877462-71-0
Chemical Structure
TriDAP
Synonym(s): L-Ala-γ-D-Glu-meso-diaminopimelic acid
- CAS No.: 877462-71-0
- Formula:C15H26N4O8
- Molecular Weight:390.39
InChIKey: FMNCPUGORYYCEM-AUXWQGHOSA-N
SMILES: C[C@H](N)C(N[C@@H](C(O)=O)CCC(NC(C(O)=O)CCCC(N)C(O)=O)=O)=O
Biological Activity: TriDAP (L-Ala-γ-D-Glu-meso-diaminopimelic acid) is a NOD1 agonist with a Kd value of 34.5 μM. TriDAP enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP decreases IκBα levels and increases p65 levels. TriDAP induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection[1][2][3][4][5].
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TriDAP | TriDAP (L-Ala-γ-D-Glu-meso-diaminopimelic acid) is a NOD1 agonist with a Kd value of 34.5 μM. TriDAP enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP decreases IκBα levels and increases p65 levels. TriDAP induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection. | |||||||||||||||||||||
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- [1]. Enoksson M, et al. Human cord blood-derived mast cells are activated by the Nod1 agonist M-TriDAP to release pro-inflammatory cytokines and chemokines. J Innate Immun. 2011;3(2):142-149. [Content Brief]
- [2]. Laroui H, et al. L-Ala-γ-D-Glu-meso-diaminopimelic acid (DAP) interacts directly with leucine-rich region domain of nucleotide-binding oligomerization domain 1, increasing phosphorylation activity of receptor-interacting serine/threonine-protein kinase 2 and its interaction with nucleotide-binding oligomerization domain 1. J Biol Chem. 2011;286(35):31003-31013. [Content Brief]
- [3]. Garcia-Vidal E, et al. Nucleotide-Binding Oligomerization Domain 1 (NOD1) Agonists Prevent SARS-CoV-2 Infection in Human Lung Epithelial Cells through Harnessing the Innate Immune Response. Int J Mol Sci. 2024;25(10):5318. Published 2024 May 13. [Content Brief]
- [4]. Chang MC, et al. Inducing phospholipase A2 and cyclooxygenase-2 expression and prostaglandins' production of human dental pulp cells by activation of NOD receptor and its downstream signaling. Int J Biol Macromol. 2025;292:139193. [Content Brief]
- [5]. Park OJ, et al. The dual roles of peptidoglycans: NOD1 and NOD2 inversely regulate bone metabolism. Exp Mol Med. 2025;57(8):1837-1846. [Content Brief]
Keywords
