TriDAP

TriDAP (0-10 μg/mL; 6 days) dose-dependently inhibits osteogenic differentiation of primary mouse calvarial osteoblast precursors and enhances osteoclast differentiation in the co-culture system of mouse BMMs and primary calvarial osteoblast precursors^[1].
TriDAP (0-10 μg/mL; 2 days) downregulates the expression of osteogenic marker genes including Alp, Bsp and Runx2 in MC3T3-E1 mouse preosteoblasts in a dose-dependent manner^[1].
TriDAP (0-10 μg/mL; 18 h) dose-dependently inhibits the transcriptional activity of Runx2 in MC3T3-E1 mouse preosteoblasts^[1].
TriDAP (1 μg/mL; 2-24 h) reduces the stability of Runx2 protein in transiently transfected HEK293 cells. After 8 hours of co-incubation with Cycloheximide (HY-12320), the relative level of Runx2 decreases by approximately 50%, which enhances Smurf1-mediated Runx2 degradation in cells^[1].
TriDAP (1-10 μg/mL; 24 h) increases the ubiquitination level of Runx2 in transiently transfected HEK293 cells in a dose-dependent manner^[1].
TriDAP (0.1-10 μg/mL; 2 days) dose-dependently increases the RANKL/OPG ratio in primary mouse calvarial osteoprogenitor cells, through a mechanism that decreases OPG secretion and increases RANKL secretion^[1].
TriDAP (1 μg/mL; 15-90 min) activates the NF-κB pathway in MC3T3-E1 mouse osteoprogenitor cells by reducing IκBα levels and increasing p65 levels, and induces nuclear translocation of NF-κB p65^[1].
TriDAP (0.1-10 μg/mL; 24 h) dose-dependently enhances the transcriptional activity of NF-κB in MC3T3-E1 mouse preosteoblasts^[1].
TriDAP (10 μg/mL; 10 days) inhibits osteogenic mineralization of wild-type primary mouse calvarial preosteoblasts, but this effect is abolished in NOD1-deficient preosteoblasts, indicating that this action is dependent on NOD1^[1].
TriDAP (10 μg/mL; 16 h) preferentially activates the transcriptional activity of NF-κB in HEK293 cells transfected with NOD1, whereas the activity is extremely low in cells transfected with NOD2^[1].
TriDAP (10-100 μM) binds directly to purified full-length NOD1 protein, with a measured K_d value of 34.5 μM via SPR^[4].
Binding of TriDAP (0.1 mM) to purified full-length NOD1 protein increases the binding affinity between purified RICK protein and NOD1, with SPR assays showing that its K_d value decreases from 4.13 μM to 3.26 μM^[4].
TriDAP (0-5 mM; 1-4 h) induces the expression of NOD1 and secretion of IL-8 in Caco2-BBE intestinal epithelial cells, and this pro-inflammatory response depends on the expression of NOD1^[4].
TriDAP activates the NOD1 pathway in HEK-Blue hNOD1 cells, with an EC₅₀ of 700 ng/mL^[5].
TriDAP (0.4-50 µM; 6-24 h) increases the proportion of IL-8⁺ human lung epithelial A549 cells by 3.29-fold, elevates the proportion of IL-8⁺ human lung epithelial A549-Dual cells, does not reduce cell viability, and activates the NF-κB and ISRE pathways in human lung epithelial A549-Dual cells^[5].
TriDAP (50 µM; 8 h) upregulates the mRNA expression levels of IL-8, CXCL10 and ISG15 in the human lung epithelial cell line A549-Dual^[5].
TriDAP (2-50 µM; 3-hour pretreatment; 48 hours post-infection) dose-dependently inhibits SARS-CoV-2 replication in human lung epithelial A549-Dual cells, with an EC₅₀ of 7.75 µM, and reduces the number of infected cells by 49% at a concentration of 50 µM^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.