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Merck

G0500

Sigma-Aldrich

D-(+)-半乳糖胺 盐酸盐

≥99% (HPLC)

别名:

2-氨基-2-脱氧-D-半乳糖 盐酸盐, D-软骨糖胺 盐酸盐

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About This Item

经验公式(希尔记法):
C6H13NO5 · HCl
CAS号:
分子量:
215.63
Beilstein:
3697825
EC號碼:
MDL號碼:
分類程式碼代碼:
12352201
PubChem物質ID:
NACRES:
NA.25

品質等級

化驗

≥99% (HPLC)

形狀

powder

技術

HPLC: suitable

雜質

≤0.5% Glucosamine (HPAE)

顏色

white to off-white

mp

172-180  °C

溶解度

H2O: 50 mg/mL, clear to slightly hazy, colorless to very faintly yellow

儲存溫度

room temp

SMILES 字串

Cl.N[C@@H](C=O)[C@@H](O)[C@@H](O)[C@H](O)CO

InChI

1S/C6H13NO5.ClH/c7-3(1-8)5(11)6(12)4(10)2-9;/h1,3-6,9-12H,2,7H2;1H/t3-,4+,5+,6-;/m0./s1

InChI 密鑰

CBOJBBMQJBVCMW-NQZVPSPJSA-N

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一般說明

D-半乳糖胺(d-GalN)是一种特异性肝毒剂,尤其可在肝细胞内代谢。它是一种源自半乳糖的6碳氨基糖。

應用

D-(+)-半乳糖盐酸盐已用于:
  • 甘露聚糖结合凝集素(MBL)与改性云母表面的表面结合
  • 腹腔注射前的无菌磷酸盐缓冲液(PBS)中
  • 小鼠中产生原发性骨髓来源的巨噬细胞(BMDM)

D-(+)-半乳糖胺(D-软骨胺)联合脂多糖(LPS)已用于诱导急性肝衰竭模型(LPS/D-GALN诱导肝损伤、肝炎)的治疗研究,以寻找新药。

生化/生理作用

半乳糖胺(Gal)通过细胞坏死和凋亡诱导肝细胞死亡。它通过产生尿苷二磷酸己糖胺来阻止肝RNA的产生。D-半乳糖胺可降低细胞内尿嘧啶核苷酸库,进而阻止RNA和蛋白质的产生。

其他說明

为了全面了解我们针对客户研究提供的各种单糖产品,建议您访问我们的碳水化合物分类页面。

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

個人防護裝備

Eyeshields, Gloves, type N95 (US)


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分析证书(COA)

Lot/Batch Number

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其他客户在看

Xing Lin et al.
Biological & pharmaceutical bulletin, 37(4), 625-632 (2014-05-13)
This study examined the effect of genistein from Hydrocotyle sibthorpioides on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute hepatic failure. Compared to the model control, genistein treatment significantly protected against LPS/D-GalN-induced liver injury, as evidenced by the decrease in serum alanine and aspartate
Yating Li et al.
Applied microbiology and biotechnology, 103(1), 375-393 (2018-10-23)
Acute liver failure is a drastic, unpredictable clinical syndrome with high mortality. Various preventive and adjuvant therapies based on modulating the gut flora have been proposed for hepatic injury. We aimed to explore the preventive and therapeutic effects of Bifidobacterium
Aoxiang Zhuge et al.
Applied microbiology and biotechnology, 104(17), 7437-7455 (2020-07-16)
Acute liver failure is a clinical emergency associated with high mortality. Accumulating evidence indicates that gut microbiota participates in the progression of liver injury, and preventive therapies based on altering gut microbiota are of great interest. Previous studies demonstrated that
Cao-Qi Lei et al.
Journal of immunology (Baltimore, Md. : 1950), 203(1), 259-268 (2019-05-28)
The dynamic regulations of ubiquitination and deubiquitination play important roles in TGF-β-activated kinase 1 (TAK1)-mediated NF-κB activation, which regulates various physiological and pathological events. We identified ubiquitin-specific protease (USP)19 as a negative regulator of TNF-α- and IL-1β-triggered NF-κB activation by
Yinhong Zhu et al.
International immunopharmacology, 72, 131-137 (2019-04-14)
Saikosaponin a (SSa), one of the major active components of Bupleurum falcatum, has antioxidant and anti-inflammatory pharmacological properties. However, the effects of SSa on liver injury have not been reported. In the present study, we evaluated the protective effects and

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