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Merck
CN

SML2647

Sigma-Aldrich

CA3

≥97% (HPLC)

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别名:
1,1′-[[9-(Hydroxyimino)-9H-fluorene-2,7-diyl]bis(sulfonyl)]bis-piperidine, 2,7-bis(1-Piperidinylsulfonyl)-9H-fluoren-9-one oxime, CIL56
经验公式(希尔记法):
C23H27N3O5S2
分子量:
489.61
MDL编号:
UNSPSC代码:
12352200
NACRES:
NA.77

检测方案

≥97% (HPLC)

形式

powder

颜色

white to beige

溶解性

DMSO: 2 mg/mL, clear

储存温度

−20°C

生化/生理作用

CA3 is a potent and selective inhibitor of YAP1 (Hippo co-activator Yes-associated protein 1) that inhibits YAP1 expression and transcriptional activity in esophageal adenocarcinoma (EAC) cell lines. CA3 potently inhibits growth, induces apoptosis in radiation resistant CSC (cancer stem cell) enriched EAC cells. It inhibits tumor growth of in xenograft model with no apparent toxicity.

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Siyuan Hao et al.
iScience, 27(6), 109927-109927 (2024-05-24)
YAP/TEAD signaling is essential for organismal development, cell proliferation, and cancer progression. As a transcriptional coactivator, how YAP activates its downstream target genes is incompletely understood. YAP forms biomolecular condensates in response to hyperosmotic stress, concentrating transcription-related factors to activate
Shumei Song et al.
Molecular cancer therapeutics, 17(2), 443-454 (2017-11-24)
Mounting evidence suggests that the Hippo coactivator Yes-associated protein 1 (YAP1) is a major mediator of cancer stem cell (CSC) properties, tumor progression, and therapy resistance as well as often a terminal node of many oncogenic pathways. Thus, targeting YAP1
Xiao Qin et al.
Cell, 186(25), 5554-5568 (2023-12-09)
Cancer cells are regulated by oncogenic mutations and microenvironmental signals, yet these processes are often studied separately. To functionally map how cell-intrinsic and cell-extrinsic cues co-regulate cell fate, we performed a systematic single-cell analysis of 1,107 colonic organoid cultures regulated
Sina Stern et al.
Neuron, 109(21), 3436-3455 (2021-09-12)
An inhibitory extracellular milieu and neuron-intrinsic processes prevent axons from regenerating in the adult central nervous system (CNS). Here we show how the two aspects are interwoven. Genetic loss-of-function experiments determine that the small GTPase RhoA relays extracellular inhibitory signals

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