552410
5-アミノ-4-イミダゾールカルボキサミド
95%
別名:
4-Amino-5-carbamoylimidazole, 4-Aminoimidazole-5-carboxamide, 4-Carbamoyl-5-aminoimidazole, 4-Carboxamido-5-aminoimidazole, 5-Amino-1H-imidazole-4-carboxamide, 5-Amino-1H-imidazole-4-carboxylic acid amide, 5-Amino-3H-imidazole-4-carboxamide
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この商品について
実験式（ヒル表記法）:
C4H6N4O
CAS番号:
分子量:
126.12
NACRES:
NA.22
PubChem Substance ID:
UNSPSC Code:
12352005
EC Number:
206-641-4
MDL number:
製品名
5-アミノ-4-イミダゾールカルボキサミド, 95%
InChI key
DVNYTAVYBRSTGK-UHFFFAOYSA-N
InChI
1S/C4H6N4O/c5-3-2(4(6)9)7-1-8-3/h1H,5H2,(H2,6,9)(H,7,8)
SMILES string
NC(=O)c1nc[nH]c1N
assay
95%
form
solid
mp
164-170 °C (lit.)
functional group
amide
Quality Level
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関連するカテゴリー
Application
5-アミノ-4-イミダゾールカルボキサミドは、4-(N′-ベンゾイルカルバモイル)アミノ-5-イミダゾールカルボキサミドおよび5-アミノ-1-β-D-リボシル-4-イミダゾールカルボキサミド-5′-ホスフェート（AICAR）の合成に使用できます。
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
保管分類
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
Synthesis of guanosine and its derivatives from 5-amino-l-?-D-ribofuranosyl-4-imidazolecarboxamide. III. Formation of a novel cycloimidazole nucleoside and its cleavage reactions.
Okutsu M and Yamazaki A.
Nucleic Acids Research, 3(1), 237-250 (1976)
Preparation of 5-Amino-1-?-ribosyl-4-imidazolecarboxamide-5'-phosphate and N-(5-Amino-1-?-D-ribosyl-4-imidazolecarbonyl)-L-aspartic Acid 5'-Phosphate.
Huang HT.
Biochemistry, 4(1), 58-62 (1965)
James P White et al.
American journal of physiology. Endocrinology and metabolism, 304(10), E1042-E1052 (2013-03-28)
Although catabolic signaling has a well-established role in muscle wasting during cancer cachexia, the suppression of anabolic signaling also warrants further investigation. In cachectic tumor-bearing mice, circulating IL-6 levels are associated with suppressed muscle protein synthesis and mTORC1 signaling. We
Jang Han Lee et al.
American journal of physiology. Renal physiology, 304(6), F686-F697 (2013-01-18)
The epithelial-mesenchymal transition (EMT) is a novel mechanism that promotes renal fibrosis. Transforming growth factor-β (TGF-β), angiotensin II, aldosterone, high glucose, and urinary albumin are well-known causes of EMT and renal fibrosis. We examined whether and how activation of AMP-activated
Hiroyasu Hatakeyama et al.
Molecular biology of the cell, 24(6), 809-817 (2013-01-18)
Tbc1d1 is key to skeletal muscle GLUT4 regulation. By using GLUT4 nanometry combined with a cell-based reconstitution model, we uncover a shift in the regulatory mode of Tbc1d1 by showing that Tbc1d1 temporally acquires insulin responsiveness, which triggers GLUT4 trafficking
ライフサイエンス、有機合成、材料科学、クロマトグラフィー、分析など、あらゆる分野の研究に経験のあるメンバーがおります。.
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