From 11:00 pm to 12:00 pm EST ( 8:00 pm to 9:00 pm PST ) on January 6th, the website will be under maintenance. We are sorry for the inconvenience. Please arrange your schedule properly.
Adrixetinib (Q702) is an orally active triple inhibitor against CSF1R, Mer, and Axl, with Kd values of 8.7 nM, 0.8 nM, and 0.3 nM, respectively. Adrixetinib acts as a potent immune modulator that remodels the tumor microenvironment. Adrixetinib increases the abundance of M1 macrophages and CD8⁺ T cells, while decreasing the levels of M2 macrophages and myeloid-derived suppressor cells (MDSCs). Adrixetinib upregulates the expression of MHC class I and E-cadherin in tumor cells. Adrixetinib shows remarkable antitumor efficacy in syngeneic mouse tumor models. Adrixetinib is suitable for the research of breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma .
Escin IA is an oral LOXL2 inhibitor and EMT inhibitor, with selectivity for LOXL2-expressing cells. Escin IA suppresses invasion, migration, and metastasis of breast cancer cells, and acts as the primary anti-TNBC metastasis constituent of Aesculus chinensis Bunge fruit saponin fraction. Escin IA can be used for the research of triple-negative breast cancer, acute inflammation, and ethanol-induced gastric mucosal lesions .
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 .
ITX3 is a specific and nontoxic inhibitor of TrioN (N-terminal GEF domain of the multidomain Trio protein) with an IC50 value of 76 μM. ITX3 can be used for the research of agent .
LNSMGQD is a cyclic peptide fragment derived from desmoglein 1 (amino acids 81-86), which mimics trans-interactions and acts as part of the tandem peptide binding interface of desmoglein 2. LNSMGQD not only binds to desmoglein 1 and 3, but also effectively inhibits their homophilic trans-interactions, while reducing the probability of homophilic or heterophilic binding between desmoglein 2 and Dsc2, N-cadherin and E-cadherin. LNSMGQD is applicable to the research on disease mechanisms such as Crohn's disease and pemphigus vulgaris .
ZLDI-8 is a Notch activating/cleaving enzyme ADAM-17 inhibitor and inhibits the cleavage of Notch protein. ZLDI-8 decreases the expression of pro-survival/anti-apoptosis and epithelial-mesenchymal transition (EMT) related proteins. ZLDI-8 is also a competitive and irreversible tyrosine phosphatase (Lyp) inhibitor with an IC50 of 31.6 μM and a Ki of 26.22 μM. ZLDI-8 inhibits the growth of MHCC97-H cells with an IC50 of 5.32 μM .
BAS00602705 is an E-cadherin inhibitor. BAS00602705 exerts its function by blocking the trans-interactions of E-cadherin molecules within junctional complexes, without permanently altering E-cadherin expression levels. BAS00602705 significantly impairs invadopodia formation in pancreatic cancer cells. BAS00602705 can be used for the study of anti-invasive therapeutic strategies in cancers characterized by dysregulated E-cadherin-mediated invadopodia activity, such as pancreatic ductal adenocarcinoma (PDAC) .
(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 .
PRMT7-IN-2 (A33) is a selective PRMT7 inhibitor with an IC50 of 0.50 μM. PRMT7-IN-2 arrests cell cycle at G0/G1 phase, induces cell apoptosis, and inhibits cell growth in vivo and in vitro. PRMT7-IN-2 decreases the monomethylarginine level of PRMT7, increases expression of epithelial marker (E-cadherin, and reduces expression of mesenchymal markers such as N-cadherin, Vimentin, and ZEB2 .
Hakin-1 is a E3 Ubiquitin-Ligase Hakai inhibitor. Hakin-1 blocks Hakai-mediated global ubiquitination and specific ubiquitination of E-cadherin and inhibits epithelial-mesenchymal transition (EMT) progression. Hakan-1 inhibits tumor progression and cancer metastasis. Hakin-1 can be used for the study of carcinoma such as colorectal cancer .
TRPM7-IN-1 (compound SUD), a benzoylurea derivative, is an effective TRPM7 inhibitor. TRPM7-IN-1 induces cell cycle arrest and apoptosis, decreases the migration of MCF-7 and BGC-823 cells. TRPM7-IN-1 decreases vimentin expression and increases E-cadherin expression. TRPM7-IN-1 potentially reduces the TRPM7-like current and decreases TRPM7 expression through the PI3K/Akt signaling pathway. TRPM7-IN-1 is a potential agent to suppress the metastasis of breast and gastric cancer by inhibiting TRPM7 expression and function .
(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) .
Anti-CDH1/E-cadherin/CD324 Antibody is a humanized antibody expressed in CHO, targeting CDH1/E-cadherin/CD324. The Anti-CDH1/E-cadherin/CD324 Antibody contains a huIgG1 heavy chain and a huκ light chain, with a predicted molecular weight (MW) of 146.6 kDa. The isotype control for Anti-CDH1/E-cadherin/CD324 Antibody can be referenced as Human IgG1 kappa, Isotype Control (HY-P99001).
BAS00093476 is an E-cadherin inhibitor. BAS00093476 exhibits inhibitory activity against E-cadherin-mediated cell-cell adhesion in human pancreatic tumor BxPC-3 cells. BAS00093476 can be applied to the research on the modulation of E-cadherin-mediated cell-cell adhesion in solid tumors expressing cadherins .
BAS00132635 (Compound AS9) is an E-cadherin inhibitor. BAS00132635 can block trans-interactions of E-cadherin molecules in junctional complexes and reduce the number of cancer cells exhibiting invadopodia. BAS00132635 can be used for the research of cancer, such as Pancreatic cancer .
Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) is an anti-mouse E-Cadherin/CD324 IgG1 monoclonal antibody. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can downregulate the HER signaling axis and PI3K/Akt/mTOR signaling pathway. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can inhibit the proliferation of tumor cells and induce their apoptosis. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can be used for researches on cancer and inflammation conditions such as breast cancer, chronic compression injury (CCI) and asthma .
BML-284 hydrochloride is a potent and cell-permeable Wnt signaling activator. BML-284 induces TCF-dependent transcriptional activity with an EC50 of 700 nM .
SLEC-11 is a CDH1/E-cadherin modulator that potently inhibits cell death in E-cadherin-deficient cells (EC50=8.2 μM). SLEC-11 can be used to study potential synthetic lethal therapies for gastric cancer .
Apoptosis inducer 44 is an apoptosis inducer. Apoptosis inducer 44 triggers apoptosis in MDA-MB-231 cells by increasing the levels of Bax and Cyt C, reducing Bcl-2, and initiating caspase-3 cleavage. Apoptosis inducer 44 suppresses the invasion and migration of MDA-MB-231 cells by down-regulating MMP-2 and MMP-9 expression and up-regulating E-cadherin protein levels. Apoptosis inducer 44 can be used for the study of breast cancer .
Ovalitenone is a flavonoid compound that can be isolated from the plant Millettia peguensis. It shows no cytotoxic effects on lung cancer H460 and A549 cells, but it significantly inhibits anchorage-independent growth, CSC-like phenotypes, colony formation, and the migration and invasion capabilities of cancer cells. Ovalitenone can significantly reduce the levels of N-cadherin, snail, and slug, while increasing E-cadherin, thus inhibiting the EMT pathway. Additionally, Ovalitenone suppresses the signaling pathways regulated by focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (AKT), mammalian target of rapamycin (mTOR), and cell division cycle 42 (Cdc42) .
SHP2 ATTEC degrader-1 is a SHP2ATTEC degrader. SHP2 ATTEC degrader-1 has degradation rate of 83.31 at 1.0 μM for 24 h in the PANC-1 cell line. SHP2 ATTEC degrader-1 inhibits cell growth in vivo and in vitro. SHP2 ATTEC degrader-1 induces apoptosis and increases the expression of the epithelial marker (E-cadherin)， and reduces the expression of interstitial markers (such as N-cadherin, Vimentin) (Pink: LC3 ligand (HY-174085); Black :linker HY-140468; Blue: SHP2 ligand (HY-174084) .
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 .
Adrixetinib (Q702) TFA is an orally active triple inhibitor against CSF1R, Mer, and Axl, with Kd values of 8.7 nM, 0.8 nM, and 0.3 nM, respectively. Adrixetinib TFA acts as a potent immune modulator that remodels the tumor microenvironment. Adrixetinib TFA increases the abundance of M1 macrophages and CD8⁺ T cells, while decreasing the levels of M2 macrophages and myeloid-derived suppressor cells (MDSCs). Adrixetinib TFA upregulates the expression of MHC class I and E-cadherin in tumor cells. Adrixetinib TFA shows remarkable antitumor efficacy in syngeneic mouse tumor models. Adrixetinib TFA is suitable for the research of breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma .
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 .
AW01178 is a Class I HDAC inhibitor. AW01178 induces the upregulation of E-cadherin at both mRNA and protein levels and inhibits the EMT of breast cancer cells .
anti-TNBC agent-9 (Compound 3as) is an anti-cancer agent for triple-negative breast cancer (TNBC). anti-TNBC agent-9 exhibits significant inhibitory activity against MDA-MB-453 cells with an IC50 value of 8.5 μM. anti-TNBC agent-9 inhibits tumor cell migration by upregulating E-cadherin and downregulating N-cadherin, matrix metalloproteinase 2 (MMP2), and MMP9. anti-TNBC agent-9 induces apoptosis by increasing the expression of the pro-apoptotic protein BAX and decreasing the expression of the anti-apoptotic protein BCL-2, thereby inhibiting tumor cell proliferation .
Aristolactam I (Standard) is the analytical standard of Aristolactam I. This product is intended for research and analytical applications. 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 .
AL-GDa62 is a derivative of the CDH1/E-cadherin modulator SLEC-11 (HY-145268) and induces apoptosis in CDH1 -/- cells. AL-GDa62 has an EC50 of 3.2 μM and 2 μM for isogenic mammary epithelial cells MCF10A-WT (wild type) and mutant MCF10A-CDH1 -/-, respectively. AL-GDa62 specifically inhibits TCOF1, ARPC5, and UBC9, and suppresses SUMOylation at low micromolar concentrations .
CT1-3 is a potent anticancer agent. CT1-3 induces mitochondria-mediated apoptosis by regulating JNK/Bcl-2/Bax/XIAP pathway. CT1-3 suppresses the epithelial mesenchymal transition (EMT) potential of human cancer cells (HCCs) via regulating the E-cadherin/Snail axis, thus inhibits tumorigenesis. CT1-3 has a strong antitumor effect in mice model and exhibits no significant hepatic and renal toxicity .
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 .
ML327 (Standard) is the analytical standard of ML327 (HY-103038). This product is intended for research and analytical applications. ML327 is a blocker of MYC which can also de-repress E-cadherin transcription and reverse Epithelial-to-Mesenchymal Transition (EMT).
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 .
TKL002 is a blood-brain barrier-permeable inhibitor of the CTH/H2S/NF-κB/EMT signaling axis. TKL002 induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells. TKL002 inhibits the migration and invasion of glioblastoma cells by upregulating E-cadherin and downregulating N-cadherin and vimentin. TKL002 is applicable to relevant research on glioblastoma .
OSU-03013 is a Celecoxib (HY-14398) analog. OSU-03013 can promote apoptosis, up-regulate E-cadherin, and down-regulate β-catenin, c-myc, Wnt1, and N-cadherin. OSU-03013 reduces cell migration and invasion. OSU-03013 regulates both Wnt and mTOR expression to inhibit colon cancer (CC) cell proliferation. OSU-03013 can be used for CC cancer 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 .
JNK3-IN-11 is a selective JNK3 inhibitor with an IC50 of 2.08 nM. JNK3-IN-11 binds to the JNK3 ATP-binding pocket, forming conserved hydrogen bonds with Met149 and a water-mediated hydrogen bond with Lys93. JNK3-IN-11 suppresses TGF-β1-induced c-Jun phosphorylation, reduces profibrotic markers COL1A1 and PAI-1, restores E-cadherin expression, and has protection against podocyte injure. JNK3-IN-11 can be used for the research of chronic kidney disease .
NUAK1-IN-3 is a potent and selective NUAK1 inhibitor with an IC50 of 0.49 nM. NUAK1-IN-3 also inhibits NUAK2 and JAK3 with IC50 values of265 and 225 nM. NUAK1-IN-3 engages Glu139 of NUAK1, forms a salt bridge between its bicyclic ring nitrogen and Asp142, and uses a fluorine atom to enhance hydrophobic binding interactions. NUAK1-IN-3 attenuates MYPT1 phosphorylation, suppresses the NUAK1-MYPT1 signaling axis, and inhibits proliferation, migration, and invasion of triple-negative breast cancer cells. NUAK1-IN-3 reverses TGF-β1-induced epithelial-mesenchymal transition (EMT) marker alterations, downregulates Snail and N-cadherin, and upregulates E-cadherin in tumor tissues. NUAK1-IN-3 suppresses tumor growth in triple-negative breast cancer xenograft models. NUAK1-IN-3 can be used for the research of triple-negative breast cancer .
BML-284 (Standard) is the analytical standard of BML-284. This product is intended for research and analytical applications. BML-284 is a potent and cell-permeable Wnt signaling activator. BML-284 induces TCF-dependent transcriptional activity with an EC50 of 700 nM .
LNSMGQD is a cyclic peptide fragment derived from desmoglein 1 (amino acids 81-86), which mimics trans-interactions and acts as part of the tandem peptide binding interface of desmoglein 2. LNSMGQD not only binds to desmoglein 1 and 3, but also effectively inhibits their homophilic trans-interactions, while reducing the probability of homophilic or heterophilic binding between desmoglein 2 and Dsc2, N-cadherin and E-cadherin. LNSMGQD is applicable to the research on disease mechanisms such as Crohn's disease and pemphigus vulgaris .
SWELYYPLRANL-NH2 is an E-cadherin and N-cadherin antagonist. SWELYYPLRANL-NH2 inhibits phage clone binding to E- or N-cad/Fc chimeric protein (IC50: 0.7 and 0.09 μM respectively). SWELYYPLRANL-NH2 inhibits cell aggregation. SWELYYPLRANL-NH2 can be used to promote drug delivery through epithelial and endothelial permeability barriers .
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 .
SWELYYPLRANL-NH2 TFA is an E-cadherin and N-cadherin antagonist. SWELYYPLRANL-NH2 TFA inhibits phage clone binding to E- or N-cad/Fc chimeric protein (IC50: 0.7 and 0.09 μM respectively). SWELYYPLRANL-NH2 TFA inhibits cell aggregation. SWELYYPLRANL-NH2 can be used to promote drug delivery through epithelial and endothelial permeability barriers .
Anti-CDH1/E-cadherin/CD324 Antibody is a humanized antibody expressed in CHO, targeting CDH1/E-cadherin/CD324. The Anti-CDH1/E-cadherin/CD324 Antibody contains a huIgG1 heavy chain and a huκ light chain, with a predicted molecular weight (MW) of 146.6 kDa. The isotype control for Anti-CDH1/E-cadherin/CD324 Antibody can be referenced as Human IgG1 kappa, Isotype Control (HY-P99001).
Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) is an anti-mouse E-Cadherin/CD324 IgG1 monoclonal antibody. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can downregulate the HER signaling axis and PI3K/Akt/mTOR signaling pathway. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can inhibit the proliferation of tumor cells and induce their apoptosis. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can be used for researches on cancer and inflammation conditions such as breast cancer, chronic compression injury (CCI) and asthma .
Escin IA is an oral LOXL2 inhibitor and EMT inhibitor, with selectivity for LOXL2-expressing cells. Escin IA suppresses invasion, migration, and metastasis of breast cancer cells, and acts as the primary anti-TNBC metastasis constituent of Aesculus chinensis Bunge fruit saponin fraction. Escin IA can be used for the research of triple-negative breast cancer, acute inflammation, and ethanol-induced gastric mucosal lesions .
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 .
Ovalitenone is a flavonoid compound that can be isolated from the plant Millettia peguensis. It shows no cytotoxic effects on lung cancer H460 and A549 cells, but it significantly inhibits anchorage-independent growth, CSC-like phenotypes, colony formation, and the migration and invasion capabilities of cancer cells. Ovalitenone can significantly reduce the levels of N-cadherin, snail, and slug, while increasing E-cadherin, thus inhibiting the EMT pathway. Additionally, Ovalitenone suppresses the signaling pathways regulated by focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (AKT), mammalian target of rapamycin (mTOR), and cell division cycle 42 (Cdc42) .
Aristolactam I (Standard) is the analytical standard of Aristolactam I. This product is intended for research and analytical applications. 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 .
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 .
Cadherin-1/CD324 protein, a calcium-dependent adhesion molecule, mediates cell processes. It interacts homophilically with other cadherin molecules, sorting and organizing cell types. CDH1 regulates adhesion, mobility, and proliferation of epithelial cells. It serves as an integrin ligand, suppressing invasion and promoting non-amyloidogenic degradation. CDH1 inhibits APP C99 and C83 production. Cadherin-1/CD324 Protein, Rat (HEK293, His) is the recombinant rat-derived Cadherin-1/CD324 protein, expressed by HEK293 , with C-His labeled tag.
Cadherin-1/CD324 protein, a calcium-dependent adhesion molecule, mediates cell processes. It interacts homophilically with other cadherin molecules, sorting and organizing cell types. CDH1 regulates adhesion, mobility, and proliferation of epithelial cells. It serves as an integrin ligand, suppressing invasion and promoting non-amyloidogenic degradation. CDH1 inhibits APP C99 and C83 production. Cadherin-1/CD324 Protein, Rat (HEK293, Fc) is the recombinant rat-derived Cadherin-1/CD324 protein, expressed by HEK293 , with C-hFc labeled tag.
Cadherin-1/CD324 is a calcium-dependent cell adhesion protein that orchestrates homogeneous interactions, promoting cell cohesion and potential cell type sorting. CDH1 regulates epithelial cell adhesion, mobility, and proliferation and acts as an invasive suppressor. Cadherin-1/CD324 Protein, Mouse (HEK293, His) is the recombinant mouse-derived Cadherin-1/CD324 protein, expressed by HEK293 , with C-6*His labeled tag.
The Cadherin-1/CD324 protein is a calcium-dependent cell adhesion protein that interacts with homology in junctional cells to facilitate cell type sorting. CDH1 is involved in regulating intercellular adhesion, mobility, and epithelial cell proliferation. Cadherin-1/CD324 Protein, Human (HEK293, Fc) is the recombinant human-derived Cadherin-1/CD324 protein, expressed by HEK293 , with C-hFc labeled tag.
The Cadherin-1/CD324 protein is a calcium-dependent cell adhesion protein that interacts with homology in junctional cells to facilitate cell type sorting. CDH1 is involved in regulating intercellular adhesion, mobility, and epithelial cell proliferation. Cadherin-1/CD324 Protein, Human (Biotinylated, HEK293, Fc) is the recombinant human-derived Cadherin-1/CD324 protein, expressed by HEK293 , with C-hFc labeled tag.
The Cadherin-1/CD324 protein is a calcium-dependent receptor on myeloid cells that binds to carbohydrates on neutrophils and monocytes. It promotes interactions between activated endothelial cells or platelets and leukocytes. Cadherin-1/CD324 Protein, Cynomolgus (HEK293, His) is the recombinant cynomolgus-derived Cadherin-1/CD324 protein, expressed by HEK293 , with C-His labeled tag.
The Cadherin-1/CD324 protein is a calcium-dependent cell adhesion protein that interacts with homology in junctional cells to facilitate cell type sorting. CDH1 is involved in regulating intercellular adhesion, mobility, and epithelial cell proliferation. Cadherin-1/CD324 Protein, Human (Biotinylated, HEK293, His, Avi) is the recombinant human-derived Cadherin-1/CD324 protein, expressed by HEK293, with C-Avi and C-His labeled tag.
Cadherin-1/CD324 Protein, Human (HEK293, His) is a recombinant human E-cadherin produced in HEK293 cells, with His tag. Cadherin-1/CD324/E-cadherin is one of the most important molecules in cell-cell adhesion in epithelial tissues.
Phospho-E-Cadherin (Ser838/Ser840) Antibody (YA2579) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-E-Cadherin (Ser838/Ser840).
Phospho-E-Cadherin (Ser838/Ser840) Antibody (YA2579) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-E-Cadherin (Ser838/Ser840).
AW01178 is a Class I HDAC inhibitor. AW01178 induces the upregulation of E-cadherin at both mRNA and protein levels and inhibits the EMT of breast cancer cells .
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 .
Inquiry Online
Your information is safe with us. * Required Fields.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
MedchemExpress Validation 03
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
MedchemExpress Validation 04
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedChemExpress values your privacy and your trust is important to us. We use cookies to enhance your website experience. Some cookies are necessary to run the website.
Privacy and Cookie Policy
