S4696
SB-505124 hydrochloride hydrate
≥98% (HPLC), activin receptor-like kinase (ALK) 5 inhibitor, powder
동의어(들):
2-(5-Benzo[1,3]dioxol-5-yl-2-tert-butyl-3H-imidazol-4-yl)-6-methylpyridine hydrochloride hydrate
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크기 선택
제품정보 (DICE 배송 시 비용 별도)
실험식(Hill 표기법):
C20H21N3O2 · xHCl · yH2O
CAS 번호:
Molecular Weight:
335.40 (anhydrous free base basis)
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
제품 이름
SB-505124 hydrochloride hydrate, ≥98% (HPLC)
SMILES string
O.Cl.Cc1cccc(n1)-c2[nH]c(nc2-c3ccc4OCOc4c3)C(C)(C)C
InChI key
DIDCCMVWCVRTNB-UHFFFAOYSA-N
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
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
color
yellow
solubility
DMSO: >10 mg/mL, H2O: insoluble
originator
GlaxoSmithKline
storage temp.
2-8°C
Quality Level
Application
SB-505124 hydrochloride hydrate was used to study the role of TGF-β pathway in development and differentiation studies.3,4
Biochem/physiol Actions
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.
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
Features and Benefits
This compound was developed by GlaxoSmithKline. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
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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