おすすめの製品
アッセイ
≥98% (HPLC)
フォーム
powder
色
light orange to dark orange
溶解性
DMSO: 5 mg/mL, clear (warmed)
保管温度
−20°C
SMILES記法
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
InChI Key
NVNSXBXKNMWKEJ-UHFFFAOYSA-N
アプリケーション
UCF-101 has been used to study its cytoprotective activity in a mouse model of spinal cord injury.
生物化学的/生理学的作用
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.
UCF-101 is a selective inhibitor of the pro-apoptotic mitochondrial serine protease Omi/HtrA2.
特徴および利点
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.
保管分類コード
11 - Combustible Solids
WGK
WGK 3
引火点(°F)
Not applicable
引火点(℃)
Not applicable
適用法令
試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。
Jan Code
SML1105-25MG:
SML1105-VAR:
SML1105-BULK:
SML1105-5MG:
最新バージョンのいずれかを選択してください:
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
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