1 μg/mL; 6 h)-induced IL8 expression in human brain pericytes depends on the NOD1/RIPK2/p38/NF-κB signaling pathway. NOD1 knockdown reduces IL8 induction by >62%, while inhibitors of RIPK2, p38 or NF-κB can significantly suppress this response[1].
C12-iE-DAP (1 μg/mL) acts synergistically with LPS (5 ng/mL) for 6 h to enhance IL8 mRNA expression in primary human brain pericytes, and the induced level is higher than that of LPS (100 ng/mL) alone[1].
C12-iE-DAP (2,000 ng/mL) increases the adhesion of HT29 cells to fibronectin, collagen I and collagen IV by approximately 2-fold, 2-fold and 1.5-fold, respectively, enhances the migration of HT29 cells by approximately 2-fold, and simultaneously increases the adhesion of MC38 cells to both collagen I and fibronectin by approximately 1.5-fold[4].
C12-iE-DAP (up to 2,000 ng/mL; up to 80 min) increases p38 phosphorylation in colorectal cancer cells by up to approximately 7-fold in a dose- and time-dependent manner, but does not induce corresponding changes in IκBα degradation[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human monocytic THP-1 cells
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Concentration:1-100 μg/mL
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Incubation Time:24 h
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Result:Induced IL-8 production in a dose-dependent manner.
Produced IL-8 production levels greater than the sum of levels induced by individual stimulation when combined with Curdlan or TDB, demonstrating a synergistic potentiation effect.
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Cell Line:human monocytic THP-1 cells
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Concentration:10 μg/mL
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Incubation Time:24 h (agonist incubation); inhibitors added 1 h prior to agonist treatment
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Result:Abrogated IL-8 production induced by individual treatment when RIP2 was inhibited via gefitinib.
Reduced IL-8 production induced by combined treatment with TDB to near baseline levels when RIP2 was inhibited via gefitinib.
Showed no significant effect on IL-8 production induced by individual treatment when Syk was inhibited via piceatannol.
Reduced IL-8 production induced by combined treatment with TDB to levels equivalent to individual treatment when Syk was inhibited via piceatannol.
Completely abrogated IL-8 production induced by both individual and combined treatment when dexamethasone was used.
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Cell Line:human colorectal cancer HT29 cells
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Concentration:2000 ng/mL
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Incubation Time:60 min (following 30 min DMSO pre-incubation)
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Result:Induced a 2-fold increase in HT29 cell migration compared to DMSO vehicle control, with statistical significance.
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Cell Line:human colorectal cancer HT29 cells
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Concentration:500-2000 ng/mL (fixed incubation time); 2000 ng/mL (time-dependent analysis)
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Incubation Time:fixed time (dose-dependent analysis); 20-80 min (2000 ng/mL)
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Result:Induced a dose-dependent increase in p38 phosphorylation, with up to a 7-fold increase at 2000 ng/mL compared to DMSO contro.
Induced a time-dependent increase in p38 phosphorylation, with up to a 2.3-fold increase at 80 min compared to baseline.
Activation of the NOD1 signaling pathway via C12-iE-DAP (1 mM; intracerebroventricular injection; once every 3 days for 4 weeks) abolishes the cognitive-improving, anti-inflammatory and anti-Aβ plaque effects of Avn-C in obese 5×FAD mice, with significant reversals observed in key indicators including the novel object recognition index, time spent in the target quadrant of the MWM, pro-inflammatory cytokine levels and Aβ load[3].
When MC38 cells pretreated with C12-iE-DAP (2,000 ng/mL) are injected intrasplenically into C57BL/6 mice, 37 metastatic nodules form on the liver surface on day 21[4].
Intrasplenic injection of HT29 or MC38 cells pretreated with C12-iE-DAP (2,000 ng/mL) increases their adhesion to liver sinusoids in C57BL/6 mice by approximately 2-fold, and this effect is blocked by ML130 (10 μM)[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (female, SPF, 5-6 weeks old)[2]
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Dosage:C12-iE-DAP: 1 μg/mouse; Curdlan; TDB: 10 μg/mouse
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Administration:i.m.; single dose
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Result:Co-stimulation synergistically increased serum IL-6 and KC levels at 3 h.
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Animal Model:5×FAD (male, 2 months old, high-fat diet-induced obesity-accelerated Alzheimer's disease)[3]
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Dosage:1 mM
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Administration:i.c.v.; once every three days; 4 weeks
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Result:Reduced object-recognition and spatial-memory performance.
Reversed the reductions in NOD1/RIP2/NF-κB signaling, inflammatory cytokines and Aβ deposition induced by Avenanthramide-C.
Chemical Information
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CAS No. 1269619-57-9
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Molecular Weight 501.61
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Formula C24H43N3O8
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Synonyms
Lauroyl-γ-D-glutamyl-meso-diaminopimelic acid; γ-D-glutamyl-meso-diaminopimelic acid
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Sequence
Lauroyl-γ-d-Glu-meso-diaminopimelic acid
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
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J Extracell Vesicles
Tumour-Derived Extracellular Vesicles Reprogramme Tumour-Associated Macrophages Into Immunosuppressive Phenotype via NOD1 Signalling in Clear Cell Renal Cell Carcinoma. [Abstract]2026 Jun;15(6):e70317. PMID: 42226559
Purity & Documentation
References
[1]. Navarro R, et al. Role of nucleotide-binding oligomerization domain 1 (NOD1) in pericyte-mediated vascular inflammation. Journal of cellular and molecular medicine. 2016 May;20(5):980-6. [Content Brief]
[2]. Tukhvatulin AI, et al. NOD1/2 and the C-Type Lectin Receptors Dectin-1 and Mincle Synergistically Enhance Proinflammatory Reactions Both In Vitro and In Vivo. Journal of inflammation research. 2020;13:357-368. [Content Brief]
[3]. Wang M, et al. Avenanthramide-C Mitigates High-Fat Diet-Accelerated Alzheimer's Pathologies via NOD1-Driven Neuroinflammation in 5×FAD Mice. Nutrients. 2025 Aug 19;17(16):2679. [Content Brief]
[4]. Jiang HY, et al. Activation of the pattern recognition receptor NOD1 augments colon cancer metastasis. Protein & cell. 2020 Mar;11(3):187-201. [Content Brief]
[5]. Agnihotri G, et al. Structure-activity relationships in nucleotide oligomerization domain 1 (Nod1) agonistic γ-glutamyldiaminopimelic acid derivatives. Journal of medicinal chemistry. 2011 Mar 10;54(5):1490-510. [Content Brief]
Calculators
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