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Merck
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Key Documents

SML2822

Sigma-Aldrich

AZ12601011

≥98% (HPLC)

Sinônimo(s):

1-(2-Pyridin-2-yl-6,7dihydro-5H-cyclopenta[e]pyrimidin-4-yl)pyrrolo[3,2-c]pyridine, 2-(2-Pyridinyl)-4-(1H-pyrrolo[3,2-c]pyridin-1-yl)-6,7-dihydro-5H-cyclopenta[d]pyrimidine, AZ 12601011, AZ-12601011

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About This Item

Fórmula empírica (Notação de Hill):
C19H15N5
Peso molecular:
313.36
Código UNSPSC:
12352200
NACRES:
NA.77

Nível de qualidade

Ensaio

≥98% (HPLC)

forma

powder

cor

white to light brown

solubilidade

DMSO: 2 mg/mL, clear

temperatura de armazenamento

2-8°C

Ações bioquímicas/fisiológicas

AZ12601011 is an orally active, subtype-selective TGF-β type I receptors active site inhibitor (active-site affinity: ALK4/5/6 Kd = 2.6/2.9/42 nM, ALK1/2/3 Kd = 40/15/40 μM) that prevents ALK4/5/7-mediated Smad2, but not ALK1/2/3/6-mediated Smad1, phosphorylation (10 μM; NIH3T3 expressing respective constitutively active receptors). AZ12601011 inhibits 4T1 murine mammary carcinoma growth in cultures (IC50 = 400 nM) and in vivo (50 mg/kg bid. po. mice). AZ12601011 also causes heart valve lesions and physeal dysplasia in rats (150 mg/kg/day po. for 7 days), consistent with a critical role of ALK5 in maintaining the integrity of heart valve and physis.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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Thomas G Bird et al.
Science translational medicine, 10(454) (2018-08-17)
Liver injury results in rapid regeneration through hepatocyte proliferation and hypertrophy. However, after acute severe injury, such as acetaminophen poisoning, effective regeneration may fail. We investigated how senescence may underlie this regenerative failure. In human acute liver disease, and murine
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
Rene Jackstadt et al.
Cancer cell, 36(3), 319-336 (2019-09-19)
The metastatic process of colorectal cancer (CRC) is not fully understood and effective therapies are lacking. We show that activation of NOTCH1 signaling in the murine intestinal epithelium leads to highly penetrant metastasis (100% metastasis; with >80% liver metastases) in

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