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Merck

SML1671

Sigma-Aldrich

NCT-503 Inactive Control

≥98% (HPLC)

别名:

N-(4,6-Dimethylpyridin-2-yl)-4-(pyridin-4-yl)piperazine-1-carbothioamide

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About This Item

经验公式(希尔记法):
C17H21N5S
分子量:
327.45
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 beige

溶解度

DMSO: 5 mg/mL, clear (warmed)

儲存溫度

2-8°C

SMILES 字串

CC1=CC(NC(N2CCN(C3=CC=NC=C3)CC2)=S)=NC(C)=C1

InChI

1S/C17H21N5S/c1-13-11-14(2)19-16(12-13)20-17(23)22-9-7-21(8-10-22)15-3-5-18-6-4-15/h3-6,11-12H,7-10H2,1-2H3,(H,19,20,23)

InChI 密鑰

ITLPIAAGIQAGRA-UHFFFAOYSA-N

應用

NCT-503 Inactive Control has been used as a small molecule inhibitor of phosphoglycerate dehydrogenase in neuroblastoma cells.

生化/生理作用

NCT-503 Inactive Control is the inactive control probe for NCT-503, which is an inhibitor of phosphoglycerate dehydrogenase (PHGDH), the enzyme that catalyzes the first, rate-limiting step of glucose-derived serine synthesis. NCT-503 Inactive Control has an IC50 value >57 μM for PHGDH. NCT-503 has an IC50 value of 2.5 μM for PHGDH. NCT-503 Inactive Control is water soluble and has good stability, similar to NCT-503.

推薦產品

The active PHGDH inhibitor, NCT-503, is available from Sigma. To learn more about and purchase NCT-503, click here.

象形圖

Exclamation mark

訊號詞

Warning

危險聲明

危險分類

Skin Irrit. 2

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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Birte Arlt et al.
Journal of enzyme inhibition and medicinal chemistry, 36(1), 1282-1289 (2021-07-02)
The small-molecule inhibitor of phosphoglycerate dehydrogenase, NCT-503, reduces incorporation of glucose-derived carbons into serine in vitro. Here we describe an off-target effect of NCT-503 in neuroblastoma cell lines expressing divergent phosphoglycerate dehydrogenase (PHGDH) levels and single-cell clones with CRISPR-Cas9-directed PHGDH
Yingfeng Xia et al.
Cancer research, 79(15), 3837-3850 (2019-05-16)
MYCN amplification drives the development of neuronal cancers in children and adults. Given the challenge in therapeutically targeting MYCN directly, we searched for MYCN-activated metabolic pathways as potential drug targets. Here we report that neuroblastoma cells with MYCN amplification show

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