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S7071

Sigma-Aldrich

SD-208

≥98% (HPLC), powder

Sinónimos:

2-(5-Chloro-2-fluorophenyl)pteridin-4-yl]pyridin-4-yl-amine

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About This Item

Fórmula empírica (notación de Hill):
C17H10ClFN6
Número de CAS:
627536-09-8
Peso molecular:
352.75
Número MDL:
MFCD11519969
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
24899731
NACRES:
NA.77

Nivel de calidad

100

Análisis

≥98% (HPLC)

formulario

powder

color

off-white to tan

solubilidad

DMSO: >5 mg/mL

temp. de almacenamiento

2-8°C

cadena SMILES

Fc1ccc(Cl)cc1-c2nc(Nc3ccncc3)c4nccnc4n2

InChI

1S/C17H10ClFN6/c18-10-1-2-13(19)12(9-10)15-24-16-14(21-7-8-22-16)17(25-15)23-11-3-5-20-6-4-11/h1-9H,(H,20,22,23,24,25)

Clave InChI

BERLXWPRSBJFHO-UHFFFAOYSA-N

Aplicación

SD-208 was used to inhibit the activity of ALK5 kinase in bovine retinal vascular cells.2

Acciones bioquímicas o fisiológicas

SD-208 is TGF-βR I kinase inhibitor with IC50 =49 nM based on direct enzymatic assay of TGFRI kinase (ALK5) activity with a specificity of >100-fold against TGFRII and at least 17-fold over members of a panel of related protein kinases including p38a, p38b, p38d, JNK1, EGFR, MAPKAPK2, MKK6, ERK2, PKC, PKA, PKD, CDC2, and CaMKII.
SD-208 is an inhibitor of TGF β receptor 1 kinase that is reportedly effective against human malignant gliomas. It increases the lytic activity and tumor infiltration by polyclonal natural killer cells, CD8 T cells and macrophages.1

Pictogramas

Exclamation mark
GHS07

Palabra de señalización

Warning

Frases de peligro

H302

Clasificaciones de peligro

Acute Tox. 4 Oral

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Equipo de protección personal

dust mask type N95 (US), Eyeshields, Gloves

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Katharina Seystahl et al.
Neuro-oncology, 17(2), 254-265 (2014-08-29)
The transforming growth factor (TGF)-β and vascular endothelial growth factor (VEGF) pathways have a major role in the pathogenesis of glioblastoma, notably immunosuppression, migration, and angiogenesis, but their interactions have remained poorly understood. We characterized TGF-β pathway activity in 9
Tanja Stüber et al.
Journal for immunotherapy of cancer, 8(1) (2020-04-19)
Immunotherapy with chimeric antigen receptor (CAR)-engineered T-cells is effective in some hematologic tumors. In solid tumors, however, sustained antitumor responses after CAR T-cell therapy remain to be demonstrated both in the pre-clinical and clinical setting. A perceived barrier to the
Martin Uhl et al.
Cancer research, 64(21), 7954-7961 (2004-11-03)
The cytokine transforming growth factor (TGF)-beta, by virtue of its immunosuppressive and promigratory properties, has become a major target for the experimental treatment of human malignant gliomas. Here we characterize the effects of a novel TGF-beta receptor (TGF-betaR) I kinase
Chandan K Nagaraju et al.
Scientific reports, 9(1), 8879-8879 (2019-06-22)
After myocardial infarction, resident fibroblasts (Fb) differentiate towards myofibroblasts (MyoFb), generating the scar tissue and the interstitial fibrosis seen in the adjacent myocardium. Fb and MyoFb have the potential to interact with cardiac myocytes (CMs) but insight into the phenotype-specific
Elisa Ventura et al.
Journal of immunology (Baltimore, Md. : 1950), 198(12), 4569-4574 (2017-05-10)
Glioblastoma is the most common and aggressive intrinsic brain tumor in adults. Self-renewing, highly tumorigenic glioma-initiating cells (GIC) have been linked to glioma invasive properties, immunomodulation, and increased angiogenesis, leading to resistance to therapy. TGF-β signaling has been associated with
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