TGF-beta/Smad
Transforming growth factor beta
Transforming growth factor-beta (TGF-β) is a member of a superfamily of pleiotropic proteins that regulate multiple cellular processes such as growth, development and differentiation. The intracellular effectors of TGF-beta signalling, the Smad proteins, are activated by receptors and translocate into the nucleus, where they regulate transcription. Although this pathway is inherently simple, combinatorial interactions in the heteromeric receptor and Smad complexes, receptor-interacting and Smad-interacting proteins, and cooperation with sequence-specific transcription factors allow substantial versatility and diversification of TGF-beta family responses. Other signalling pathways further regulate Smad activation and function.
In addition, TGF-beta receptors activate Smad-independent pathways that not only regulate Smad signalling, but also allow Smad-independent TGF-beta responses. Aberrant TGF-β signaling is associated with a variety of diseases, such as fibrosis, cardiovascular disease and cancer. Hence, the TGF-β signaling pathway is recognized as a potential drug target.
TGF-beta/Smad Isoform Specific Products
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TGF-beta/Smad Inhibitors
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TGF-beta/Smad Agonists
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TGF-beta/Smad Antagonist
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TGF-beta/Smad Activators
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TGF-beta/Smad Modulators
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TGF-beta/Smad Inducers
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TGF-beta/Smad Control
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TGF-β1 Proteins
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TGF-β2 Proteins
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TGF-β3 Proteins
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Smad Family Proteins
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SMAD2 Proteins
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SMAD3 Proteins
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SMAD4 Proteins
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SMAD5 Proteins
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TGF-β Proteins
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TGF-beta/Smad Related Products (281)
Related Products (281)
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Recombinant Proteins (62)
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Antibodies (18)
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TGF-beta/Smad Isoform Comparison
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Hydrochlorothiazide-13C6
0 ImagesSynonyms: HCTZ-13C6Hydrochlorothiazide-13C6 is the 13C labeled Hydrochlorothiazide. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect.
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Mogroside III-E
0 ImagesMogroside III-E is a cucurbitane-type triterpenoid glycoside extracted from Siraitia grosvenorii, and it is an orally active TLR4 inhibitor. Mogroside III-E downregulates the expression of TLR4 and MyD88, and blocks the phosphorylation of downstream ERK, JNK and p38 MAPK molecules; meanwhile, it inhibits TGF-β- or LPS-mediated transdifferentiation of primary pulmonary fibroblasts into myofibroblasts, reduces the content of fibrosis markers such as hydroxyproline, suppresses the pro-fibrotic TGF-β/Smad signaling pathway, and downregulates the levels of inflammatory factors MPO and IL-1β. Mogroside III-E alleviates Bleomycin (HY-108345)-induced pulmonary collagen deposition and inflammatory infiltration in mice. Mogroside III-E can be used in studies related to idiopathic pulmonary fibrosis.
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Lobeglitazone sulfate
0 ImagesLobeglitazone sulfate is a new type of thiazolidinedione. Lobeglitazone sulfate is the orally active agonist for PPAR with EC50 of 137.4 nM and 546.3 nM for PPARγ and PPARα. Lobeglitazone sulfate is the inhibitor for ERK/JNK/Smad/NF-κB signaling pathway. Lobeglitazone sulfate exhibits anti-inflammatory, anti-diabetic, anti-fibrotic and anti-atherosclerotic properties.
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KS370G
0 ImagesKS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy.
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Isoviolanthin
0 ImagesIsoviolanthin is a flavonoid glycoside. Isoviolanthin can be extracted from Dendrobium officinale. Isoviolanthin has a strong affinity for binding to KDM6B, CHAC2, ESCO2, and IPO4. Isoviolanthin decreases MMP-2 and MMP-9. Isoviolanthin inhibits TGF-β/Smad and PI3K/Akt/mTOR signaling pathways. Isoviolanthin increases Fhl3 expression. Isoviolanthin has cytoprotective effects. Isoviolanthin has anticancer activity against hepatocellular carcinoma.
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DGM
0 ImagesDGM 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.
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MORF-627
0 ImagesCat. No.: HY-149136CAS No.: 2412688-16-3MORF-627 is a highly selective, orally active integrin αvβ6 inhibitor. By blocking TGF-β1 activation and pSMAD2 signaling, MORF-627 significantly reduces collagen deposition, epithelial-mesenchymal transition markers, and structural changes in fibrotic cells. MORF-627 exhibits significant antifibrotic efficacy without genotoxicity in idiopathic pulmonary fibrosis models. However, MORF-627 induces bladder epithelial proliferation and early invasive urothelial carcinoma in cynomolgus monkeys and human cells, and this toxic effect can be reversed by exogenous TGF-β. MORF-627 can be used for studying the pathological mechanisms of pulmonary fibrosis and evaluating drug safety.
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BI-4659
0 ImagesBI-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.
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3,7-DMF
0 Images3,7-DMF is an orally active inhibitor of TGF-β1-induced activation of HSCs. 3,7-DMF induces antioxidant genes and quenches ROS away, which can be used to study liver fibrosis.
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P162-0948
0 ImagesP162-0948 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.
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TGFβRII-IN-3
0 ImagesTGFβRII-IN-3 (Compound 2r) is a selective inhibitor of the TGFβ type II receptor (TGFβ RII) (IC50 = 4.1 μM). TGFβRII-IN-3 inhibits TGFβ signaling by promoting the proteolytic degradation of TGFβ RII. TGFβRII-IN-3 can block endothelial-to-mesenchymal transition and cell migration. TGFβRII-IN-3 can be used in cancer research.
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CDD-2789
0 ImagesCat. No.: HY-173149CAS No.: 3052084-77-9
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CBT-295
0 ImagesCBT-295 is an orally active autotaxin (ATX) inhibitor. CBT-295 exhibits a significant reduction in inflammatory cytokines like TGF-β, TNF-α and IL-6 levels, also reduced bile duct proliferation marker CK-19 and lowered liver fibrosis. The reversal of liver fibrosis with CBT-295 led to a reduction in blood and brain ammonia levels. CBT-295 also reduced neuroinflammation induced by ammonia. CBT-295 is promising for research of liver cirrhosis and associated encephalopathy.
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CMF9
0 ImagesCat. No.: HY-P11223Purity: 98.65%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.
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Nickel(II) oxide
0 ImagesCat. No.: HY-W075770CAS No.: 1313-99-1Synonyms: Nickel monoxideNickel(II) oxide (nickel monoxide) is a chemical warfare agent that can enter the body through the respiratory tract and other routes, distributing to organs such as the lungs and testes. The nanoparticle form of nickel(II) oxide (NiO NPs) exhibits antibacterial, anti-leishmanial, anti-diabetic, and anti-cancer activities. NiO NPs can be activated by ultraviolet and visible light, generating reactive oxygen species (ROS). Nickel(II) oxide induces oxidative stress by generating reactive oxygen species, activating the TGF-β1-mediated MAPK and PI3K/AKT pathways, disrupting the MMPs/TIMPs balance, and upregulating the expression of inflammatory factors (IL-1β, IL-6) and apoptosis-related molecules (Bax, caspase-3, p53), while inhibiting the activity of the anti-apoptotic molecule Bcl-2. Nickel(II) oxide induces cytotoxicity, promotes fibrosis, triggers inflammatory responses, and causes apoptosis. Nickel(II) oxide can be applied in research on the safety assessment of nanomaterials, such as in the context of pulmonary fibrosis and reproductive system toxicity.
