Cadherin Activator

Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease.

Aristolactam I is an AQP1 inhibitor and Aristolochic acid I metabolite. Aristolactam I can be isolated from Aristolochia plants. Aristolactam I downregulates Twist1 expression, increases E-cadherin expression, and activates the TGF-β/Smad signaling pathway. Aristolactam I has anticancer activity against breast cancer. Aristolactam I is nephrotoxic. Aristolactam I is mainly used in the study of breast cancer and kidney diseases such as renal interstitial fibrosis.

E-cadherin activator-1 (Compound 13m) is an E-Cadherin activator. E-cadherin activator-1 can be used in the study of colorectal carcinoma.

NKP608 is a non-peptidic derivative of 4-aminopiperidine, a highly selective, orally active, neurokinin-1 (NK₁) receptor antagonist with IC₅₀ of 2.6 nM. NKP608 is active both in vitro and in vivo, showing extremely low affinity for NK₂, NK₃ receptors. NKP608 exerts its effects by blocking the NK₁ receptor, regulate cell proliferation and apoptosis, affect neurotransmitter functions and gastric mucosal repair mechanisms, and suppress the Wnt/β-catenin pathway in antitumor research. NKP608 is applicable to research related to various diseases, including cough, anxiety disorders, depression, gastric mucosal injury, and colorectal cancer.

7-Hydroxystaurosporine (UCN-01), a derivative of Staurosporine (HY-15141), is a selective protein kinase C (PKC) inhibitor with antitumor activity. 7-hydroxystaurosporine induces apoptosis and inhibits cell proliferation in colon carcinoma and leukemia cells, suppresses invasion and migration in glioblastoma cells. 7-Hydroxystaurosporine exhibits efficacy in breast cancer xenograft mouse models. 7-Hydroxystaurosporine can be used for colon carcinoma, breast cancer, glioblastoma and leukemia research.

(R)-MMP408 is an isomer of MMP408 (HY-12093). MMP408 is an orally active MMP-12 inhibitor (IC₅₀=2.0 nM for hMMP-12) that effectively interferes with the epithelial-mesenchymal transition (EMT) process. MMP408 significantly upregulates the expression of E-cadherin in nasal epithelial cells, while inhibiting mesenchymal markers such as vimentin, α-smooth muscle actin and fibronectin, thereby reversing the EMT phenotype. MMP408 is used in studies of airway remodeling-related diseases, including chronic rhinosinusitis with nasal polyps, chronic obstructive pulmonary disease (COPD) and asthma.

Nef-M1 (Nef-Motif-1) is an antagonist peptide targeting CXCR4 and an apoptosis inducer derived from a myristoylated protein encoded by the nef gene in HIV. Nef-M1 inhibits tumor angiogenesis and epithelial-mesenchymal transition (EMT). Nef-M1 activates the apoptosis pathway by increasing the level of caspase-3 in cancer cells. Nef-M1 simultaneously inhibits VEGF-A, p-GSK-3β and vimentin, and enhances E-cadherin, thereby inhibiting angiogenesis and EMT processes. Nef-M1 can be used in the study of colorectal cancer and breast cancer.

(Rac)-AAA is a regulator and inhibitor targeting GPR75. By blocking the 20-HETE-induced downregulation of GPR75 expression, (Rac)-AAA effectively inhibits the activation of key downstream signaling pathways including EGFR, AKT, NF-κB and FAK. (Rac)-AAA reverses 20-HETE-mediated epithelial-mesenchymal transition, which is specifically characterized by downregulating vimentin (vimentin), upregulating E-Cadherin, as well as reducing MMP-2 activity and cancer cell migration ability. (Rac)-AAA also abolishes the 20-HETE-induced upregulation of HIC-5 expression and anchorage-independent growth, and modulates the subcellular localization of PKC-α and phosphorylated AKT. (Rac)-AAA is investigated in androgen-independent prostate cancer (castration-resistant prostate cancer).

Salviamarinic acid A is a water-soluble phenolic acid that can be extracted from Salvia miltiorrhiza with potent anti-pulmonary fibrosis activity. Salviamarinic acid A significantly increases cell viability, cell index, cell motility and E-cadherin expression, and reduces TGF-β1, α-SMA and Collagen I levels. Salviamarinic acid A can be used for pulmonary fibrosis research.

Picrasidine J is a selective inhibitor targeting the KLK-10 protease and the ERK signaling pathway. Picrasidine J inhibits epithelial-mesenchymal transition (EMT) by upregulating E-Cadherin and ZO-1 and downregulating β-catenin and Snail, while simultaneously reducing KLK-10 expression and inhibiting ERK phosphorylation, thereby exhibiting significant anti-migratory and anti-invasive activity. Picrasidine J can inhibit the metastasis of head and neck squamous cell carcinoma (HNSCC) and is primarily used in anti-metastasis research for head and neck tumors.

NF-κB/STAT3/iNOS-IN-1 is a NF-κB/STAT3/iNOS inhibitor. NF-κB/STAT3/iNOS-IN-1 reduces the expression of inflammatory mediators TNF-α, IL-1β, IL-6, IL-8 and COX-2. NF-κB/STAT3/iNOS-IN-1 upregulates the expression of epithelial barrier-related proteins E-cadherin, Occludin and Zonula occludens-1. NF-κB/STAT3/iNOS-IN-1 alleviates disease severity and histopathological damage in mouse colitis models. NF-κB/STAT3/iNOS-IN-1 can be used for the research of inflammatory bowel disease (colitis).

JNK3-IN-10 is a blood-brain barrier-impermeable JNK3 inhibitor (IC₅₀=0.257 nM) with over 400-fold selectivity over JNK1. JNK3-IN-10 blocks the JNK3-mediated signaling pathway downstream of TGF-β₁, inhibits TGF-β₁-induced phosphorylation of c-Jun, reduces the expression of pro-fibrotic markers, and restores the expression of the epithelial protein E-cadherin. JNK3-IN-10 exhibits low cytotoxicity, anti-fibrotic, cytoprotective and renoprotective effects, and alleviates albuminuria, glomerulosclerosis and podocyte foot process fusion. JNK3-IN-10 can be used for the research of chronic kidney disease, glomerulosclerosis and adriamycin-induced nephropathy.

Cystatin B agonist 1 is an orally active MMP-2/9 inhibitor. Cystatin B agonist 1 exhibits inhibitory effects with IC₅₀ values of 3.95 and 3.43 μM against U87 and T98G cells, respectively. Cystatin B agonist 1 induces the cell-cycle arrest at S phase, inhibits angiogenesis, and suppresses migration and invasion of MG cells. Cystatin B agonist 1 inhibits tumor growth in U87 MG xenograft model. Cystatin B agonist 1 can be used for the study of malignant glioma (MG).

Ecad saRNA is a small activating RNA (saRNA) targeting the E-cadherin genes. Ecad saRNA induce expression of the E-cadherin genes, and targets the E-cadherin promoters at ?215 relative to gene's transcription start site.