PZ0299
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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모든 사진(1)
About This Item
추천 제품
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)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
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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