Ugrás a tartalomra
Merck

SML2376

Sigma-Aldrich

GSK′963

≥98% (HPLC)

Szinonimák:

1-[(5S)-4,5-Dihydro-5-phenyl-1H-pyrazol-1-yl]-2,2-dimethyl-1-propanone; 2,2-Dimethyl-1-(5(S)-phenyl-4,5-dihydro-pyrazol-1-yl)-propan-1-one, GSK 963, GSK′ 963A, GSK′963A, GSK-963, GSK-963A, GSK963, GSK963A

Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez


About This Item

Tapasztalati képlet (Hill-képlet):
C14H18N2O
CAS-szám:
Molekulatömeg:
230.31
UNSPSC kód:
12352200
NACRES:
NA.77

Teszt

≥98% (HPLC)

Forma

powder

szín

white to beige

oldhatóság

DMSO: 2 mg/mL, clear

tárolási hőmérséklet

2-8°C

SMILES string

O=C(C(C)(C)C)N1[C@H](C2=CC=CC=C2)CC=N1

Biokémiai/fiziológiai hatások

GSK′963 (GSK′963A) is a brain-penetrant, highly potent and selective ATP site-targeting receptor-interacting protein 1 kinase (RIP1; RIPK1) inhibitor (IC50 = 0.8-8 nM with 50 μM ATP; IC50 >10 μM against RIPK2/3/5 and 335 other kinases) that protects against TNFα/zVAD-induced necroptosis (EC50 = 1/4 nM in mouse L929/human U937 cultures) and blocks Y. pestis-induced death of murine fetal liver macrophages (1 μM). GSK′963 prevents lethal hypothermia by acute sterile shock (2 mg/kg i.p. 15 min prior to TNFα/zVAD i.v.) and protects against acute neuronal death upon autologous blood intracerebral hemorrhage induction in mice in vivo (25 mg/kg/3 hr i.p.).

Tárolási osztály kódja

11 - Combustible Solids

WGK

WGK 3

Lobbanási pont (F)

Not applicable

Lobbanási pont (C)

Not applicable


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Analitikai tanúsítványok (COA)

Lot/Batch Number

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Dokumentumtár megtekintése

Anne von Mässenhausen et al.
Cell death & disease, 9(3), 359-359 (2018-03-04)
Receptor-interacting protein kinases 1 and 3 (RIPK1/3) have best been described for their role in mediating a regulated form of necrosis, referred to as necroptosis. During this process, RIPK3 phosphorylates mixed lineage kinase domain-like (MLKL) to cause plasma membrane rupture.
Hongyan Guo et al.
Cell host & microbe, 17(2), 243-251 (2015-02-13)
Herpes simplex virus (HSV)-1 and HSV-2 are significant human pathogens causing recurrent disease. During infection, HSV modulates cell death pathways using the large subunit (R1) of ribonucleotide reductase (RR) to suppress apoptosis by binding to and blocking caspase-8. Here, we demonstrate
Sevda Lule et al.
Stroke, 48(9), 2549-2556 (2017-08-03)
Recent studies using cultured cells and rodent intracerebral hemorrhage (ICH) models have implicated RIPK1 (receptor interacting protein kinase-1) as a driver of programmed necrosis and secondary injury based on use of chemical inhibitors. However, these inhibitors have off-target effects and
Dan Weng et al.
Proceedings of the National Academy of Sciences of the United States of America, 111(20), 7391-7396 (2014-05-07)
A number of pathogens cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as the "Black Death" in medieval Europe, induces considerable cytotoxicity. The rapid killing of macrophages induced by Y. pestis
S B Berger et al.
Cell death discovery, 1, 15009-15009 (2015-01-01)
Necroptosis and signaling regulated by RIP1 kinase activity is emerging as a key driver of inflammation in a variety of disease settings. A significant amount has been learned about how RIP1 regulates necrotic cell death through the use of the

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