SML0506
LY-411575
≥97% (HPLC), γ-secretase inhibitor , powder
别名:
LSN-411575, LY 411575, N2-[（2S）-2-（3,5-二氟苯基）-2-羟基乙酰]-N1-[（7S）-5-甲基-6-氧代-6,7-二氢-5H-二苯并[b，d]氮杂-7-基]-L-丙氨酰胺
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关于此项目
经验公式（希尔记法）:
C26H23F2N3O4
化学文摘社编号:
分子量:
479.48
MDL编号:
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77
产品名称
LY-411575, ≥97% (HPLC)
质量水平
方案
≥97% (HPLC)
表单
powder
颜色
white to beige
溶解性
DMSO: 5 mg/mL, clear
运输
wet ice
储存温度
−20°C
SMILES字符串
C[C@H](NC(=O)[C@@H](O)c1cc(F)cc(F)c1)C(=O)N[C@@H]2C(=O)N(C)c3ccccc3-c4ccccc24
InChI
1S/C26H23F2N3O4/c1-14(29-25(34)23(32)15-11-16(27)13-17(28)12-15)24(33)30-22-20-9-4-3-7-18(20)19-8-5-6-10-21(19)31(2)26(22)35/h3-14,22-23,32H,1-2H3,(H,29,34)(H,30,33)/t14-,22-,23-/m0/s1
InChI key
ULSSJYNJIZWPSB-CVRXJBIPSA-N
相关类别
应用
LY-411575已被用作有效的γ-分泌酶抑制剂和Notch抑制剂。
生化/生理作用
LY-411575是一种有效的细胞渗透性和选择性 γ-分泌酶抑制剂，可在急性或慢性治疗后降低 Aβ40/42，并阻断Notch活化。
LY-411575是一种有效的细胞渗透性和选择性γ-分泌酶抑制剂，可在急性或慢性治疗后降低Aβ/42，并阻断Notch活化。研究（癌细胞）已显示用LSN-411575治疗可通过抑制HES1表达和ERK磷酸化，阻滞KrasG12V驱动的NSCLC。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
K Pandya et al.
British journal of cancer, 105(6), 796-806 (2011-08-19)
We reported that Notch-1, a potent breast oncogene, is activated in response to trastuzumab and contributes to trastuzumab resistance in vitro. We sought to determine the preclinical benefit of combining a Notch inhibitor (γ-secretase inhibitor (GSI)) and trastuzumab in both
Enzymatic assays for studying intramembrane proteolysis.
Bolduc D M, et al.
Methods in Enzymology, 584, 295-308 (2017)
Julia Freudenblum et al.
Frontiers in cell and developmental biology, 8, 586651-586651 (2020-10-27)
Pancreatic islets, discrete microorgans embedded within the exocrine pancreas, contain beta cells which are critical for glucose homeostasis. Loss or dysfunction of beta cells leads to diabetes, a disease with expanding global prevalence, and for which regenerative therapies are actively
Different developmental histories of beta-cells generate functional and proliferative heterogeneity during islet growth.
Singh S P, et al.
Nature Communications, 8(1), 664-664 (2017)
Kyung-Won Park et al.
Molecular therapy : the journal of the American Society of Gene Therapy, 29(7), 2294-2307 (2021-03-02)
Numerous aggregation inhibitors have been developed with the goal of blocking or reversing toxic amyloid formation in vivo. Previous studies have used short peptide inhibitors targeting different amyloid β (Aβ) amyloidogenic regions to prevent aggregation. Despite the specificity that can be
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