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Key Documents

Inne dokumenty

SML1128

Sigma-Aldrich

NMS-873

≥98% (HPLC)

Synonim(y):

3-[3-(Cyclopentylthio)-5-[[[2-methyl-4′-(methylsulfonyl)[1,1′-biphenyl]-4-yl]oxy]methyl]-4H-1,2,4-triazol-4-yl]-pyridine, 3-[3-Cyclopentylsulfanyl-5-(4′-methanesulfonyl-2-methylbiphenyl-4-yloxymethyl)-[1,2,4]triazol-4-yl]-pyridine

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About This Item

Wzór empiryczny (zapis Hilla):
C27H28N4O3S2
Numer CAS:
1418013-75-8
Masa cząsteczkowa:
520.67
Numer MDL:
MFCD28009371
Kod UNSPSC:
12352200
Identyfikator substancji w PubChem:
329825666
NACRES:
NA.77

Próba

≥98% (HPLC)

Postać

powder

kolor

white to beige

rozpuszczalność

DMSO: 25 mg/mL, clear

temp. przechowywania

2-8°C

ciąg SMILES

CC1=CC(OCC2=NN=C(SC3CCCC3)N2C4=CN=CC=C4)=CC=C1C5=CC=C(S(C)(=O)=O)C=C5

InChI

1S/C27H28N4O3S2/c1-19-16-22(11-14-25(19)20-9-12-24(13-10-20)36(2,32)33)34-18-26-29-30-27(35-23-7-3-4-8-23)31(26)21-6-5-15-28-17-21/h5-6,9-17,23H,3-4,7-8,18H2,1-2H3

Klucz InChI

UJGTUKMAJVCBIS-UHFFFAOYSA-N

Zastosowanie

MS-873 has been used as an allosteric inhibitor of ATPase valosin-containing protein (VCP)/p97.

Działania biochem./fizjol.

NMS-873 is a selective allosteric non–ATP-competitive inhibitor of the AAA ATPase family member valosine containing protein (VCP), also known as p97 (VCP/p97), an integral component of the ubiquitin fusion degradation (UFD) pathway. VCP/p97 plays a role in degradation of misfolded proteins, Golgi membrane reassembly, membrane transport, myofibril assembly, autophagosome maturation, and cell division, and is overexpressed in many tumor types. NMS-873 is the most potent and specific VCP inhibitor described to date. NMS-873 has an IC50 of 30 nM for VCP/p97 compared to IC50 >10 μM against all of the AAA ATPases, HSP90 or the 53 kinases analyzed. NMS-873 inhibited proliferation of HCT116 cancer cell line cells with an IC50 value of 400 nM.
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Kod klasy składowania

11 - Combustible Solids

Klasa zagrożenia wodnego (WGK)

WGK 3

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable

Certyfikaty analizy (CoA)

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Odwiedź Bibliotekę dokumentów

Replication-dependent unhooking of DNA interstrand cross-links by the NEIL3 glycosylase.
Semlow D R, et al.
Cell, 167(2), 498-511 (2016)
Sahradha Albert et al.
Proceedings of the National Academy of Sciences of the United States of America, 117(2), 1069-1080 (2019-12-29)
To promote the biochemical reactions of life, cells can compartmentalize molecular interaction partners together within separated non-membrane-bound regions. It is unknown whether this strategy is used to facilitate protein degradation at specific locations within the cell. Leveraging in situ cryo-electron
Irene Gallina et al.
Molecular cell, 81(3), 442-458 (2020-12-16)
Lesions on DNA uncouple DNA synthesis from the replisome, generating stretches of unreplicated single-stranded DNA (ssDNA) behind the replication fork. These ssDNA gaps need to be filled in to complete DNA duplication. Gap-filling synthesis involves either translesion DNA synthesis (TLS)
Lin Deng et al.
Molecular cell, 73(5), 915-929 (2019-03-09)
DNA replication errors generate complex chromosomal rearrangements and thereby contribute to tumorigenesis and other human diseases. One mechanism that triggers these errors is mitotic entry before the completion of DNA replication. To address how mitosis might affect DNA replication, we
Eva M van Well et al.
The EMBO journal, 38(9) (2019-03-20)
Neurodegenerative diseases are characterized by the accumulation of misfolded proteins in the brain. Insights into protein quality control mechanisms to prevent neuronal dysfunction and cell death are crucial in developing causal therapies. Here, we report that various disease-associated protein aggregates
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