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Pathways Recommended: Neuronal Signaling JAK/STAT Signaling
Results for "

EMT signaling

" in MedChemExpress (MCE) Product Catalog:

30

Inhibitors & Agonists

2

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2

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1

Peptides

1

Inhibitory Antibodies

9

Natural
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2

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-15244
    Alpelisib
    Maximum Cited Publications
    125 Publications Verification

    BYL-719

    		 PI3K Apoptosis Cancer
    Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
    Alpelisib
  • HY-111431
    p-Cresyl sulfate
    5+ Cited Publications

    p-Tolyl sulfate

    		 JNK p38 MAPK Reactive Oxygen Species (ROS) Metabolic Disease
    p-Cresyl sulfate (p-Tolyl sulfate) is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate shows antiproliferation activity. p-Cresyl sulfate increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate activates the JNK and p38 MAPK signaling pathways .
    p-Cresyl sulfate
  • HY-N0837
    Veratramine
    1 Publications Verification

    NSC17821; NSC23880

    		 PI3K Akt mTOR Autophagy Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Veratramine (NSC17821; NSC23880) is an orally active inhibitor of the PI3K/Akt/mTOR signaling pathway and a SIGMAR1 modulator. Veratramine induces autophagic apoptosis of tumor cells, arrests the cell cycle at the G0/G1 phase, and inhibits epithelial-mesenchymal transition (EMT)-related proteins to reduce tumor migration. Veratramine reduces spinal cord and sciatic nerve pathological damage in a neuropathy model by inhibiting SIGMAR1 binding to NMDAR and phosphorylation of NMDAR Ser896. Veratramine has anti-tumor proliferation, apoptosis induction, anti-inflammatory and neuroprotective activities, and can be used in the study of cancers such as liver cancer and osteosarcoma, as well as diabetic peripheral neuropathy .
    Veratramine
  • HY-101275
    EMT inhibitor-1
    2 Publications Verification

    		 Hippo (MST) TGF-beta/Smad Wnt Cancer
    EMT inhibitor-1 is an inhibitor of of Hippo, TGF-β, and Wnt signaling pathways with antitumor activities.
    EMT inhibitor-1
  • HY-B0449
    Methacycline hydrochloride
    2 Publications Verification

    		 Bacterial Antibiotic Infection
    Methacycline hydrochloride is a tetracycline antibiotic and can inhibits bacterial protein synthesis. Methacycline hydrochloride is a potent epithelial-mesenchymal transition (EMT) inhibitor. Methacycline hydrochloride blocks EMT in vitro and fibrogenesis in vivo without directly affecting TGF-β1 Smad signaling. Methacycline hydrochloride is an antimicrobial and has the potential for pulmonary fibrosis .
    Methacycline hydrochloride
  • HY-138657
    NCGC00378430
    2 Publications Verification

    		 Phosphatase Cancer
    NCGC00378430 is a potent SIX1/EYA2 interaction inhibitor. NCGC00378430 partially reverses transcriptional and metabolic profiles mediated by SIX1 overexpression and reverses SIX1-induced TGF-β signaling and epithelial-mesenchymal transition (EMT). NCGC00378430 inhibits SIX1-mediated breast cancer metastasis in a mouse model .
    NCGC00378430
  • HY-15244A
    Alpelisib hydrochloride
    Maximum Cited Publications
    125 Publications Verification

    BYL-719 hydrochloride

    		 PI3K Apoptosis Cancer
    Alpelisib (BYL-719) hydrochloride is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib hydrochloride also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib hydrochloride not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib hydrochloride can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
    Alpelisib hydrochloride
  • HY-18766
    EW-7195
    1 Publications Verification

    		 TGF-β Receptor p38 MAPK Cancer
    EW-7195 is a potent and selective ALK5 (TGFβR1) inhibitor with an IC50 of 4.83 nM. EW-7195 has >300-fold selectivity for ALK5 over p38α. EW-7195 efficiently inhibits TGF-β1-induced Smad signaling, epithelial-to-mesenchymal transition (EMT) and breast tumour metastasis to the lung .
    EW-7195
  • HY-122965
    Batatasin III

    		FAK Akt Cancer
    Batatasin III, a stilbenoid, inhibits cancer migration and invasion by suppressing epithelial to mesenchymal transition (EMT) and FAK-AKT signals. Batatasin III has anti-cancer activities .
    Batatasin III
  • HY-170964
    HPH-15

    		DNA/RNA Synthesis TGF-β Receptor Cancer
    HPH-15 is an anti-migration compound that inhibits cell migration by binding to hnRNP U or suppressing TGF-β signaling. In addition, HPH-15 can also inhibit epithelial-mesenchymal transition (EMT). HPH-15 holds promise for research in the fields of anti-tumor metastasis and anti-fibrosis .
    HPH-15
  • HY-W005379
    DGM

    		TGF-beta/Smad Inflammation/Immunology
    DGM is an inhibitor of the TGF-β1/Smad signaling pathway with significant antifibrotic effects. DGM inhibits the epithelial-mesenchymal transition (EMT) process in alveolar epithelial cells and slows the progression of pulmonary fibrosis in vivo by reducing lung inflammation, improving lung function, and decreasing extracellular matrix (ECM) remodeling. DGM can be used in research on idiopathic pulmonary fibrosis (IPF) and EMT-related diseases .
    DGM
  • HY-N13009
    MO-2097

    		Raf HIF/HIF Prolyl-Hydroxylase ERK MEK Reactive Oxygen Species (ROS) Apoptosis Caspase Cancer
    MO-2097 is a RAF-1/HIF-1α inhibitor. MO-2097 induces RAF-1 destabilization, leading to a reduction in EMT-associated transcription factors and mesenchymal markers. MO-2097 inhibits HIF-1a protein expression mediated by hnRNPA2B1 under hypoxic and mimetic hypoxia. MO-2097 induces mitochondrial ROS, which leads to apoptosis in cells. MO-2097 effectively suppresses colorectal cancer metastasis by inhibiting the RAF/MEK/ERK signaling pathway. MO-2097 attenuates tumor growth in a xenograft HCT116 cell mouse model. MO-2097 can be used for the study of colorectal cancer .
    MO-2097
  • HY-151802
    CPUL1

    		TrxR Cancer
    CPUL1 is a TrxR inhibitor, which shows proliferation-inhibitory and anti-metastatic activity against A549 cells. CPUL1 influences EMT (epithelial-mesenchymal transition) via inducing ROS-mediated ERK/JNK signaling by inhibiting TrxR1 enzyme activity. CPUL1 in combination with α-Lipoic Acid (HY-N0492) or Dithiodipropionic acid (HY-W014395) is more effective .
    CPUL1
  • HY-N0837R
    Veratramine (Standard)

    NSC17821 (Standard); NSC23880 (Standard)

    		 Reference Standards PI3K Akt mTOR Autophagy Apoptosis Neurological Disease Metabolic Disease Cancer
    Veratramine (NSC17821; NSC23880) (Standard) is the analytical standard of Veratramine (HY-N0837). This product is intended for research and analytical applications. Veratramine (NSC17821; NSC23880) is an orally active inhibitor of the PI3K/Akt/mTOR signaling pathway and a SIGMAR1 modulator. Veratramine induces autophagic apoptosis of tumor cells, arrests the cell cycle at the G0/G1 phase, and inhibits epithelial-mesenchymal transition (EMT)-related proteins to reduce tumor migration. Veratramine reduces spinal cord and sciatic nerve pathological damage in a neuropathy model by inhibiting SIGMAR1 binding to NMDAR and phosphorylation of NMDAR Ser896. Veratramine has anti-tumor proliferation, apoptosis induction, anti-inflammatory and neuroprotective activities, and can be used in the study of cancers such as liver cancer and osteosarcoma, as well as diabetic peripheral neuropathy .
    Veratramine (Standard)
  • HY-111431AR
    p-Cresyl sulfate potassium (Standard)

    p-Tolyl sulfate potassium (Standard)

    		 JNK p38 MAPK Reactive Oxygen Species (ROS) Reference Standards Metabolic Disease
    p-Cresyl sulfate (potassium) (Standard) is the analytical standard of p-Cresyl sulfate (potassium). This product is intended for research and analytical applications. p-Cresyl sulfate (p-Tolyl sulfate) potassium is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate potassium shows antiproliferation activity. p-Cresyl sulfate potassium increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate potassium induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways .
    p-Cresyl sulfate potassium (Standard)
  • HY-153858
    PHI-501

    		Raf Discoidin Domain Receptor MEK TNF Receptor Interleukin Related JAK STAT Ras Cancer
    PHI-501 is a dual inhibitor targeting RAF/DDR. PHI-501 exhibits significant anti-proliferative effects in melanoma cell lines and significantly inhibits the colony formation of drug-resistant cells. PHI-501 strongly inhibits ERK and AKT phosphorylation. PHI-501 downregulates the gene sets in drug-resistant cells of TNFA-NFKB, IL6-JAK-STAT3, and KRAS signaling pathways as well as the epithelial-mesenchymal transition (EMT) signaling pathways. PHI-501 demonstrates significant anti-tumor effects in the SK-MEL3DR xenograft model. PHI-501 can be used for research on the problem of drug resistance in melanoma .
    PHI-501
  • HY-W587701
    Methacycline

    		Bacterial Antibiotic
    Methacycline is a tetracycline antibiotic that inhibits bacterial protein synthesis. Methacycline is a potent inhibitor of epithelial-to-mesenchymal transition (EMT). Methacycline blocks EMT in vitro and inhibits fibrogenesis in vivo without directly affecting TGF-β1 Smad signaling. Methacycline is an antimicrobial agent with potential for use in pulmonary fibrosis research .
    Methacycline
  • HY-170813
    P162-0948

    		CDK TGF-beta/Smad Infection
    P162-0948 is a selective CDK8 inhibitor with an IC50 value of 50.4 nM. P162-0948 reduces cell migration and protein expression of EMT-related proteins in A549 human alveolar epithelial cell lines. P162-0948 reduces phosphorylation of Smad, which suggests disruption of the TGF-β/Smad signaling pathway. P162-0948 is promising for research of pulmonary fibrosis .
    P162-0948
  • HY-N15267
    Ovalitenone

    		FAK Akt mTOR 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) .
    Ovalitenone
  • HY-B0449R
    Methacycline hydrochloride (Standard)

    		Reference Standards Bacterial Antibiotic Infection
    Methacycline (hydrochloride) (Standard) is the analytical standard of Methacycline (hydrochloride). This product is intended for research and analytical applications. Methacycline hydrochloride is a tetracycline antibiotic and can inhibits bacterial protein synthesis. Methacycline hydrochloride is a potent epithelial-mesenchymal transition (EMT) inhibitor. Methacycline hydrochloride blocks EMT in vitro and fibrogenesis in vivo without directly affecting TGF-β1 Smad signaling. Methacycline hydrochloride is an antimicrobial and has the potential for pulmonary fibrosis .
    Methacycline hydrochloride (Standard)
  • HY-P11198
    AC-P19M

    		Apoptosis VEGFR ERK Akt Caspase Bcl-2 Family Cancer
    AC-P19M is an anticancer peptide. AC-P19M induces apoptosis by disrupting the cell membrane of cancer cells. AC-P19M reverses epithelial-mesenchymal transition (EMT). AC-P19M shows anti-angiogenic activity through the inhibition of VEGF-VEGFR2/ERK/Akt signaling. AC-P19M can be used for lung cancer research .
    AC-P19M
  • HY-101275R
    EMT inhibitor-1 (Standard)

    		Hippo (MST) Reference Standards TGF-beta/Smad Wnt Cancer
    EMT inhibitor-1 (Standard) is the analytical standard of EMT inhibitor-1 (HY-101275). This product is intended for research and analytical applications. EMT inhibitor-1 is an inhibitor of of Hippo, TGF-β, and Wnt signaling pathways with antitumor activities.
    EMT inhibitor-1 (Standard)
  • HY-N17888
    Ephemeranthol A

    		NF-κB p38 MAPK FAK Akt Apoptosis NO Synthase COX TNF Receptor Interleukin Related Inflammation/Immunology Cancer
    Ephemeranthol A is a phenanthrene compound with anticancer and anti-inflammatory activities. Ephemeranthol A exerts significant anti-inflammatory effects in macrophages by inhibiting the NF-κB and MAPK signaling pathways. Ephemeranthol A induces apoptosis and inhibits metastasis of lung cancer cells by suppressing the FAK/Akt signaling and EMT processes. Ephemeranthol A can be used for the research of acute and chronic inflammatory diseases and non-small cell lung cancer .
    Ephemeranthol A
  • HY-181717
    TKL002

    		NF-κB Apoptosis Cadherin Caspase Bcl-2 Family Neurological Disease Cancer
    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 .
    TKL002
  • HY-N16719
    Picrasidine J

    		Kallikrein ERK Cadherin β-catenin Cancer
    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 .
    Picrasidine J
  • HY-P992200
    Anti-CD146 Antibody (AA98)

    		Transmembrane Glycoprotein PI3K Akt p38 MAPK NF-κB MMP Apoptosis Caspase Bcl-2 Family Cardiovascular Disease Cancer
    Anti-CD146 Antibody (AA98) is an antibody targeting CD146 and an angiogenesis inhibitor. Anti-CD146 Antibody (AA98) blocks the dimerization of CD146 as well as its downstream PI3K/AKT, p38 MAPK and NF-κB signaling pathways; it inhibits the expression of MMP9 and ICAM1, epithelial-mesenchymal transition (EMT), and the proliferation, migration and tube formation of endothelial cells. Anti-CD146 Antibody (AA98) enhances radiation-induced cancer cell apoptosis and survival inhibition, reduces tumor microvessel density, and suppresses tumor growth, invasion and vasculogenic mimicry. Anti-CD146 Antibody (AA98) can be used in research related to cervical cancer, liver cancer, malignant phyllodes tumor of the breast, uveal melanoma, leiomyosarcoma, pancreatic cancer, other tumors and angiogenesis .
    Anti-CD146 Antibody (AA98)
  • HY-179535
    Axl-IN-21

    		TAM Receptor Discoidin Domain Receptor TGF-β Receptor Hedgehog Cancer
    Axl-IN-21 is an orally active and selective AXL inhibitor (Kd = 2.7 nM, IC50 = 4.0 nM). Axl-IN-21 displays kinase selectivity and retains strong activity against cancer-related mul-kinases (Mer with Kd = 1.4 nM, DDR1 with IC50 = 22.2 nM, HIPK4 with Kd = 11.0 nM and LOK with Kd =10 nM). Axl-IN-21 overcomes tumor microenvironment-driven resistance by blocking CAF-derived GAS6-induced AXL/STAT3/ABCG1 signaling, restoring chemosensitivity and inhibiting drug efflux in gastric cancer (GC). Axl-IN-21 suppresses TGF-β1-induced epithelial-mesenchymal transition (EMT), migration, and invasion in MDA-MB-231 cells. Axl-IN-21 exhibits no significant cytotoxicity in non-cancerous cells. Axl-IN-21 can be research for triple negative breast cancer and gastric cancer [1] [2] .
    Axl-IN-21
  • HY-182361
    NUAK1-IN-3

    		AMPK JAK Cadherin Cancer
    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 of 265 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 .
    NUAK1-IN-3
  • HY-13689G
    Go 6983

    		PKC Histone Methyltransferase DNA Methyltransferase DNA/RNA Synthesis Inflammation/Immunology
    Go 6983 GMP is Go 6983 (HY-13689) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Go 6983 is a dual inhibitor targeting Suv39h1/2 (KMT1A/KMT1B) and PKC, as well as a transcriptional activator capable of inducing DNA hypomethylation. Go 6983 stimulates the transcription of Prdm14 by reducing Suv39h1/2 protein levels, decreasing histone modifications in the Prdm14 promoter region, and increasing the recruitment of RNA polymerase II. Go 6983 induces genome-wide DNA hypomethylation by inhibiting de novo methyltransferase expression and increasing Tet1/Tet2 levels, thereby promoting self-renewal and pluripotency maintenance of stem cells. Meanwhile, Go 6983 can block PKC-mediated signaling pathways to reduce the expression of EMT-related genes and eliminate the upregulation of antioxidant genes downstream of NRF2. Go 6983 is mainly used in mechanism studies related to myocardial ischemia/reperfusion injury .
    Go 6983
  • HY-15244G
    Alpelisib

    		PI3K Apoptosis Cancer
    Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
    Alpelisib

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