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Pathways Recommended: TGF-beta/Smad
Results for "

Tgfβ1/Smad

" in MedChemExpress (MCE) Product Catalog:

33

Inhibitors & Agonists

1

Fluorescent Dye

1

Biochemical Assay Reagents

1

Peptides

6

Natural
Products

1

Isotope-Labeled Compounds

2

Oligonucleotides

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-163536
    TGF-β1/Smad3-IN-1

    		TGF-beta/Smad Inflammation/Immunology
    TGF-β1/Smad3-IN-1 (Compound 5aa) is an inhibitor of the TGF-β1/Smad3 signaling pathway(IC50=1.07 μM). TGF-β1/Smad3-IN-1 possesses antifibrotic activity and oral potency [1].
    TGF-β1/Smad3-IN-1
  • HY-P10363
    Tiger17

    		TGF-β Receptor Others
    Tiger17 is an effective wound healing agent. Tiger17 is able to induce the secretion of TGF-β1 and acts through the Smad signaling pathway, specifically promoting wound healing by increasing the phosphorylation of Smad2 and Smad3 [1].
    Tiger17
  • HY-13013
    SIS3
    Maximum Cited Publications
    94 Publications Verification

    		 TGF-beta/Smad Inflammation/Immunology
    (E)-SIS3 is a potent and selective inhibitor of Smad3 with an IC50 of 3 μM for Smad3 phosphorylation. (E)-SIS3 inhibits the myofibroblast differentiation of fibroblasts by TGF-β1 [1].
    SIS3
  • HY-100444
    SIS3 free base
    Maximum Cited Publications
    94 Publications Verification

    		 TGF-beta/Smad Inflammation/Immunology
    SIS3 free base is a potent and selective inhibitor of Smad3 phosphorylation. SIS3 free base inhibits the myofibroblast differentiation of fibroblasts by TGF-β1. SIS3 free base does not affect the phosphorylation of Smad2 [1].
    SIS3 free base
  • HY-N6985
    Baccatin III
    2 Publications Verification

    		 Others Cancer
    Baccatin III is an orally available, selective inhibitor of the TGF-β1 signaling pathway and myeloid-derived suppressor cell (MDSC) activation. Baccatin III targets the AKT/STAT6 and Smad2/3 pathways, blocking TGF-β1-induced fibroblast differentiation and MDSC-mediated immunosuppression. Baccatin III exerts anti-inflammatory and anti-fibrotic effects by inhibiting macrophage activation and extracellular matrix deposition, and shows potential in the treatment of pulmonary fibrosis and cancer in terms of regulating the tumor immune microenvironment[1][2].
    Baccatin III
  • HY-145721A
    Mongersen sodium

    GED-0301 sodium

    		 TGF-beta/Smad Inflammation/Immunology
    Mongersen sodium is a specific and orally active SMAD7 antisense oligonucleotide. Mongersen sodium restores TGF-β1 activity leading to inhibition of inflammatory signals. Mongersen sodium can attenuate Crohn's disease-like experimental colitis in mice [1] .
    Mongersen sodium
  • HY-176737
    TGF-β1/Smad-IN-1

    		TGF-beta/Smad Inflammation/Immunology
    TGF-β1/Smad-IN-1 (compound C9) is a potent TGF-β1/Smad inhibitor. TGF-β1/Smad-IN-1 inhibits the expression of fibrosis markers (α-SMA and COL1A1) induced by TGF-β1. TGF-β1/Smad-IN-1 shows antifibrotic effects. TGF-β1/Smad-IN-1 has the potential for the research of hepatic fibrosis [1].
    TGF-β1/Smad-IN-1
  • HY-145721
    Mongersen

    GED-0301

    		 TGF-beta/Smad Inflammation/Immunology
    Mongersen (GED-0301) is a specific and orally active SMAD7 antisense oligonucleotide. Mongersen restores TGF-β1 activity leading to inhibition of inflammatory signals. Mongersen can attenuate Crohn's disease-like experimental colitis in mice [1] .
    Mongersen
  • HY-163507
    ALK5-IN-79

    		Anaplastic lymphoma kinase (ALK) Cancer
    ALK5-IN-79 (compound 57) is an ALK inhibitor with anticancer activity, by blocking TGF-β1/SMAD signaling pathway. ALK5-IN-79 attenuates the production of extracellular matrix (ECM) and deposition of collagen. ALK5-IN-79 exhibits adequate pharmacokinetic (PK) properties and good in vivo tolerance.
    ALK5-IN-79
  • HY-168607
    ALK5-IN-83

    		TGF-beta/Smad Cancer
    ALK5-IN-83 (compound 13b) is a ALK5 inhibitor with the IC50 of 0.13 μM. ALK5-IN-83 inhibits TGF-β1-induced Smad2 phosphorylation and cell motility in A549 cells [1].
    ALK5-IN-83
  • 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 [1].
    Methacycline hydrochloride
  • HY-12274
    ML347
    5+ Cited Publications

    LDN 193719

    		 TGF-β Receptor Cancer
    ML347 (LDN193719) is a highly selective ALK1/ALK2 inhibitor. ML347 has IC50 values of 46 and 32 nM against ALK1 and ALK2, respectively, >300-fold selective over ALK3. ML347 block the phosphorylation of Smad1/5 by TGF-β1 [1] .
    ML347
  • HY-128439
    BT173

    		DYRK Cancer
    BT173 is a potent homeodomain interacting protein kinase 2 (HIPK2) inhibitor. BT173 binds to HIPK2 and does not inhibit HIPK2 kinase activity but rather, interfered allosterically with the ability of HIPK2 to associate with Smad3. BT173 attenuates renal fibrosis through suppression of the TGF-β1/Smad3 pathway. BT173 can be studied in research for kidney diseases such as renal fibrosis [1].
    BT173
  • HY-W587701
    Methacycline
    2 Publications Verification

    		 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 [1].
    Methacycline
  • HY-170540
    NOX4-IN-1

    		NADPH Oxidase TGF-beta/Smad Reactive Oxygen Species (ROS) Inflammation/Immunology
    NOX4-IN-1 (Compound 14m) is the inhibitor for NADPH oxidase 4 (NOX4), and blocks the generation of ROS. NOX4-IN-1 inhibits TGF-β1/Smad signaling pathway, decreases the expression of fibrosis-related proteins. NOX4-IN-1 inhibits the cell migration of NRK-49F [1].
    NOX4-IN-1
  • HY-18766
    EW-7195

    		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 [1].
    EW-7195
  • 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 [1].
    DGM
  • HY-124748
    ENMD-1068

    		Protease Activated Receptor (PAR) Apoptosis Inflammation/Immunology
    ENMD-1068 is a selective protease-activated receptor 2 (PAR2) antagonist. ENMD-1068 reduces hepatic stellate cell activation and collagen expression by inhibiting TGF-β1/Smad signaling. ENMD-1068 also inhibits the proliferation of endometrial cells and induces apoptosis of epithelial cells in the lesion. ENMD-1068 can be used in the study of endometriosis and liver fibrosis [1] .
    ENMD-1068
  • HY-124748A
    ENMD-1068 hydrochloride
    2 Publications Verification

    		 Protease Activated Receptor (PAR) Apoptosis Inflammation/Immunology
    ENMD-1068 hydrochloride is a selective protease-activated receptor 2 (PAR2) antagonist. ENMD-1068 hydrochloride reduces hepatic stellate cell activation and collagen expression by inhibiting TGF-β1/Smad signaling. ENMD-1068 hydrochloride also inhibits the proliferation of endometrial cells and induces apoptosis of epithelial cells in the lesion. ENMD-1068 hydrochloride can be used in the study of endometriosis and liver fibrosis [1] .
    ENMD-1068 hydrochloride
  • HY-118528A
    TP0427736 hydrochloride
    1 Publications Verification

    		 TGF-β Receptor Endocrinology
    TP0427736 hydrochloride is a potent inhibitor of ALK5 kinase activity with an IC50 of 2.72 nM and this effect is 300-fold higher than the inhibitory effect on ALK3 (IC50=836 nM). TP0427736 hydrochloride also inhibits Smad2/3 phosphorylation in A549 cells induced by TGF-β1 with an IC50 value of 8.68 nM. TP0427736 hydrochloride can be used for the research of androgenic alopecia (AGA) [1].
    TP0427736 hydrochloride
  • HY-W012977
    3,3-Dimethyl-1-butanol

    DMB; Neohexanol

    		 TGF-beta/Smad NF-κB Endogenous Metabolite Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    3,3-Dimethyl-1-butanol (DMB) is an orally active inhibitor of trimethylamine (TMA) and trimethylamine N-oxide (TMAO). 3,3-Dimethyl-1-butanol inhibits the signaling pathway of p65 NF-κB and TGF-β1/Smad3. 3,3-Dimethyl-1-butanol has potential applications in cardiovascular disease (CVD) [1] .
    3,3-Dimethyl-1-butanol
  • 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 [1].
    Methacycline hydrochloride (Standard)
  • HY-107614G
    1-Oleoyl lysophosphatidic acid sodium

    1-Oleoyl-sn-glycero-3-phosphate sodium; 1-Oleoyl-LPA sodium

    		 TGF-beta/Smad Neurological Disease
    1-Oleoyl lysophosphatidic acid sodium (GMP) is a GMP-grade 1-Oleoyl lysophosphatidic acid sodium (HY-107614) that can be used as an auxiliary reagent in cell therapy. 1-Oleoyl lysophosphatidic acid sodium can stimulate neuronal differentiation in neural progenitor cells from mice or rats, and it also promotes the differentiation of human adipose-derived mesenchymal stem cells into myofibroblast-like cells in vitro by activating the autocrine TGF-β1-Smad signaling pathway [1] .
    1-Oleoyl lysophosphatidic acid sodium
  • HY-149136
    MORF-627

    		Integrin TGF-beta/Smad Inflammation/Immunology
    MORF-627 is a selective, orally active inhibitor for integrin αvβ6 with an IC50 of 9.2 nM measuring by human serum ligand binding assay. MORF-627 inhibits αvβ6-mediated TGF-β1 activation with an IC50 of 2.63 nM, inhibits SMAD2/3 phosphorylation with an IC50 of 8.3 nM. MORF-627 ameliorates the Bleomycin (HY-108345)-induced mouse lung fibrosis [1].
    MORF-627
  • HY-121246
    Fluorofenidone
    1 Publications Verification

    AKF-PD

    		 NF-κB ERK TGF-beta/Smad Inflammation/Immunology Cancer
    Fluorofenidone (AKF-PD) is an orally active compound with anti-fibrotic, antioxidant, and anti-inflammatory pharmacological effects. Fluorofenidone downregulates the expression of ACSL4, upregulates GPX4 expression and inhibits the NF-κB signaling pathway to alleviate inflammation and fibrosis. Fluorofenidone ameliorates cholestasis and fibrosis by inhibiting hepatic Erk/-Egr-1 signaling and Tgfβ1/Smad pathway in mice. Fluorofenidone demonstrates protective effects against chronic lung injury in mice. Fluorofenidone can be used for the study of chronic obstructive pulmonary disease (COPD), pulmonary interstitial fibrosis (PIF) and non-small cell lung cancer (NSCLC) [1] .
    Fluorofenidone
  • HY-121246R
    Fluorofenidone (Standard)

    		Reference Standards NF-κB ERK TGF-beta/Smad Inflammation/Immunology
    Fluorofenidone (Standard) is the analytical standard of Fluorofenidone (AKF-PD) (HY-121246). This product is intended for research and analytical applications. Fluorofenidone is an orally active compound with anti-fibrotic, antioxidant, and anti-inflammatory pharmacological effects. Fluorofenidone downregulates the expression of ACSL4, upregulates GPX4 expression and inhibits the NF-κB signaling pathway to alleviate inflammation and fibrosis. Fluorofenidone ameliorates cholestasis and fibrosis by inhibiting hepatic Erk/-Egr-1 signaling and Tgfβ1/Smad pathway in mice. Fluorofenidone demonstrates protective effects against chronic lung injury in mice. Fluorofenidone can be used for the study of chronic obstructive pulmonary disease (COPD), pulmonary interstitial fibrosis (PIF) and non-small cell lung cancer (NSCLC) [1] .
    Fluorofenidone (Standard)
  • HY-N1472
    Levistolide A
    4 Publications Verification

    		 Apoptosis Reactive Oxygen Species (ROS) PPAR GSK-3 Tau Protein Ras TGF-β Receptor Infection Neurological Disease Inflammation/Immunology
    Levistolide A is an apoptosis inducer and a PEDV virus inhibitor. Levistolide A can induce apoptosis in colon cancer cells and suppress the replication of porcine epidemic diarrhea virus (PEDV) by promoting ROS generation. Levistolide A activates peroxisome proliferator-activated receptor γ (PPARγ) in N2a/APP695swe cells and reduces excessive phosphorylation of tau through the GSK3α/β pathway, improving symptoms in Alzheimer’s mice. Levistolide A improves kidney damage in 5/6 nephrectomy (Nx) mice by inhibiting the RAS,TGF-β1/Smad, and MAPK pathways [1] .
    Levistolide A
  • HY-121246S
    Fluorofenidone-d3

    AKF-PD-d3

    		 Isotope-Labeled Compounds NF-κB ERK TGF-beta/Smad Inflammation/Immunology Cancer
    Fluorofenidone-d3 (AKF-PD-d3) is deuterium labeled Fluorofenidone (AKF-PD) (HY-121246). Fluorofenidone is an orally active compound with anti-fibrotic, antioxidant, and anti-inflammatory pharmacological effects. Fluorofenidone downregulates the expression of ACSL4, upregulates GPX4 expression and inhibits the NF-κB signaling pathway to alleviate inflammation and fibrosis. Fluorofenidone ameliorates cholestasis and fibrosis by inhibiting hepatic Erk/-Egr-1 signaling and Tgfβ1/Smad pathway in mice. Fluorofenidone demonstrates protective effects against chronic lung injury in mice. Fluorofenidone can be used for the study of chronic obstructive pulmonary disease (COPD), pulmonary interstitial fibrosis (PIF) and non-small cell lung cancer (NSCLC) [1] .
    Fluorofenidone-d3
  • HY-128483
    Fusaric acid

    		TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor Cardiovascular Disease Endocrinology Cancer
    Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β1/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer [1] .
    Fusaric acid
  • HY-128483R
    Fusaric acid (Standard)

    		TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor Cardiovascular Disease Endocrinology Cancer
    Fusaric acid (Standard) is the analytical standard of Fusaric acid (HY-128483). This product is intended for research and analytical applications. Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β1/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer [1] .
    Fusaric acid (Standard)
  • HY-N1326
    Santamarine

    Santamarin; Balchanin

    		 Keap1-Nrf2 Inflammation/Immunology
    Santamarine (Santamarin), a sesquiterpene lactone, increases HO-1 expression through Nrf2 translocation and suppresses NO, PGE2, TNF-α, and IL-1β production through inhibition of NF-κB translocation in LPS-induced macrophages. Santamarine shows anti-photoaging properties via inhibition of MAPK/AP-1 and stimulation of TGF-β/Smad signaling in UVA-irradiated human dermal fibroblasts (HDFs). Antioxidant activities [1] .
    Santamarine
  • HY-16141
    Cilengitide
    55+ Cited Publications

    EMD 121974

    		 Integrin Autophagy Apoptosis STAT PD-1/PD-L1 Cancer
    Cilengitide (EMD 121974) is a potent integrins antagonist with IC50s of 0.61 nM (ανβ3), 8.4 nM (ανβ5) and 14.9 nM (α5β1), respectively. Cilengitide inhibits the binding of ανβ3 and ανβ5 to Vitronectin with IC50s of 4 nM and 79 nM, respectively. Cilengitide inhibits TGF-β/Smad signaling, mediates PD-L1 expression. Cilengitide also induces apoptosis, shows antiangiogenic effect in the research against glioblastoma and other cancers [1] .
    Cilengitide
  • HY-16141R
    Cilengitide (Standard)

    		Integrin Autophagy Apoptosis STAT PD-1/PD-L1 Cancer
    Cilengitide (Standard) is the analytical standard of Cilengitide. This product is intended for research and analytical applications. Cilengitide (EMD 121974) is a potent integrins antagonist with IC50s of 0.61 nM (ανβ3), 8.4 nM (ανβ5) and 14.9 nM (α5β1), respectively. Cilengitide inhibits the binding of ανβ3 and ανβ5 to Vitronectin with IC50s of 4 nM and 79 nM, respectively. Cilengitide inhibits TGF-β/Smad signaling, mediates PD-L1 expression. Cilengitide also induces apoptosis, shows antiangiogenic effect in the research against glioblastoma and other cancers [1] .
    Cilengitide (Standard)

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