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product name
SANT-1 型, ≥98% (HPLC), powder
品質等級
化驗
≥98% (HPLC)
形狀
powder
溶解度
DMSO: 5 mg/mL, clear (warmed)
儲存溫度
−20°C
SMILES 字串
Cc1nn(-c2ccccc2)c(C)c1\C=N\N3CCN(CC3)Cc4ccccc4
InChI
1S/C23H27N5/c1-19-23(20(2)28(25-19)22-11-7-4-8-12-22)17-24-27-15-13-26(14-16-27)18-21-9-5-3-6-10-21/h3-12,17H,13-16,18H2,1-2H3/b24-17+
InChI 密鑰
FOORCIAZMIWALX-JJIBRWJFSA-N
應用
使用 SANT-1 处理间变性淋巴瘤激酶(ALK)阳性间变性大细胞淋巴瘤细胞 2 和慢性淋巴细胞白血病细胞 3 会导致细胞死亡。
生化/生理作用
SANT-1 在胶质母细胞瘤细胞中通过 Ras/NF-κB 途径抑制 Sonic hedgehog 信号传导,并诱导细胞凋亡。
SANT-1 是一种有效的 sonic hedgehog 信号途径(Shh)拮抗剂,通过与平滑(Smo)受体结合直接抑制。SANT-1 抑制野生型和致癌 Smo 的效率相同。
儲存類別代碼
11 - Combustible Solids
水污染物質分類(WGK)
WGK 3
閃點(°F)
Not applicable
閃點(°C)
Not applicable
個人防護裝備
Eyeshields, Gloves, type N95 (US)
其他客户在看
Cancer letters, 336(2), 347-358 (2013-04-04)
Since Shh pathway effector, Gli1, is overexpressed in gliomas, we investigated the effect of novel Shh inhibitor SANT-1 on glioma cell viability. Though SANT-1 failed to induce apoptosis, it reduced proliferation of glioma stem-like cells. Apart from canonical Shh cascade
Oncogene, 29(35), 4885-4895 (2010-07-07)
The Hedgehog (Hh) pathway regulates cell proliferation and survival and contributes to tumorigenesis. We investigated the expression and function of this pathway in B-cell chronic lymphocytic leukemia (CLL) cells and in healthy B lymphocytes. Profiling of cognate Hh pathway members
Cancer research, 69(6), 2550-2558 (2009-02-27)
Deregulation of the sonic hedgehog (SHH) signaling pathway has been implicated in several cancers but has not been explored in T-cell lymphomas. Here, we report that the SHH/GLI1 signaling pathway is activated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell
eLife, 2, e01340-e01340 (2013-10-31)
The Hedgehog (Hh) signal is transduced across the membrane by the heptahelical protein Smoothened (Smo), a developmental regulator, oncoprotein and drug target in oncology. We present the 2.3 Å crystal structure of the extracellular cysteine rich domain (CRD) of vertebrate
PloS one, 12(8), e0181812-e0181812 (2017-08-17)
The gallbladder and cystic duct (GBCs) are parts of the extrahepatic biliary tree and share a common developmental origin with the ventral pancreas. Here, we report on the very first genetic reprogramming of patient-derived human GBCs to β-like cells for
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