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Results for "

αSMA

" in MedChemExpress (MCE) Product Catalog:

32

Inhibitors & Agonists

4

Peptides

1

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-151932

    FXR Inflammation/Immunology
    FXR agonist 3 is an anti-NASH agent, acting by activating FXR. FXR agonist 3 inhibits COL1A1, TGF-β1, α-SMA and TIMP1 expression with anti-fibrogenic activity. FXR agonist 3 significantly reduces liver steatosis and inflammation, improves liver fibrosis level .
    FXR agonist 3
  • HY-133897
    (Rac)-Indoximod
    1 Publications Verification

    1-Methyl-DL-tryptophan; (Rac)-NLG-8189

    Indoleamine 2,3-Dioxygenase (IDO) Apoptosis Inflammation/Immunology Cancer
    (Rac)-Indoximod (1-Methyl-DL-tryptophan) is an indoleamine 2,3-dioxygenase (IDO) inhibitor. Co-treatment with IFN-γ and (Rac)-Indoximod markedly reduces the activity of human cardiac myofibroblasts (hCMs) expressing α-SMA and induces apoptosis through up-regulating the IRF-1, Fas, and FasL genes .
    (Rac)-Indoximod
  • HY-143237

    Phosphodiesterase (PDE) Others
    ATX inhibitor 11 (compound 13c) is a potent ATX (autotaxin) inhibitor, with an IC50 of 2.7 nM. ATX inhibitor 11 can typically alleviate the severity of fibrosis tissues and effectively reduce the deposition of fibrotic biomarker α-SMA in mice fibrosis model. ATX inhibitor 11 can be used for lung fibrosis research .
    ATX inhibitor 11
  • HY-N12703

    Others Inflammation/Immunology
    N-Acetyldopamine dimmers A (Compound (+)-2) can be isolated from the cast-off shell of the cicada of Cryptotympana sp. N-Acetyldopamine dimmers A increases collagen and α-SMA expression .
    N-Acetyldopamine dimmers A
  • HY-170578

    Sirtuin Neurological Disease
    SIRT2-IN-17 (compound Z18) is a potent SIRT2 inhibitor. SIRT2-IN-17 reduces the expression of α-SMA and p-Smad2/3 .
    SIRT2-IN-17
  • HY-162929

    TGF-β Receptor Inflammation/Immunology
    TP-DEA2, a predictable-release Triptolide (HY-32735) prodrug, block Bleomycin-induced pulmonary fibrosis and inflammation. TP-DEA2 significantly inhibits α-SMA production .
    TP-DEA2
  • HY-P11112

    β-catenin Wnt Inflammation/Immunology
    PTD-DBM is a competitive peptide that blocks the CXXC5-Dvl interaction and induces the expression of β-catenin, α-SMA, and type I collagen. PTD-DBM has skin wound healing activity .
    PTD-DBM
  • HY-116307

    P2Y Receptor Cardiovascular Disease
    2-Thio-UTP is a selective P2Y2 inhibitor with an EC50 value of 50 nM. 2-Thio-UTP reduces pro-fibrotic gene expression and protein α-smooth muscle actin. 2-Thio-UTP has the potential for the research of calcific aortic valve stenosis (CAVS) .
    2-Thio-UTP
  • HY-172105

    PPAR Metabolic Disease Inflammation/Immunology
    Anti-NASH agent 2 (compound 21) is an inhibitor of de novo adipogenesis activity and α-SMA gene expression. Anti-NASH agent 2 improves hepatic steatosis, edema, inflammatory infiltrates, and liver fibrosis in NASH mouse models .
    Anti-NASH agent 2
  • HY-114366

    CXCR Others
    BC-1485 is a small molecule inhibitor of Fibrosis-inducing E3 ligase 1 (FIEL1). BC-1485 protects PIAS4 from ubiquitin-mediated degradation. BC-1485 decreases α-SMA, BAL and CXCL1. BC-1485 ameliorates fibrotic lung injury in murine models .
    BC-1485
  • HY-100446

    Glutaminase Apoptosis Metabolic Disease Inflammation/Immunology
    NTU281 is a potent transglutaminase-2 inhibitor. NTU281 can reduce the increases in serum creatinine and albuminuria in diabetic rats. NTU281 can also reduce glomerular collagen I accumulation, Hic-5 and α-SMA expression, and apoptosis. NTU281 can be used for researching glomerulosclerosis caused by diabetes .
    NTU281
  • HY-151427
    TGFβ1-IN-1
    2 Publications Verification

    TGF-β Receptor Inflammation/Immunology
    TGFβ1-IN-1 (compound 42) is a potent, orally active TGF-β1 inhibitor. TGFβ1-IN-1 inhibits the upregulation of TGF-β1-induced fibrosis markers (α-SMA and fibronectin) and can be used in liver fibrosis disease studies .
    TGFβ1-IN-1
  • HY-178328

    VD/VDR Collagen TGF-beta/Smad MMP JAK Metabolic Disease Inflammation/Immunology Endocrinology
    VDR agonist 4 is an orally active potent VDR agonist. VDR agonist 4 exerts VDR-dependent antifibrotic activity by regulating multiple fibrosis-related genes to suppress α-SMA and collagen I production, thereby inhibiting hepatic stellate cell (HSC) activation. VDR agonist 4 improves CCl4 (HY-RS16594)-induced hepatic fibrosis in mice. VDR agonist 4 can be used for liver fibrosis research .
    VDR agonist 4
  • HY-162147

    mTOR Autophagy Inflammation/Immunology
    Nur77 modulator 3 (9e) can bind to Nur77 and inhibit TGF-β1-induced α-SMA and COLA1 expression in a Nur77-dependent manner. Nur77 modulator 3 induces Nur77 expression and enhances autophagic flux by inhibiting the mTORC1 signaling pathway in vitro and in vivo. Nur77 modulator 3 blocks the progression of hepatic fibrosis .
    Nur77 modulator 3
  • HY-170227

    Phosphodiesterase (PDE) TGF-β Receptor Inflammation/Immunology
    Autotaxin-IN-7 (45), a pyridine-2-carboxylic derivative, demonstrates subnanomolar ATX inhibition (IC50 = 0.086 nM), with a favorable heart safety profile (hERG > 30 μM) and minimal fibroblast toxicity. Autotaxin-IN-7 (45) suppresses the TGF-β/Smad signaling pathway, downregulating α-smooth muscle actin (α-SMA) and extracellular matrix components (ECM). Autotaxin-IN-7 (45) is used in the research for pulmonary fibrosis .
    Autotaxin-IN-7
  • HY-117485

    Hedgehog Inflammation/Immunology
    CBR-096-4 is a derivative of Itraconazole (HY-17514). CBR-096-4 is an orally active antifibrotic agent with no CYP3A4 inhibitory activity. CBR-096-4 inhibits the formation of matrix-secreting activated myofibroblasts (MFBs) from multiple tissue types. CBR-096-4 inhibits Hedgehog reporter activity (GLI-LUC), VEGF-dependent growth, and αSMA-LUC reporter activity. CBR-096-4 can be used for research of fibrosis .
    CBR-096-4
  • HY-146434
    TGFβ-IN-2
    1 Publications Verification

    TGF-beta/Smad Inflammation/Immunology
    TGFβ-IN-2 is an orally active TGF-β inhibitor. TGFβ-IN-2 suppresses the TGF-β-induced protein expression of COL1A1, α-SMA, and p-Smad3 in vitro. TGFβ-IN-2 demonstrates excellent anti-fibrotic efficacy in Bleomycin (HY-108345)-induced pulmonary fibrosis model. TGFβ-IN-2 can be used for the study of pulmonary fibrosis .
    TGFβ-IN-2
  • HY-175603

    Amine N-methyltransferase Cancer
    NCGC00685960 is a Nicotinamide N-methyltransferase (NNMT) inhibitor with an IC50 < 10  nM. NCGC00685960 has potent antitumor activity. NCGC00685960 increases H3K27 trimethylation levels in ovarian cancer cells and inhibits α-SMA expression in NNMT-expressing ovarian fibroblasts. NCGC00685960 reduces 1-MNA levels, reverses SAM and H3K27 hypomethylation and significantly impairs collagen contractility in cancer-associated fibroblasts (CAFs). NCGC00685960 can be used for cancers research .
    NCGC00685960
  • HY-175277

    Pim NF-κB Interleukin Related Inflammation/Immunology
    PIM1-IN-8 is a PIM1/p65 pathway inhibitor. PIM1-IN-8 suppresses the expression of α-SMA and collagen I in activated fibroblasts and blocks TGF-β induced migration. PIM1-IN-8 alleviates pulmonary fibrosis in a Bleomycin (BLM) (HY-17565A)-induced pulmonary fibrosis mice model. PIM1-IN-8 can be used for the study of idiopathic pulmonary fibrosis (IPF) .
    PIM1-IN-8
  • HY-170839

    TRP Channel Inflammation/Immunology
    TRPV1-IN-3 (compound 14) is a TRPV1 inhibitor that can be used for the research of idiopathic pulmonary fibrosis. TRPV1-IN-3 affects the expression of fibrosis markers collagen I and α-SMA by inhibiting the TGF-β/Smads and MAPK pathways, thereby exerting antifibrotic activity in vitro (IC50=0.51 μM). TRPV1-IN-3 significantly inhibits collagen deposition in lung tissue, improves the alveolar structure, and also increases the survival rate of mice with pulmonary fibrosis induced by Bleomycin (HY-108345) .
    TRPV1-IN-3
  • HY-162902

    TGF-β Receptor Cardiovascular Disease
    ALK5-IN-82 is a potent and selective inhibitor against activin receptor-like kinase 5 (ALK5) with an IC50 value of 9.1 nM. ALK5-IN-82 inhibits the protein expression of α-smooth muscle actin (α-SMA), collagen I and tissue inhibitor of metalloproteinase 1 (TIMP-1)/matrix metalloproteinase 13 (MMP-13) in transforming growth factor-β-induced human umbilical vein endothelial cells. ALK5-IN-82 is promising for research of cardiac fibrosis .
    ALK5-IN-82
  • HY-176737

    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 .
    TGF-β1/Smad-IN-1
  • HY-173235

    Galectin Cardiovascular Disease Inflammation/Immunology Cancer
    Galectin-3-IN-6 (Compound 12) is an orally active inhibitor of galectin-3 (Gal-3), with an IC50 value of 12 nM and a Kd value of 13 nM for Gal-3. In a mouse model of acute liver injury and fibrosis induced by CCl4, Galectin-3-IN-6 can significantly reduce the levels of fibrosis markers collagen-1 and α-smooth muscle actin (αSMA) by 64% and 71%, respectively, showing significant anti-fibrotic activity. Galectin-3-IN-6 can be used in the research of fibrotic diseases, cancer, and cardiovascular diseases .
    Galectin-3-IN-6
  • HY-P11223

    TGF-beta/Smad Inflammation/Immunology
    CMF9, a cyclic peptide molecule, is an inhibitor of the SMAD2-SMAD4 interaction. CMF9 effectively blocks the formation of the heterodimeric complex of SMAD2 and SMAD4 by inhibiting the phosphorylation of SMAD2. CMF9 has no effect on the phosphorylation of SMAD3 or SMAD1/5/8. CMF9 downregulates the expression of fibrotic markers α-SMA and COL1A1. CMF9 exhibits potent anti-fibrotic effects in mouse models by promoting the degradation of pathological extracellular matrix (ECM) and inhibiting inflammation. CMF9 can be used for the study of liver fibrosis .
    CMF9
  • HY-P3136A

    TRV120055 hydrochloride

    Angiotensin Receptor Cardiovascular Disease
    TRV055 (TRV120055) (hydrochloride) is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV120055 induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. TRV055 activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. TRV055 induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. TRV055 can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses [1]
    TRV055 hydrochloride
  • HY-162888

    PDGFR ERK Cardiovascular Disease
    WQ-C-401 is an orally active platelet-derived growth factor receptor (PDGFR) inhibitor. WQ-C-401 inhibits cell proliferation by blocking PDGFR autophosphorylation in a concentration-dependent manner, with EC50 values of 3.5 nM for PDGFRα Y849 and 5.8 nM for PDGFRβ Y1021. Additionally, WQ-C-401 can inhibit PASMCs proliferation and migration by blocking PDGF-BB-induced ERK1/2 phosphorylation, reducing collagen I synthesis, and increasing α-SMA expression, thereby preventing pulmonary vascular remodeling. WQ-C-401 holds promise for research in the field of pulmonary arterial hypertension .
    WQ-C-401
  • HY-P3136

    TRV120055

    Angiotensin Receptor ERK Cardiovascular Disease
    TRV055 (TRV120055) is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV120055 induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. TRV055 activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. TRV055 induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. TRV055 can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses [1]
    TRV055
  • HY-169177

    JNK Inflammation/Immunology
    JNK-1-IN-4 (Compound E1) is an inhibitor for JNK, that inhibits JNK-1, JNK-2 and JNK-3 with IC50s of 2.7, 19.0 and 9.0 nM, respectively. JNK-1-IN-4 inhibits the phosphorylation of c-Jun, and reduces the expression of TGF-β1-induced EMT marker proteins, such as fibronectin and α-SMA. JNK-1-IN-4 exhibits good pharmacokinetic characteristics with a bioavailability of 69%. JNK-1-IN-4 exhibits anti-fibrotic effect in Bleomycin (HY-17565)-induced mice idiopathic pulmonary fibrosis models .
    JNK-1-IN-4
  • HY-172258

    5-HT Receptor Cancer
    5-HT2B antagonist-2 (Compound 19c) is a 5HT2B receptor antagonist with an IC50 of 1.09 nM. 5-HT2B antagonist-2 can downregulate the expression of fibrosis-related genes α-SMA, Timp1, Col1a1, and Col3a1, and significantly reduce the deposition of fibrosis, thereby reducing the fibrotic area and inhibiting the fibrotic process in CCl4-induced liver fibrosis mouse models. 5-HT2B antagonist-2 can be used in the study of immune inflammatory-related diseases, particularly in the research of pulmonary fibrosis diseases .
    5-HT2B antagonist-2
  • HY-175033

    Epigenetic Reader Domain Phosphatase c-Myc Apoptosis Inflammation/Immunology
    BRD4-IN-11 is an orally active and selective BRD4 inhibitor (IC50 = 26.35 nM (BD1), IC50 = 72.81 nM (BD2)). BRD4-IN-11 is approximately 3- to 18-fold more potent against BRD4 than againstBRD2, BRD3, and BRDT. BRD4-IN-11 enhances H2S release and inhibits the upregulation of fibrotic markers (α-SMA and fibronectin), c-Myc, and CDC25B. BRD4-IN-11 reduces apoptosis in LO2 hepatocytes. BRD4-IN-11 significantly improves liver and lung function in a hepatopulmonary fibrosis model and can be used to study hepatopulmonary fibrosis .
    BRD4-IN-11
  • HY-179042

    TGF-beta/Smad p38 MAPK Phosphodiesterase (PDE) Inflammation/Immunology
    TGF-β/Smad-IN-3 (Compound 4w) is an effective TGF-β/Smad inhibitor. TGF-β/Smad-IN-3 exerts anti-pulmonary fibrosis activity by simultaneously inhibiting the TGF-β/Smad and MAPK signaling pathways. TGF-β/Smad-IN-3 significantly inhibits collagen deposition induced by TGF-β1, with its IC50 value being 3.21 μM. TGF-β/Smad-IN-3 has an IC₅₀ of 46.77 nM for the autocrine motility factor (ATX). TGF-β/Smad-IN-3 significantly reduces the expression levels of α-SMA, COL1A1 and FN in TGF-β1-induced CCC-HPF-1 cells, and effectively inhibited TGF-β1-induced cell migration. TGF-β/Smad-IN-3 can be used for the study of pulmonary fibrosis .
    TGF-β/Smad-IN-3
  • HY-170846

    FGFR VEGFR Bcr-Abl FLT3 Cytochrome P450 Inflammation/Immunology
    FGFRs-IN-1 (Compound A16) is the orally active inhibitor for FGFR, that inhibits FGFR1/2/3/4 with IC50s of 2.3, 7, 11, and 163 nM, respectively. FGFRs-IN-1 also inhibits VEGFR1/2/3, Abl, and Flt3 with IC50s of 61, 176, 112, 26, and 353 nM, respectively. FGFRs-IN-1 exhibits weak inhibitory efficacy against CYP enzymes. FGFRs-IN-1 reduces the expression of α-SMA and collagen I, and inhibits epithelial-mesenchymal transition (EMT) in TGF-β1 stimulated A549 cell. FGFRs-IN-1 exhibits anti-inflammatory activity in Bleomycin (HY-17565)-induced mouse pulmonary fibrosis model and CCl4 (HY-Y0298)-induced mouse liver fibrosis model .
    FGFRs-IN-1

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