SML1409
Madrasin
≥98% (HPLC)
别名:
2-[（（7-甲氧基-4-甲基-2-喹唑啉基）氨基] -5,6-二甲基-4（1H）-嘧啶酮（9CI）, 2-（7-甲氧基-4-甲基-喹唑啉-2-基氨基）-5,6-二甲基-3H-嘧啶-4-酮, 4（1H）-嘧啶酮，2-[（（7-甲氧基-4-甲基-2-喹唑啉基）氨基] -5,6-二甲基-（9CI）, 4（3H）-嘧啶酮，2-[（（7-甲氧基-4-甲基-2-喹唑啉基）氨基] -5,6-二甲基-, DDD00107587, RNA剪接抑制剂
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关于此项目
经验公式（希尔记法）:
C16H17N5O2
化学文摘社编号:
分子量:
311.34
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
产品名称
Madrasin, ≥98% (HPLC)
InChI
1S/C16H17N5O2/c1-8-9(2)17-16(20-14(8)22)21-15-18-10(3)12-6-5-11(23-4)7-13(12)19-15/h5-7H,1-4H3,(H2,17,18,19,20,21,22)
SMILES string
CC1=NC(NC(NC(C)=C2C)=NC2=O)=NC3=CC(OC)=CC=C31
InChI key
QQJIYKXTEMDJFM-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
, white to dark brown
solubility
DMSO: 0.5 mg/mL, clear (warmed)
storage temp.
2-8°C
Quality Level
相关类别
Application
Madrasin已作为剪接体抑制剂，抑制3T3-L1细胞中前体RNA的剪接加工。
Biochem/physiol Actions
Madrasin 是一种高效的、细胞渗透性剪接抑制剂。
Madrasin 是一种高效的、细胞渗透性剪接抑制剂，可干扰剪接体组装的早期阶段。 Madrasin 使 A 复合体的剪接体装配停滞。
Madrasin在较高浓度下具有细胞毒性。在极低浓度下，Madrasin可诱导蛋白亚细胞核定位和引起细胞周期停滞。
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Yves Mugabo et al.
The Journal of biological chemistry, 293(18), 6736-6750 (2018-03-14)
Adipogenesis involves a complex signaling network requiring strict temporal and spatial organization of effector molecules. Molecular scaffolds, such as 14-3-3 proteins, facilitate such organization, and we have previously identified 14-3-3ζ as an essential scaffold in adipocyte differentiation. The interactome of
Andrea Pawellek et al.
The Journal of biological chemistry, 289(50), 34683-34698 (2014-10-05)
Eukaryotic pre-mRNA splicing is an essential step in gene expression for all genes that contain introns. In contrast to transcription and translation, few well characterized chemical inhibitors are available with which to dissect the splicing process, particularly in cells. Therefore
Andrey A Parkhitko et al.
PLoS genetics, 17(2), e1009354-e1009354 (2021-02-17)
The RB1 tumor suppressor is recurrently mutated in a variety of cancers including retinoblastomas, small cell lung cancers, triple-negative breast cancers, prostate cancers, and osteosarcomas. Finding new synthetic lethal (SL) interactions with RB1 could lead to new approaches to treating
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