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Merck
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SML2819

Sigma-Aldrich

AZ12799734

≥98% (HPLC)

Synonyme(s) :

4-[[4-[(2,6-Dimethyl-3-pyridinyl)oxy]-2-pyridinyl]amino]benzenesulfonamide, 4-[[4-[(2,6-Dimethylpyridin-3-yl)oxy]pyridin-2-yl]amino]benzenesulfonamide, AZ 12799734, AZ-12799734

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About This Item

Formule empirique (notation de Hill):
C18H18N4O3S
Numéro CAS:
1117684-36-2
Poids moléculaire :
370.43
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 2 mg/mL, clear

Température de stockage

2-8°C

Actions biochimiques/physiologiques

AZ12799734 is an orally active TGF-β type I receptors active site inhibitor (ALK1/2/3/4/5/6 Kd = 7.1/6.2/40/1/0.74/0.017 μM) that inhibits ALK5-dependent Smad2 nuclear translocation upon TGF-β1 stimulation (IC50 = 17 nM; MDA-MB-468), as well as ALK1/2/3/6-mediated Smad1 and ALK4/5/7-mediated Smad2 phosphorylation (10 μM; NIH3T3 expressing respective constitutively active receptors). AZ12799734 oral administration in rats results in heart valve lesions (200 mg/kg/day for 5 days) and physeal dysplasia (400 mg/kg/day for 6 days), consistent with a critical role of ALK5 in maintaining the integrity of heart valve and physis.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

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Frederick W Goldberg et al.
Journal of medicinal chemistry, 52(23), 7901-7905 (2009-09-10)
A novel class of 4-pyridinoxy-2-anilinopyridine-based TGF-beta type I receptor (also known as activin-like kinase 5 or ALK5) inhibitors is reported. The binding mode of this scaffold was successfully predicted by analyzing possible docked binding modes of literature inhibitors and novel
Mark J Anderton et al.
Toxicologic pathology, 39(6), 916-924 (2011-08-24)
Aberrant signaling by transforming growth factor-β (TGF-β) and its type I (ALK5) receptor has been implicated in a number of human diseases and this pathway is considered a potential target for therapeutic intervention. Transforming growth factor-β signaling via ALK5 plays
Jason S L Yu et al.
Stem cells (Dayton, Ohio), 37(7), 958-972 (2019-04-02)
Direct in vivo reprogramming of cardiac fibroblasts into myocytes is an attractive therapeutic intervention in resolving myogenic deterioration. Current transgene-dependent approaches can restore cardiac function, but dependence on retroviral delivery and persistent retention of transgenic sequences are significant therapeutic hurdles.
Lindsay C Spender et al.
Molecular pharmacology, 95(2), 222-234 (2018-11-22)
The transforming growth factor β (TGFβ) superfamily includes TGFβ, activins, inhibins, and bone morphogenetic proteins (BMPs). These extracellular ligands have essential roles in normal tissue homeostasis by coordinately regulating cell proliferation, differentiation, and migration. Aberrant signaling of superfamily members, however

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