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SML2971

Sigma-Aldrich

K03861

≥98% (HPLC)

Sinônimo(s):

1-[4-(2-Aminopyrimidin-4-yloxy)phenyl]-3-[4-[(4-methylpiperazin-1-yl)methyl]-3-trifluoromethylphenyl]urea, AUZ 454, AUZ-454, AUZ454, CCG 269702, CCG-269702, CCG269702, K 03861, K-03861, N-[4-[(2-Amino-4-pyrimidinyl)oxy]phenyl]-N′-[4-[(4-methyl-1-piperazinyl)methyl]-3-(trifluoromethyl)phenyl]urea

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About This Item

Fórmula empírica (Notação de Hill):
C24H26F3N7O2
Número CAS:
853299-07-7
Peso molecular:
501.50
Número MDL:
MFCD19443769
Código UNSPSC:
12352200
NACRES:
NA.77

Nível de qualidade

100

Ensaio

≥98% (HPLC)

Formulário

powder

cor

white to beige

solubilidade

DMSO: 2 mg/mL, clear

temperatura de armazenamento

−20°C

InChI

1S/C24H26F3N7O2/c1-33-10-12-34(13-11-33)15-16-2-3-18(14-20(16)24(25,26)27)31-23(35)30-17-4-6-19(7-5-17)36-21-8-9-29-22(28)32-21/h2-9,14H,10-13,15H2,1H3,(H2,28,29,32)(H2,30,31,35)

chave InChI

PWDLXPJQFNVTNL-UHFFFAOYSA-N

Ações bioquímicas/fisiológicas

K03861 is an ATP site-binding, cyclin-competitive, type II CDK2 inhibitor that selectively targets and locks the kinase in its inactive DFG-out conformation (CDK2 Kd = 50 nM, DFG-out stabilizing CDK2-C118L/A144C mutant Kd = 9.7 nM without vs. 134.1 nM with bound cycB; CDK2-C118L/A144C-cycA IC50 = 0.8 μM), rendering it incompatible for cyclin bining. K03861 selectively inhibits CDK2-C118L/A144C over CycA-bound wt CDK2 by in vitro kinase assay (IC50 = 0.8 vs. >10 μM) and inhibits the proliferation of immortalized multipotent otic progenitor (iMOP) murine cell line (by 81% and 92%, resepectively, at 0.1 and 1.0 μM).

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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Carrow I Wells et al.
Nature communications, 11(1), 2743-2743 (2020-06-04)
Concerted multidisciplinary efforts have led to the development of Cyclin-Dependent Kinase inhibitors (CDKi's) as small molecule drugs and chemical probes of intracellular CDK function. However, conflicting data has been reported on the inhibitory potency of CDKi's and a systematic characterization
Atsushi Okuma et al.
Nature communications, 8(1), 2050-2050 (2017-12-14)
p16Ink4a and p21Cip1/Waf1 act as tumour suppressors through induction of cellular senescence. However, senescence-independent roles of these CDK inhibitors are not well understood. Here, we report an unexpected function of p16Ink4 and p21Cip1/Waf1, namely, tumour promotion through chemotaxis. In monocytic
Zhichao Song et al.
Stem cell reports, 9(5), 1516-1529 (2017-10-17)
Loss of spiral ganglion neurons (SGNs) significantly contributes to hearing loss. Otic progenitor cell transplantation is a potential strategy to replace lost SGNs. Understanding how key transcription factors promote SGN differentiation in otic progenitors accelerates efforts for replacement therapies. A
Zhichao Song et al.
Frontiers in cell and developmental biology, 7, 87-87 (2019-06-14)
Stem cell replacement therapy is a potential method for repopulating lost spiral ganglion neurons (SGNs) in the inner ear. Efficacy of cell replacement relies on proper differentiation. Defining the dynamic expression of different transcription factors essential for neuronal differentiation allows

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