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Merck
모든 사진(1)

Key Documents

PZ0299

Sigma-Aldrich

PF-05175157

≥98% (HPLC)

동의어(들):

1,4-Dihydro-1′-[(2-methyl-1H-benzimidazol-6-yl)carbonyl]-1-(1-methylethyl)-spiro[5H-indazole-5,4′-piperidin]-7(6H)-one, 1-Isopropyl-1-(2-methyl-1H-benzo[d]imidazole-6-carbonyl)-1,4-dihydrospiro[indazole-5,4-piperidin]-7(6H)-one

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About This Item

실험식(Hill 표기법):
C23H27N5O2
CAS Number:
Molecular Weight:
405.49
UNSPSC 코드:
12352200
NACRES:
NA.77

Quality Level

분석

≥98% (HPLC)

형태

powder

색상

white to beige

solubility

DMSO: 5 mg/mL, clear (warmed)

저장 온도

room temp

SMILES string

CC(C)N(N=C1)C2=C1CC3(CCN(C(C4=CC(NC(C)=N5)=C5C=C4)=O)CC3)CC2=O

애플리케이션

PF-05175157 has been used as an acetyl-Coenzyme A carboxylase (ACC) inhibitor to study its effects on the infection of flavivirus.

생화학적/생리학적 작용

PF-05175157 is a potent and selective inhibitor of both acetyl-CoA carboxylase isoform ACC1 located primarily in liver and adipose tissue and isoform ACC2 dominant in skeletal and heart muscle, with IC50 values of 27 nM and 33 nM, respectively. Acetyl CoA carboxylase (ACC) generates malonyl CoA, which is a substrate for de novo lipogenesis and is also an inhibitor of mitochondrial fatty acid β-oxidation through inihbition of carnitine-palmitoyl transferase I (CPT-1), responsible for the transport of long-chain fatty acyl-CoAs across the mitochondrial membrane. ACC inihibitors are hoped to inhibit de novo lipogenesis and increase β-oxidation of long-chain fatty acids with potential for treatment of type 2 diabetes, hepatic steatosis, and cancer. In Phase I clinical studies for diabetes treatment, PF-05175157 inhibited de novo lipogenesis and increased net whole-body fatty acid utilization.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

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문서 라이브러리 방문

Nereida Jiménez de Oya et al.
Emerging microbes & infections, 8(1), 624-636 (2019-04-20)
Flaviviruses are (re)-emerging RNA viruses strictly dependent on lipid metabolism for infection. In the search for host targeting antivirals, we explored the effect of pharmacological modulation of fatty acid metabolism during flavivirus infection. Considering the central role of acetyl-Coenzyme A

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