SB-525334 was used to study TGFβ1-mediated human trophoblast differentiation.7
Biochem./physiol. Wirkung
SB-525334 blocks the activation of Smad2/3 induced by TGFβ1 in renal proximal tubule cells.4 The sensitivity of TGFβ1 is decreased by SB-525334 that benefits the pulmonary arterial hypertension condition by reversing the pulmonary arterial pressure.5 SB-525334 is reduces the tumor incidence and size of mesenchymal tumors such as uterine leiomyoma.6
SB-525334 is a potent activin receptor-like kinase (ALK5)/ type I TGFβ-receptor kinase inhibitor with IC50 = 14.3 nM.
SB-525334 is an ALK5/type I TGFβ-R kinase inhibitor.
Leistungsmerkmale und Vorteile
This compound was developed by GlaxoSmithKline. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
Lagerklassenschlüssel
11 - Combustible Solids
WGK
WGK 3
Persönliche Schutzausrüstung
dust mask type N95 (US), Eyeshields, Faceshields, Gloves
The Journal of pharmacology and experimental therapeutics, 313(3), 943-951 (2005-03-17)
SB-525334 (6-[2-tert-butyl-5-(6-methyl-pyridin-2-yl)-1H-imidazol-4-yl]-quinoxaline) has been characterized as a potent and selective inhibitor of the transforming growth factor-beta1 (TGF-beta1) receptor, activin receptor-like kinase (ALK5). The compound inhibited ALK5 kinase activity with an IC(50) of 14.3 nM and was approximately 4-fold less potent
The use of novel tools to understand tumour-fibrosis in pancreatic ductal adenocarcinoma (PDAC) and novel anti-fibrotic treatments are highly needed. We established a pseudo-3D in vitro model including humane pancreatic fibroblasts (PFs) and pancreatic cancer-associated fibroblasts (CAFs) in combination with
The American journal of pathology, 174(2), 380-389 (2009-01-01)
Mutations in the gene for the transforming growth factor (TGF)-beta superfamily receptor, bone morphogenetic protein receptor II, underlie heritable forms of pulmonary arterial hypertension (PAH). Aberrant signaling via TGF-beta receptor I/activin receptor-like kinase 5 may be important for both the
The development of therapies to prevent or treat salivary gland dysfunction has been limited by a lack of functional in vitro models. Specifically, critical markers of salivary gland secretory phenotype downregulate rapidly ex vivo. Here, we utilize a salivary gland
Excessive extracellular matrix (ECM) deposition is a hallmark feature in fibrosis and tissue remodelling diseases. Typically, mesenchymal cells will produce collagens under standard 2D cell culture conditions, however these do not assemble into fibrils. Existing assays for measuring ECM production
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