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Key Documents

SML2216

Sigma-Aldrich

Takinib

≥98% (HPLC)

Synonym(s):

N1-(1-Propyl-1H-benzimidazol-2-yl)-1,3-benzenedicarboxamide

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About This Item

Empirical Formula (Hill Notation):
C18H18N4O2
CAS Number:
Molecular Weight:
322.36
UNSPSC Code:
12352200
NACRES:
NA.77

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

SMILES string

CCCN1C2=CC=CC=C2N/C1=N\C(C3=CC(C(N)=O)=CC=C3)=O

General description

Takinib belongs to the aminobenzimidazole class of inhibitors.

Application

Takinib has been used as an inhibitor of transforming 28 growth factor - β-activated kinase -1 (TAK-1) in human leukemia monocytic THP-1 cells. It may be used as a TAK1 inhibitor in Jurkat cells.

Biochem/physiol Actions

Takinib is a selective inhibitor of TAK1/MAP3K7 kinase, which is a member of the MAP3K family and a key regulator of cell death. It binds in the TAk1 ATPbinding pocket with an IC50 value of 9.5 nM. Takinib selectively induced apoptosis following TNF-α stimulation in rheumatoid arthritis and breast cancer.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Juliane Totzke et al.
Cell chemical biology, 24(8), 1029-1039 (2017-08-19)
Tumor necrosis factor alpha (TNF-α) has both positive and negative roles in human disease. In certain cancers, TNF-α is infused locally to promote tumor regression, but dose-limiting inflammatory effects limit broader utility. In autoimmune disease, anti-TNF-α antibodies control inflammation in
Constanza E Espada et al.
Journal of virology, 95(3) (2020-11-13)
Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) restricts HIV-1 replication by limiting the intracellular deoxynucleoside triphosphate (dNTP) pool. SAMHD1 also suppresses the activation of NF-κB in response to viral infections and inflammatory stimuli. However, the mechanisms by which

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