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Merck

616452

RepSox

≥95% (HPLC), solid, TGF-β RI kinase inhibitor, Calbiochem

別名:

TGF-β RI Kinase Inhibitor II, ALK5 Inhibitor II, Transforming Growth Factor-β Type I Receptor Kinase Inhibitor II, 2-(3-(6-Methylpyridin-2-yl)-1H-pyrazol-4-yl)-1,5-naphthyridine

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この商品について

実験式（ヒル表記法）:
C17H13N5
CAS番号:
446859-33-2
分子量:
287.32
UNSPSC Code:
51111800
NACRES:
NA.77
MDL number:
MFCD09037561
Assay:
≥95% (HPLC)
Form:
solid
Quality level:
100
Storage condition:
OK to freeze
protect from light

主要文書

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製品名

TGF-β RI Kinase Inhibitor II, TGF-β RI Kinase Inhibitor II, CAS 446859-33-2, is a cell-permeable, potent, reversible, ATP-competitive inhibitor of TGF-β R1 kinase (IC50 = 23 nM and 4 nM for ALK5 binding & auto-phosphorylation).

SMILES string

[nH]1ncc(c1c4nc(ccc4)C)c2nc3c(nccc3)cc2

InChI

1S/C17H13N5/c1-11-4-2-5-16(20-11)17-12(10-19-22-17)13-7-8-14-15(21-13)6-3-9-18-14/h2-10H,1H3,(H,19,22)

InChI key

LBPKYPYHDKKRFS-UHFFFAOYSA-N

assay

≥95% (HPLC)

form

solid

potency

23 nM IC50

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

yellow

solubility

DMSO: 5 mg/mL
methanol: 5 mg/mL

shipped in

ambient

Quality Level

100

storage temp.

2-8°C

関連するカテゴリー

Biochem/physiol Actions

Cell permeable: yes
Primary Target
ALKS binding
Product competes with ATP.
Secondary Target
ALK 5 auto phosphorylation (IC₅₀ = 4 nM)

Disclaimer

Toxicity: Standard Handling (A)

General description

A cell-permeable naphthyridinyl pyrazolo compound that acts as a potent, selective, reversible, and ATP-competitive inhibitor of TGF-β type I receptor (ALK5; IC50 = 23 nM, 4 nM and 18 nM for ALK5 binding, ALK5 auto-phosphorylation and TGF-β cellular assay in HepG2 cells, respectively). Minimally affects a panel of 9 closely related kinases including p38 MAPK at IC50 >16 µM. Also available as a 50 mM solution in DMSO (Cat. No. 508158).

Other Notes

Gellibert, F., et al. 2004. J. Med. Chem.47, 4494.
Ichida, J. K., et al. 2009. Cell Stem Cell 5, 491.

Packaging

Packaged under inert gas

Preparation Note

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

保管分類

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

試験成績書（COA）

製品のロット番号・バッチ番号を入力して、試験成績書（COA） を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。

以前この製品を購入いただいたことがある場合

文書ライブラリで、最近購入した製品の文書を検索できます。

文書ライブラリにアクセスする

Satoru Shinriki et al.
The Journal of pathology, 244(3), 367-379 (2017-12-14)
Oral squamous cell carcinoma (OSCC) has a very poor prognosis because of its highly invasive nature, and the 5-year survival rate has not changed appreciably for the past 30 years. Although cylindromatosis (CYLD), a deubiquitinating enzyme, is thought to be a
Mikolaj M Kozlowski et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 40(13), 2618-2632 (2020-02-23)
Sensory hair cell losses underlie the vast majority of permanent hearing and balance deficits in humans, but many nonmammalian vertebrates can fully recover from hearing impairments and balance dysfunctions because supporting cells (SCs) in their ears retain lifelong regenerative capacities
Ana Guerrero et al.
Nature aging, 2, 851-866 (2022-11-29)
Cellular senescence is a stable type of cell cycle arrest triggered by different stresses. As such, senescence drives age-related diseases and curbs cellular replicative potential. Here, we show that 3-deazaadenosine (3DA), an S-adenosyl homocysteinase (AHCY) inhibitor, alleviates replicative and oncogene-induced
Ayumi Kanemaru et al.
Cancer cell international, 22(1), 358-358 (2022-11-16)
Tumor suppressor CYLD dysfunction by loss of its expression, triggers malignant transformation, especially drug resistance and tumor invasion/metastasis. Although loss of CYLD expression is significantly associated with poor prognosis in a large variety of tumors, no clinically-effective treatment for CYLD-negative
Sayaka Imatsuji et al.
Oncology research, 32(1), 139-150 (2024-01-08)
Growing evidence suggests an association between epithelial-mesenchymal transition (EMT), a hallmark of tumor malignancy, and chemoresistance to a number of anti-cancer drugs. However, the mechanism of EMT induction in the process of acquiring anti-cancer drug resistance remains unclear. To address
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グローバルトレードアイテム番号

カタログ番号GTIN
616452-2MGCN04055977185829

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