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Pathways Recommended: TGF-beta/Smad
Results for "

Tgfβ1/Smad

" in MedChemExpress (MCE) Product Catalog:

46

Inhibitors & Agonists

2

Peptides

3

Inhibitory Antibodies

11

Natural
Products

1

Isotope-Labeled Compounds

2

Oligonucleotides

Targets Recommended:
Cat. No. Nombre del producto Target Áreas de investigación Chemical Structure
  • HY-13013
    SIS3
    Maximum Cited Publications
    106 Publications Verification

    		 TGF-beta/Smad Inflammation/Immunology
    SIS3 is a potent and selective inhibitor of Smad3 with an IC50 of 3 μM for Smad3 phosphorylation. SIS3 inhibits the myofibroblast differentiation of fibroblasts by TGF-β1 [1].
    SIS3
  • HY-16141
    Cilengitide
    65+ Cited Publications

    EMD 121974

    		 Integrin Autophagy Apoptosis STAT PD-1/PD-L1 Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Cilengitide (EMD 121974) is a BBB-permeable 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-W012977
    3,3-Dimethyl-1-butanol
    1 Publications Verification

    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-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-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-N0657
    Pinoresinol Diglucoside
    1 Publications Verification

    		 NF-κB Keap1-Nrf2 Heme Oxygenase (HO) TGF-beta/Smad Akt mTOR PI3K Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Pinoresinol Diglucoside is an orally active lignan with multifunctional bioactivity. Pinoresinol Diglucoside interacts with targets including ALB, HIF1A, GSK3B, BCL2, MARK3, IL6, NF-κB p65, Nrf2, HO-1, and TLR4, and modulates pathways including PI3K-Akt, estrogen, MAPK, Rap1, AKT/mTOR/NF-κB, and TGF-β1/Smads. Pinoresinol Diglucoside regulates osteogenesis, bone resorption, oxidative stress, inflammation, apoptosis, ferroptosis, ferritinophagy, cardiac fibrosis, and vasorelaxation. Pinoresinol Diglucoside can be used for the research of osteoporosis, ischemia/reperfusion-induced brain injury, Alzheimer’s disease, myocardial ischemia-reperfusion injury, chondrodysplasia, diabetic cardiomyopathy, cardiac hypertrophy, hypertension, cisplatin-induced hearing loss, atherosclerotic cardiovascular diseases, and disuse osteoporosis [1] .
    Pinoresinol Diglucoside
  • 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] .
    Baccatin III
  • 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-100444
    SIS3 free base
    Maximum Cited Publications
    106 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-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-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 [1].
    EW-7195
  • 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-121246
    Fluorofenidone
    1 Publications Verification

    AKF-PD

    		 ACSL Family 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-N1472
    Levistolide A
    5 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-N6082
    Rhein 8-O-β-D-Glucopyranoside
    1 Publications Verification

    		 Apoptosis Bcl-2 Family Caspase TGF-beta/Smad Bacterial Infection Metabolic Disease Inflammation/Immunology
    Rhein 8-O-β-D-Glucopyranoside is an orally active glycoside found in Rhubarb. Rhein 8-O-β-D-Glucopyranoside attenuates high glucose-induced apoptosis, recovers altered lincRNA ANRIL and let-7a expression, reverses high glucose-altered Bcl-2 and cleaved caspase-3 protein expression, and inhibits TGF-β1/Smad signaling. Rhein 8-O-β-D-Glucopyranoside accelerates Sennoside A (HY-N0365) metabolism, stimulates sennoside A purgative activity. Rhein 8-O-β-D-Glucopyranoside inhibits bacterial biofilm formation, suppresses its virulence gene expression, and exerts antibacterial activity. Rhein 8-O-β-D-Glucopyranoside can be used for the research of diabetic nephropathy, constipation, and infection [1] .
    Rhein 8-O-β-D-Glucopyranoside
  • HY-P5542
    Vicatertide

    SB-01; Peniel 2000

    		 Factor Xa TGF-beta/Smad Inflammation/Immunology
    Vicatertide (SB-01, Peniel 2000) is a polypeptide with both competitive inhibitory activity against TGF-β1 and selective inhibitory activity against human factor XIa (hFXIa, with a Ka of 80 nM for hFXIa). Vicatertide binds allosterically to the two binding sites of dimeric hFXI/hFXIa, while directly binding to activated TGF-β1, selectively blocking the Smad1/5/8 pathway and maintaining low-level activation of the Smad2 pathway to enhance the synthesis of type Ⅱ collagen and aggrecan. Vicatertide inhibits thrombus formation in arteriovenous thrombosis models, and also reduces thrombus weight and thrombus incidence in mouse lung cancer models. Vicatertide can be used for research on degenerative disc disease and thrombosis-related diseases [1] .
    Vicatertide
  • 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-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-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-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-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-171878
    BI-4659

    		TGF-β Receptor PDGFR TGF-beta/Smad Inflammation/Immunology Cancer
    BI-4659 is a TGFβRI and PDGFRα inhibitor with IC50 values of 19 nM and 99 nM, respectively. BI-4659 inhibits the kinase activities of TGFβRI and PDGFRα, blocks the downstream TGFβRI signaling pathway, and reduces the phosphorylation level of Smad2/3 without altering the expression of TGF-β1. BI-4659 is applicable to research related to pulmonary fibrosis, cancer, and renal ischemia-reperfusion injury [1] .
    BI-4659
  • 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-118528A
    TP0427736 hydrochloride
    2 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-179042
    TGF-β/Smad-IN-3

    		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 [1].
    TGF-β/Smad-IN-3
  • 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 [1].
    Methacycline
  • 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-N0887
    Isoastragaloside I
    2 Publications Verification

    Isoastragaloside-I

    		 Akt NF-κB p38 MAPK PI3K FXR Keap1-Nrf2 NO Synthase COX Interleukin Related Integrin TGF-β Receptor Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Inflammation/Immunology
    Isoastragaloside I is a natural compound found in Astragalus membranaceus, with oral activity and multiple biological activities such as anti-inflammatory and antioxidant properties. Isoastragaloside I inhibits Akt, NF-κB, MAPKs and PI3K, enhances the activity of hepatic FXR, regulates the TGF-β/Smads signaling pathway, and upregulates antioxidant molecules downstream of Nrf2. Isoastragaloside I inhibits the expression of NO, TNF-α, iNOS, COX-2, IL-1β and VCAM-1, and reduces intracellular ROS levels. Isoastragaloside I attenuates blood-brain barrier disruption, restores intestinal barrier function, increases β-cell mass, improves glucose homeostasis, and elevates circulating adiponectin levels. Isoastragaloside I can be used for the study of neuroinflammation-related neurodegenerative diseases, cholestatic liver disease, and diabetes [1] .
    Isoastragaloside I
  • HY-182038
    TGF-β1/Smad3-IN-2

    		VD/VDR TGF-beta/Smad Collagen Hippo (MST) Metabolic Disease
    TGF-β1/Smad3-IN-2 is an orally active antifibrotic agent. TGF-β1/Smad3-IN-2 has high affinity for VDR and can inhibit the TGFβ/SMAD3 signaling pathway. TGF-β1/Smad3-IN-2 inhibits hepatic stellate cell activation, reduces extracellular matrix deposition, and alleviates liver fibrosis in a bile duct ligation mouse model. TGF-β1/Smad3-IN-2 can be used for the research of liver fibrosis [1].
    TGF-β1/Smad3-IN-2
  • HY-16141R
    Cilengitide (Standard)

    EMD 121974 (Standard)

    		 Integrin Autophagy Apoptosis STAT PD-1/PD-L1 Reference Standards Cancer
    Cilengitide (Standard) is the analytical standard of Cilengitide. This product is intended for research and analytical applications. Cilengitide (EMD 121974) is a BBB-permeable 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)
  • 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-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-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-121246R
    Fluorofenidone (Standard)

    		ACSL Family 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-121246S
    Fluorofenidone-d3

    AKF-PD-d3

    		 Isotope-Labeled Compounds ACSL Family 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-128483R
    Fusaric acid (Standard)

    		TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor Reference Standards 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-N0657R
    Pinoresinol Diglucoside (Standard)

    		Reference Standards NF-κB Keap1-Nrf2 Heme Oxygenase (HO) TGF-beta/Smad Akt mTOR PI3K Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Pinoresinol Diglucoside (Standard) is the analytical standard of Pinoresinol Diglucoside (HY-N0657). This product is intended for research and analytical applications. Pinoresinol Diglucoside is an orally active lignan with multifunctional bioactivity. Pinoresinol Diglucoside interacts with targets including ALB, HIF1A, GSK3B, BCL2, MARK3, IL6, NF-κB p65, Nrf2, HO-1, and TLR4, and modulates pathways including PI3K-Akt, estrogen, MAPK, Rap1, AKT/mTOR/NF-κB, and TGF-β1/Smads. Pinoresinol Diglucoside regulates osteogenesis, bone resorption, oxidative stress, inflammation, apoptosis, ferroptosis, ferritinophagy, cardiac fibrosis, and vasorelaxation. Pinoresinol Diglucoside can be used for the research of osteoporosis, ischemia/reperfusion-induced brain injury, Alzheimer’s disease, myocardial ischemia-reperfusion injury, chondrodysplasia, diabetic cardiomyopathy, cardiac hypertrophy, hypertension, cisplatin-induced hearing loss, atherosclerotic cardiovascular diseases, and disuse osteoporosis.
    Pinoresinol Diglucoside (Standard)
  • HY-N6082R
    Rhein 8-O-β-D-Glucopyranoside (Standard)

    		Reference Standards Apoptosis Bacterial Bcl-2 Family Caspase TGF-beta/Smad Infection Metabolic Disease Inflammation/Immunology
    Rhein 8-O-β-D-Glucopyranoside (Standard) is the analytical standard of Rhein 8-O-β-D-Glucopyranoside (HY-N6083). This product is intended for research and analytical applications. Rhein 8-O-β-D-Glucopyranoside is an orally active glycoside found in Rhubarb. Rhein 8-O-β-D-Glucopyranoside attenuates high glucose-induced apoptosis, recovers altered lincRNA ANRIL and let-7a expression, reverses high glucose-altered Bcl-2 and cleaved caspase-3 protein expression, and inhibits TGF-β1/Smad signaling. Rhein 8-O-β-D-Glucopyranoside accelerates Sennoside A (HY-N0365) metabolism, stimulates sennoside A purgative activity. Rhein 8-O-β-D-Glucopyranoside inhibits bacterial biofilm formation, suppresses its virulence gene expression, and exerts antibacterial activity. Rhein 8-O-β-D-Glucopyranoside can be used for the research of diabetic nephropathy, constipation, and infection [1] .
    Rhein 8-O-β-D-Glucopyranoside (Standard)
  • HY-181430
    PXS 25

    		TGF-beta/Smad Metabolic Disease Inflammation/Immunology
    PXS 25 is a cation-independent mannose 6-phosphate receptor (CI-M6PR) inhibitor that inhibits CI-M6PR-mediated activation of latent TGF-β1. PXS 25 inhibits conversion of high glucose-induced latent TGF-β1 to active TGF-β1 in proximal tubule cells under normoxic conditions. PXS 25 suppresses high glucose-induced fibronectin, collagen IV production, and phosphorylated Smad 2 in proximal tubule cells under normoxic conditions. PXS 25 has antifibrotic properties in skin fibroblasts. PXS 25 can be used for the research of diabetic nephropathy [1].
    PXS 25
  • HY-181431
    PXS 64

    		TGF-beta/Smad Inflammation/Immunology
    PXS 64, a mannose-6-phosphate (M6P) analogue. a lipophilic prodrug of PXS 25 (HY-181430). PXS 64 is an effective anti-fibrotic agent by inhibiting the activation of latent TGF-β1. PXS64, inhibits fibrosis via TGF-β1 pathway in human lung fibroblasts. PXS 64 reduces TGFβ-mediated collagen IV, fibronectin, MCP-1, and phospho-smad2 expression in kidney cells. PXS 64 reduces collagen deposition in dermal scar fibroblasts. PXS 64 can be used for the research of chronic kidney disease, idiopathic pulmonary fibrosis, scarring [1] .
    PXS 64
  • HY-181808
    HSF1/AMPK activator 1

    		AMPK TGF-beta/Smad Collagen Metabolic Disease
    HSF1/AMPK activator 1 is a compound that modulates the HSF1/AMPK axis and the TGF-β1/Smad signaling pathway. HSF1/AMPK activator 1 exhibits anti-hepatic fibrosis activity and metabolic stability. HSF1/AMPK activator 1 inhibits fibrosis formation and cell proliferation in activated hepatic stellate cells. HSF1/AMPK activator 1 alleviates liver injury and hepatic fibrosis symptoms in fibrotic mice. HSF1/AMPK activator 1 is applicable to research related to hepatic fibrosis [1].
    HSF1/AMPK activator 1
  • HY-W012977R
    3,3-Dimethyl-1-butanol (Standard)

    DMB (Standard); Neohexanol (Standard)

    		 TGF-beta/Smad Reference Standards NF-κB Endogenous Metabolite Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    3,3-Dimethyl-1-butanol (Standard) is the analytical standard of 3,3-Dimethyl-1-butanol (HY-W012977). This product is intended for research and analytical applications. 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 (Standard)
  • HY-P992108
    Efadirelaxin alfa

    RELAX10

    		 RXFP Receptor Akt NO Synthase VEGFR Cardiovascular Disease
    Efadirelaxin alfa (RELAX10) is a highly selective agonist of relaxin/insulin-like family peptide receptor RXFP1. After subcutaneous administration in animal experiments, Efadirelaxin alfa exhibits a significantly prolonged terminal half-life (7 days in mice, 3.75 days in rats), and shows no activity against related receptors such as RXFP2 and RXFP3. Efadirelaxin alfa has significant anti-cardiac hypertrophy and anti-fibrotic effects. Efadirelaxin alfa effectively attenuates and reverses cardiac hypertrophy and collagen deposition by regulating the TGF-β1/Smad2 and AKT/eNOS signaling pathways. Efadirelaxin alfa improves cardiac systolic function without causing fluctuations in blood pressure or heart rate, demonstrating favorable safety. Efadirelaxin alfa is currently mainly used in studies related to heart failure [1].
    Efadirelaxin alfa
  • HY-P992410
    MEDI-579

    		PAI-1 TGF-beta/Smad Inflammation/Immunology
    MEDI-579 is a fully human monoclonal antibody against PAI-1, with a KD value of 6 pM for human PAI-1 and 105 pM for rat PAI-1. MEDI-579 restores renal plasmin activity and inhibits PAI-1-mediated intracellular signal transduction. MEDI-579 reduces albuminuria, glomerulosclerosis severity, TGF-β1 expression level, and phosphorylated Smad2 level induced in diabetic mice. MEDI-579 decreases the levels of active PAI-1 in plasma and kidneys, and increases plasma plasmin level in a mouse model of lupus nephritis. MEDI-579 can be used in research related to diabetic nephropathy and lupus nephritis. The recommended isotype control is human IgG1 kappa (HY-P99001) [1] .
    MEDI-579
  • HY-P992076
    Anti-Candida auris β-1, 3 glucans Antibody (2G8)

    		TGF-β Receptor TGF-beta/Smad Cholinesterase (ChE) Fungal Infection Cancer
    Anti-Candida auris β-1,3-glucans Antibody (2G8) is an antibody targeting Candida auris β-1,3-glucans, and also acts as an inhibitor of AChE and TGF-β receptor 2. Anti-Candida auris β-1,3-glucans Antibody (2G8) also targets fungal cell wall components, effectively inhibits fungal growth and interferes with capsule formation, thereby significantly reducing the fungal load in mouse tissues. Anti-Candida auris β-1,3-glucans Antibody (2G8) not only blocks TGF-β receptor binding to inhibit the Smad signaling pathway, reduces fibroblast activation and collagen deposition, but also induces epithelial differentiation of tumor cells and reduces pancreatic tumor metastasis. Anti-Candida auris β-1,3-glucans Antibody (2G8) specifically binds to the conserved N-linked glycoepitope on AChE to inhibit its activity without interfering with BChE, and can be used in studies of cryptococcosis and related tumor mechanisms [1] .The isotype control is Human IgG1 kappa, Isotype Control (HY-P99001).
    Anti-Candida auris β-1, 3 glucans Antibody (2G8)

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