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SML1105

Sigma-Aldrich

UCF-101

≥98% (HPLC)

Sinônimo(s):

Dihydro-5-[[5-(2-nitrophenyl)-2-furanyl]methylene]-1,3-diphenyl-2-thioxo-4,6(1H,5H)-pyrimidinedione

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About This Item

Fórmula empírica (Notação de Hill):
C27H17N3O5S
Número CAS:
Peso molecular:
495.51
Número MDL:
Código UNSPSC:
12352200
ID de substância PubChem:
NACRES:
NA.77

Ensaio

≥98% (HPLC)

forma

powder

cor

light orange to dark orange

solubilidade

DMSO: 5 mg/mL, clear (warmed)

temperatura de armazenamento

−20°C

cadeia de caracteres SMILES

S=C(N(C1=CC=CC=C1)C2=O)N(C3=CC=CC=C3)C(C2=CC4=CC=C(C5=CC=CC=C5[N+]([O-])=O)O4)=O

InChI

1S/C27H17N3O5S/c31-25-22(17-20-15-16-24(35-20)21-13-7-8-14-23(21)30(33)34)26(32)29(19-11-5-2-6-12-19)27(36)28(25)18-9-3-1-4-10-18/h1-17H

chave InChI

NVNSXBXKNMWKEJ-UHFFFAOYSA-N

Aplicação

UCF-101 has been used to study its cytoprotective activity in a mouse model of spinal cord injury.

Ações bioquímicas/fisiológicas

UCF-101 is a selective inhibitor of the pro-apoptotic mitochondrial serine protease Omi/HtrA2, involved in the cellular response to thermal and oxidative stress. Like SMAC/Diablo, Omi/HtrA2 is an inhibitor of IAPs (inhibitor of apoptosis proteins), inhibiting the apoptosis inhibitors, thus resulting in pro-apoptotic activity. In septic rat studies, UCF-101 was found to inhibit apoptosis and have neuroprotective effects on cerebral oxidative injury and cognitive impairment. In aging rats with induced myocardial ischemia/reperfusion (MI/R) injury, UCF-101 treatment decreased XIAP degradation and caspase-3 activity and exerted cardioprotective effects.

Características e benefícios

This compound is a featured product for Apoptosis research. Click here to discover more featured Apoptosis products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


Certificados de análise (COA)

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Acute administration of ucf-101 ameliorates the locomotor impairments induced by a traumatic spinal cord injury
D.Reigada
Neuroscience, 300(6), 404-417 (2015)
Pengfei Wang et al.
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 49(6), 2163-2173 (2018-10-05)
the pathogenesis of sepsis-associated encephalopathy (SAE) is multifactorial, involving neurotransmitter alterations, inflammatory cytokines, oxidative damage, mitochondrial dysfunction, apoptosis, and other factors. Mitochondria are major producers of reactive oxygen species, resulting in cellular injury. Omi/HtrA2 is a proapoptotic mitochondrial serine protease

Conteúdo relacionado

Apoptosis, or programmed cell death (PCD), is a selective process for the removal of unnecessary, infected or transformed cells in various biological systems. As it plays a role in the homeostasis of multicellular organisms, apoptosis is tightly regulated through two principal pathways by a number of regulatory and effector molecules.

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