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Merck
모든 사진(1)

Key Documents

SML2430

Sigma-Aldrich

Kdo2-Lipid A (KLA)

≥90% (HPLC)

동의어(들):

Di[3-deoxy-D-manno-octulosonyl]-lipid A (ammonium salt), KLA, Kdo2-LipidA

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About This Item

실험식(Hill 표기법):
C110H202N2O39P2 · xNH3
CAS Number:
Molecular Weight:
2238.72 (free acid basis)
UNSPSC 코드:
12352211
NACRES:
NA.77

생물학적 소스

Escherichia coli

분석

≥90% (HPLC)

형태

solid

저장 온도

−20°C

SMILES string

O=C(O)[C@@]1(O[C@H]2[C@@H](O)C([C@H](O)CO)O[C@](C(O)=O)(OC[C@H]3O[C@@H](OC[C@H]4O[C@H](OP(O)(O)=O)[C@@H](NC(C[C@@H](CCCCCCCCCCC)O)=O)C(OC(C[C@@H](CCCCCCCCCCC)O)=O)[C@H]4O)C(NC(C[C@@H](CCCCCCCCCCC)OC(CCCCCCCCCCC)=O)=O)[C@@H](OC(C[C@@H](CCCCCCCCCCC)OC(CCCCC

관련 카테고리

일반 설명

3-deoxy-D-manno-octulosonic acid (Kdo2-Lipid A) is the essential component of lipopolysaccharide in most Gram-negative bacteria and the minimal structural component to sustain bacterial viability. It serves as the active component of lipopolysaccharide to stimulate potent host immune responses through the complex of Toll-like-receptor 4 (TLR4) and myeloid differentiation protein 2 (MD2). Therefore, Kdo2-lipid A is an important stimulator for studying the mechanism of the innate immune system and for developing bacterial vaccine adjuvants. Kdo2 Lipid A/TLR4 antagonists can also be applied in anti-inflammatory interventions. Kdo2-lipid A, induces de novo sphingolipid biosynthesis in RAW264.7 macrophages, which is essential for induction of autophagy. Kdo2-Lipid A has been used in animal atherosclerosis model.

기타 정보

Solubility: Kdo2 -Lipid A can be dissolved in a solution of 0.1-0.5% Triethylamine (Sigma Cat# 90335) at 1 mg/ml (In case of percipitation use sonication). Use sonication to directly solublized in cell culture medium. Storage: Once Kdo2-lipidA is dissolved in 0.1-0.5% Triethylamine (Sigma Cat# 90335) aliquot and store at -20°C. The solution is stable for 2 months in -20°C.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

No data available

Flash Point (°C)

No data available


시험 성적서(COA)

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문서 라이브러리 방문

Kacee Sims et al.
The Journal of biological chemistry, 285(49), 38568-38579 (2010-09-30)
Activation of RAW264.7 cells with a lipopolysaccharide specific for the TLR4 receptor, Kdo(2)-lipid A (KLA), causes a large increase in cellular sphingolipids, from 1.5 to 2.6 × 10(9) molecules per cell in 24 h, based on the sum of subspecies
Philipp Wiesner et al.
Circulation research, 107(1), 56-65 (2010-05-22)
Oxidized low-density lipoprotein (LDL) is an important determinant of inflammation in atherosclerotic lesions. It has also been documented that certain chronic infectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations of atherosclerosis. In addition, low-level but persistent metabolic
Nathanael J Spann et al.
Cell, 151(1), 138-152 (2012-10-02)
Inflammation and macrophage foam cells are characteristic features of atherosclerotic lesions, but the mechanisms linking cholesterol accumulation to inflammation and LXR-dependent response pathways are poorly understood. To investigate this relationship, we utilized lipidomic and transcriptomic methods to evaluate the effect
Christian R H Raetz et al.
Journal of lipid research, 47(5), 1097-1111 (2006-02-16)
The LIPID MAPS Consortium (www.lipidmaps.org) is developing comprehensive procedures for identifying all lipids of the macrophage, following activation by endotoxin. The goal is to quantify temporal and spatial changes in lipids that occur with cellular metabolism and to develop bioinformatic

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