n-cadherin

BML-284 (Wnt agonist 1) is a potent, selective and , cell-permeable Wnt signaling activator.

ZLDI-8 is an inhibitor of Notch activating/cleaving enzyme ADAM-17 and inhibits the cleavage of Notch protein.

ADH-1 trifluoroacetate (Exherin trifluoroacetate) is a cyclic pentapeptide vascular-targeting agent with potential antineoplastic and antiangiogenic activities. ADH-1 selectively and competitively binds to and blocks N-cadherin, which may result in disruption of tumor vasculature, inhibition of tumor cell growth, and the induction of tumor cell and endothelial cell apoptosis.

ADH-1 (Exherin) is an N-cadherin antagonist, inhibits N-cadherin mediated cell adhesion with potential antineoplastic and antiangiogenic activities.

BML-284 hydrochloride (Wnt agonist 1 HCL) is a potent, selective Wnt canonical signaling activator and tubulin polymerization inhibitor.

N-Cadherinmimic peptide is an agonist of N-cadherin. This peptide enhances β-catenin signaling to promote the homodimerization of N-cadherin, inducing early chondrogenesis and cartilage matrix production in mesenchymal stem cells (MSCs). It holds promise for studies focused on cartilage regeneration using mesenchymal stem cells.

Anti-TNBC agent-9 (Compound 3as) is an anticancer agent used for treating triple-negative breast cancer (TNBC). It exhibits significant inhibitory activity against MDA-MB-453 cells, with an IC50 value of 8.5 μM. Anti-TNBC agent-9 impedes tumor cell migration by upregulating E-cadherin and downregulating N-cadherin, matrix metalloproteinase 2 (MMP2), and MMP9. Additionally, it inhibits tumor cell proliferation by inducing apoptosis, achieved through the increased expression of pro-apoptotic protein BAX and decreased expression of anti-apoptotic protein BCL-2.

PRMT7-IN-2 (A33) is a selective inhibitor of PRMT7 with an IC50 value of 0.50 μM. It causes cell cycle arrest at the G0/G1 phase, induces apoptosis, and inhibits cell growth both in vivo and in vitro. PRMT7-IN-2 reduces monomethylation levels of arginine by PRMT7, increases the expression of the epithelial marker E-cadherin, and decreases the expression of mesenchymal markers N-cadherin, Vimentin, and ZEB2.

SHP2ATTEC degrader-1 is an ATTEC degrader targeting SHP2, achieving an 83.31% degradation rate in PANC-1 cells at 1.0 μM after 24 hours. It inhibits cell proliferation both in vitro and in vivo. SHP2ATTEC degrader-1 induces apoptosis, elevates the expression of epithelial markers (E-cadherin), and reduces the expression of mesenchymal markers (such as N-cadherin, Vimentin).

TKL002 is a blood-brain barrier-permeable inhibitor of the CTH/H₂S/NF-κB/EMT signaling axis. It induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells. TKL002 also inhibits the migration and invasion of glioblastoma cells by upregulating E-cadherin and downregulating N-cadherin and vimentin expression, and is used in glioblastoma research.

OSU-03013, an analog of Celecoxib, promotes apoptosis while upregulating E-cadherin and downregulating β-catenin, c-myc, Wnt1, and N-cadherin. It reduces cell migration and invasion capacity and inhibits the proliferation of colon cancer (CC) cells by modulating the expression of Wnt and mTOR. OSU-03013 is utilized in colon cancer research.

NUAK1-IN-3 is a potent and selective inhibitor of NUAK1, with an IC50 of 0.49 nM. It also inhibits NUAK2 and JAK3, exhibiting IC50 values of 265 nM and 225 nM respectively. The compound interacts with NUAK1 at Glu139, forming a salt bridge with its bicyclic nitrogen atom and Asp142, and enhances hydrophobic interactions through a fluorine atom. NUAK1-IN-3 reduces the phosphorylation of MYPT1, thereby inhibiting the NUAK1-MYPT1 signaling axis while suppressing the proliferation, migration, and invasion of triple-negative breast cancer cells. It can reverse TGF-β1-induced epithelial-mesenchymal transition (EMT) marker changes, downregulating Snail and N-cadherin expression, while upregulating E-cadherin expression in tumor tissues. Additionally, NUAK1-IN-3 inhibits tumor growth in triple-negative breast cancer xenograft models, making it a useful tool for research related to this cancer.

SWELYYPLRANL-NH2 TFA acts as an antagonist to both E-cadherin and N-cadherin, with inhibitory effects on phage clone binding to E- or N-cad/Fc chimeric proteins, exhibiting IC50 values of 0.7 μM and 0.09 μM, respectively. Additionally, it disrupts cell aggregation and is utilized to enhance drug delivery by increasing the permeability of epithelial and endothelial barriers [1].

SWELYYPLRANL-NH2 is a dual antagonist of E-cadherin and N-cadherin, effectively inhibiting the binding of phage clones to both E-cad/Fc and N-cad/Fc chimeric proteins with IC50 values of 0.7 μM and 0.09 μM, respectively. This compound also impedes cell aggregation and has potential applications in enhancing drug delivery by increasing epithelial and endothelial permeability barriers [1].

ANT308 is an antagonist of the vasoactive intestinal peptide (VIP receptor). It significantly enhances T cell activation and proliferation. By inhibiting VIP-VPAC2 signaling and reducing the expression of MCAM and N-cadherin, ANT308 suppresses melanoma cell migration and metastasis while inducing apoptosis. This compound is useful for research in acute myeloid leukemia (AML) and uveal melanoma (UVM).

ANT308 TFA serves as an antagonist for the vasoactive intestinal peptide (VIP receptor). It significantly enhances the activation and proliferation of T cells. By inhibiting VIP-VPAC2 signaling and reducing the expression of MCAM and N-cadherin, ANT308 TFA impedes the migration and metastasis of melanoma cells and induces apoptosis. This compound is applicable in research related to acute myeloid leukemia (AML) and uveal melanoma (UVM).