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Merck
모든 사진(2)

주요 문서

A68203

Sigma-Aldrich

6-Aminonicotinamide

99%

동의어(들):

6AN, 6-Aminopyridine-3-carboxamide

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About This Item

실험식(Hill 표기법):
C6H7N3O
CAS Number:
Molecular Weight:
137.14
Beilstein:
116042
EC Number:
MDL number:
UNSPSC 코드:
12352100
PubChem Substance ID:
NACRES:
NA.22

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Quality Level

분석

99%

양식

powder

mp

245-248 °C (lit.)

SMILES string

NC(=O)c1ccc(N)nc1

InChI

1S/C6H7N3O/c7-5-2-1-4(3-9-5)6(8)10/h1-3H,(H2,7,9)(H2,8,10)

InChI key

ZLWYEPMDOUQDBW-UHFFFAOYSA-N

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일반 설명

6-Aminonicotinamide is an aminopyridine, which is a specific pentose inhibitor and thus inhibits the NADP production.[1]

애플리케이션

6-Aminonicotinamide can be used as a reactant:
  • For the synthesis of 6-substituted imidazo[1,2-a]pyridines with potential application as chemotherapeutic drugs.[2]
  • In the dehydrative N-monobenzylation.[3]

픽토그램

Health hazard

신호어

Danger

유해 및 위험 성명서

Hazard Classifications

Repr. 1B

Storage Class Code

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

개인 보호 장비

Eyeshields, Gloves, type P2 (EN 143) respirator cartridges


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문서 라이브러리 방문

L Poulain et al.
Leukemia, 31(11), 2326-2335 (2017-03-11)
Alterations in metabolic activities are cancer hallmarks that offer a wide range of new therapeutic opportunities. Here we decipher the interplay between mTORC1 activity and glucose metabolism in acute myeloid leukemia (AML). We show that mTORC1 signaling that is constantly
A borrowing hydrogen methodology: palladium-catalyzed dehydrative N-benzylation of 2-aminopyridines in water.
Hikawa H, et al.
Green Chemistry, 20(13), 3044-3049 (2018)
6-Substituted imidazo [1, 2-a] pyridines: Synthesis and biological activity against colon cancer cell lines HT-29 and Caco-2.
Dahan-Farkas N, et al.
European Journal of Medicinal Chemistry, 46(9), 4573-4583 (2011)
Patrycja Kaczara et al.
The FEBS journal, 285(7), 1346-1358 (2018-02-22)
Carbon monoxide-releasing molecules (CO-RMs) induce nitric oxide (NO) release (which requires NADPH), and Ca2+ -dependent signalling; however, their contribution in mediating endothelial responses to CO-RMs is not clear. Here, we studied the effects of CO liberated from CORM-401 on NO
Sachin A Gupte et al.
Journal of molecular and cellular cardiology, 41(2), 340-349 (2006-07-11)
In the failing heart, NADPH oxidase and uncoupled NO synthase utilize cytosolic NADPH to form superoxide. NADPH is supplied principally by the pentose phosphate pathway, whose rate-limiting enzyme is glucose 6-phosphate dehydrogenase (G6PD). Therefore, we hypothesized that cardiac G6PD activation

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