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Merck

SML1358

Sigma-Aldrich

SGI-1027

≥98% (HPLC)

别名:

N-(4-(2-Amino-6-methylpyrimidin-4-ylamino)phenyl)-4-(quinolin-4-ylamino) benzamide

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About This Item

经验公式(希尔记法):
C27H23N7O
分子量:
461.52
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77

品質等級

化驗

≥98% (HPLC)

形狀

powder

顏色

white to light brown

溶解度

DMSO: 20 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

O=C(NC1=CC=C(NC2=NC(N)=NC(C)=C2)C=C1)C(C=C3)=CC=C3NC4=C(C=CC=C5)C5=NC=C4

InChI

1S/C27H23N7O/c1-17-16-25(34-27(28)30-17)32-20-10-12-21(13-11-20)33-26(35)18-6-8-19(9-7-18)31-24-14-15-29-23-5-3-2-4-22(23)24/h2-16H,1H3,(H,29,31)(H,33,35)(H3,28,30,32,34)

InChI 密鑰

QSYLKMKIVWJAAK-UHFFFAOYSA-N

應用

SGI-1027 has been used as a DNA methyltransferase inhibitor to study its effects on gene expression during osteogenic differentiation. It has also been used as a DNA methyltransferase 3a inhibitor to study its effects on interleukin-6 (IL-6)-induced loss of forkhead box P3 (Foxp3) gene expression in B-lymphocyte-induced maturation protein 1 (Blimp1)-Treg cells.

生化/生理作用

SGI-1027 is a DNA methyltransferase (DNMT) inhibitor with IC50 values of 6-13 μM for DNMT3B, DNMT3A and DNMT1. SGI-1027 directly inhibits DNMT activity by competing with the cofactor, S-adenosylmethionine (SAM) in the methylation reaction. SGI-1027 treatment of cancer cell lines induced degradation of DNMT1, but not DNMT3A or DNMT3B, and in RKO cells caused re-expression of the silenced tumor supressor genes p16, MLH1 and TIMP3.

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


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Rodrigo A da Silva et al.
Bone, 125, 74-86 (2019-05-06)
The HOXA gene cluster is generally recognized as a pivotal mediator of positional identity in the skeletal system, expression of different orthologues conferring alternative locational phenotype of the vertebrate bone. Strikingly, however, the molecular mechanisms that regulate orthologue-specific expression of
Garima Garg et al.
Cell reports, 26(7), 1854-1868 (2019-02-14)
Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during

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