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Merck

S4696

Sigma-Aldrich

SB-505124 hydrochloride hydrate

≥98% (HPLC)

Synonym(e):

2-(5-Benzo[1,3]dioxol-5-yl-2-tert-butyl-3H-imidazol-4-yl)-6-methylpyridine hydrochloride hydrate

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About This Item

Empirische Formel (Hill-System):
C20H21N3O2 · xHCl · yH2O
CAS-Nummer:
Molekulargewicht:
335.40 (anhydrous free base basis)
MDL-Nummer:
UNSPSC-Code:
12352200
PubChem Substanz-ID:
NACRES:
NA.77

Qualitätsniveau

Assay

≥98% (HPLC)

Form

powder

Lagerbedingungen

desiccated

Farbe

yellow

Löslichkeit

DMSO: >10 mg/mL
H2O: insoluble

Ersteller

GlaxoSmithKline

Lagertemp.

2-8°C

SMILES String

O.Cl.Cc1cccc(n1)-c2[nH]c(nc2-c3ccc4OCOc4c3)C(C)(C)C

InChI

1S/C20H21N3O2.ClH.H2O/c1-12-6-5-7-14(21-12)18-17(22-19(23-18)20(2,3)4)13-8-9-15-16(10-13)25-11-24-15;;/h5-10H,11H2,1-4H3,(H,22,23);1H;1H2

InChIKey

DIDCCMVWCVRTNB-UHFFFAOYSA-N

Anwendung

SB-505124 hydrochloride hydrate was used to study the role of TGF-β pathway in development and differentiation studies.3,4

Biochem./physiol. Wirkung

SB-505124 selectively inhibits TGF-β type I receptors, activin receptor-like kinases (ALK) 4, 5 and 7. It inhibits ALK4-, 5- and 7-mediated activation of Smad2, Smad3 and MAPK pathway induced by TGF-β.1 SB-505124 inhibits the human fibroblast trans-differentiation induced by the co-culture with Esophageal squamous cell carcinoma.2
SB-505124 is an inhibitor of activin receptor-like kinase (ALK) 5, also known as transforming growth factor-α type I receptor kinase, with an IC50 of 47 ± 5 nM.

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.

Piktogramme

Exclamation mark

Signalwort

Warning

Gefahreneinstufungen

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

Zielorgane

Respiratory system

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

dust mask type N95 (US), Eyeshields, Gloves


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

Stacey DaCosta Byfield et al.
Molecular pharmacology, 65(3), 744-752 (2004-02-24)
Clinically, there is a great need for small molecule inhibitors that could control pathogenic effects of transforming growth factor (TGF-beta) and/or modulate effects of TGF-beta in normal responses. Inhibition of TGF-beta signaling would be predicted to enhance re-epithelialization of cutaneous
Kazuhiro Noma et al.
Gastroenterology, 134(7), 1981-1993 (2008-04-29)
Esophageal squamous cell carcinoma (ESCC) is known to be a highly angiogenic tumor. Here, we investigated the role of the stromal fibroblasts in the ESCC-induced angiogenic response using a novel 3-dimensional model. A novel assay was developed where cocultures of
Masahiro Shin et al.
Mechanisms of development, 128(5-6), 268-278 (2011-03-16)
Nanog is required for the maintenance of cellular pluripotency during normal development and in cultured embryonic stem cells. A number of signaling pathways have been implicated in regulating Nanog gene expression in vitro. Using the chick model, we provide in
Hongmin Yun et al.
Immunity, 53(5), 1050-1062 (2020-11-19)
Herpes simplex virus type 1 (HSV-1)-infected corneas can develop a blinding immunoinflammatory condition called herpes stromal keratitis (HSK), which involves the loss of corneal sensitivity due to retraction of sensory nerves and subsequent hyperinnervation with sympathetic nerves. Increased concentrations of
Liming Tan et al.
Neuron, 108(4), 735-747 (2020-10-23)
High acuity stereopsis emerges during an early postnatal critical period when binocular neurons in the primary visual cortex sharpen their receptive field tuning properties. We find that this sharpening is achieved by dismantling the binocular circuit present at critical period

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