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Merck
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Key Documents

SML0795

Sigma-Aldrich

PF-670462

≥98% (HPLC)

同義詞:

4-[3-Cyclohexyl-5-(4-fluoro-phenyl)-3H-imidazol-4-yl]-pyrimidin-2-ylamine dihydrochloride, PF670462

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About This Item

經驗公式(希爾表示法):
C19H20FN5 · 2HCl
CAS號碼:
分子量::
410.32
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

化驗

≥98% (HPLC)

形狀

powder

儲存條件

desiccated

顏色

white to beige

溶解度

H2O: 2 mg/mL, clear (warmed)

儲存溫度

2-8°C

InChI

1S/C19H20FN5.2ClH/c20-14-8-6-13(7-9-14)17-18(16-10-11-22-19(21)24-16)25(12-23-17)15-4-2-1-3-5-15;;/h6-12,15H,1-5H2,(H2,21,22,24);2*1H

InChI 密鑰

PSNKGVAXBSAHCH-UHFFFAOYSA-N

生化/生理作用

PF-670462 is a selective inhibitor of the δ- and ε-isoforms of casein kinase I, with IC50 values of 7.7 and 14 nM respectively, and >30 selectivity relative to 42 other kinases tested. Casein kinase Iε phosphorylates PER proteins, which are involved in setting the period of the circadian pacemaker or clock. PF-670462 is potent (IC50 7.7 nM) and effective in vivo (i.e. it induces profound phase delays in circadian periodicity).
PF-670462 is also termed as 4-[1-cyclohexyl-4-(4-fluorophenyl)-1H-imidazol-5-yl]-2-pyrimidinamine dihydrochloride). It participates in ceramide transfer between Golgi and ER (endoplasmic reticulum) compartments. PF-670462 affects actin filament consolidation. It also hinders the stability at the front edge of cells treated with N-formyl Met-Leu-Phe.

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析證明 (COA)

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The Inhibitor Index: A Desk Reference on Enzyme Inhibitors, Receptor Antagonists, Drugs, Toxins, Poisons, Biologics, and Therapeutic Leads, 1362-1362 (2017)
Combined Pharmacological and Genetic Manipulations Unlock Unprecedented Temporal Elasticity and Reveal Phase-Specific Modulation of the Molecular Circadian Clock of the Mouse Suprachiasmatic Nucleus.
Patton AP, et al.
The Journal of Neuroscience, 36(36), 9326-9341 (2016)
David A Hicks et al.
Neurochemical research, 45(6), 1354-1364 (2019-07-08)
Motor neuron disease (MND) is a progressive neurodegenerative disease with no effective treatment. One of the principal pathological hallmarks is the deposition of TAR DNA binding protein 43 (TDP-43) in cytoplasmic inclusions. TDP-43 aggregation occurs in both familial and sporadic

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