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Kdo2-Lipid A (KLA) | 699500

Di[3-deoxy-D-manno-octulosonyl]-lipid A (ammonium salt)

699500P

Powder

1 mg
$175.00
5 mg
$720.00
10 mg
$1270.00

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Custom packaging is calculated at $4.00 per aliquot and will be charged at the time of shipping.

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  • Animal Studies
A new preparation of the saccharolipid glycan, Kdo2-Lipid A (KLA), is a nearly homogeneous Re lipopolysaccharide (LPS) substructure with endotoxin activity equal to that of native LPS. KLA is comparable to LPS and its activity is reduced by >103 in cells from TLR-4 deficient mice. The advantage of KLA over LPS is that it is a reproducible, defined natural product, and it can be detected by ESI/MS at the low concentrations used to stimulate animal cells. The purity of KLA should also facilitate the structural analysis of its complexes with signaling receptors, such as TLR-4/MD2.
 

New research* shows 1μg KLA induces

the same response as 10μg LPS.

Perform experiments at half the cost of using LPS!

* Saito, O., C.I. Svensson, M.W. Buczynski, K. Wegner, X.Y. Hua, S. Codeluppi, R.H. Schaloske, R.A. Deems, E.A. Dennis, and T.L. Yaksh. (2010). Spinal glial TLR4-mediated nociception and production of prostaglandin E and TNF. Br J Pharmacol 160:1754-64.
 
For a list of cell and solution protocols utilizing KLA, please see information on the LIPID MAPS website at the following link.
 
Purity
>95%
Stability
6 Months
Storage
-20°C
CAS Number
1246298-62-3
CAS Registry Number is a Registered Trademark of the American Chemical Society
Molecular Weight
2306.840 (based on representative structure; may not reflect exact MW of compound)
Synonyms
KLA
Download
Notes
GIF Graphics File. 
GIF Graphics File. 
MDL Molfile. 
CDX File. 
Chung, H.S. and C.R. Raetz. (2010). Interchangeable domains in the Kdo transferases of Escherichia coli and Haemophilus influenzae. Biochemistry 49:4126-37.

[Abstract]



Andreyev, A.Y., Fahy, E., Guan, Z., Kelly, S., Li, X., McDonald, J.G., Milne, S., Myers, D., Park, H., Ryan, A., Thompson, B.M., Wang, E., Zhao, Y., Brown, H.A., Merrill, A.H., Raetz, C.R., Russell, D.W., Subramaniam, S., Dennis, E.A. (2010) Subcellular organelle lipidomics in TLR-4-activated macrophages. J Lipid Res. 51:2785-97. [PubMed]

Saito, O., Svensson, C.I., Buczynski, M.W., Wegner, K., Hua, X.-Y., Codeluppi, S., Schaloske, R.H., Deems, R.A., Dennis, E.A., Yaksh, T.L. (2010) Spinal glial TLR4-mediated nociception and production of prostaglandin E2 and TNF. British Journal of Pharmacology 160:1754–1764. [Abstract]

Sasaki, H., White, S.H. (2008)Aggregation behavior of an ultra-pure lipopolysaccharide that stimulates TLR-4 receptors. Biophys J. 95:986-93. [PubMed]

Wei, J., Wang, E., Kelly, S.,Sullards, C.,Merrill, A. (2007)Up-regulation of de novo sphingolipid biosynthesis through serine palmitoyltransferease in RAW 264.7 cells upon Kdo2-Lipid A treatment. FASEB J. 21:487.11 [Abstract]

Allegood, J.,Wang, E.,Sullards, M.C.,Merrill, A.H., Jr. (2007)Quantitative analysis of sulfatides in RAW 264.7 cells treated with Kdo2-Lipid A. FASEB J. 21:779.12 [Abstract]

Raetz, C.R., Garrett, T.A., Reynolds, C.M., Shaw, W.A., Moore, J.D., Smith, D.C., Jr, Ribeiro, A.A., Murphy, R.C., Ulevitch, R.J., Fearns, C., Reichart, D., Glass, C.K., Benner, C., Subramaniam, S., Harkewicz, R., Bowers-Gentry, R.C., Buczynski, M.W., Cooper, J.A., Deems, R.A., Dennis, E.A. (2006) Kdo2-Lipid A of Escherichia coli, a defined endotoxin that activates macrophages via TLR-4. J Lipid Res. 47:1097-111. [PubMed]



Packaging for animal studies available. Please contact technical@avantilipids.com.
 
References:
 
Gu, B.B., J.F. Miao, Y.M. Zhu, Y.E. Deng, and S.X. Zou. (2009). Protective effect of retinoid against endotoxin-induced mastitis in rats.  Inflamm Res 58:81-8.
 
Yajima, S., H. Morisaki, R. Serita, T. Suzuki, N. Katori, T. Asahara, K. Nomoto, F. Kobayashi, A. Ishizaka, and J. Takeda. (2009). Tumor necrosis factor-alpha mediates hyperglycemia-augmented gut barrier dysfunction in endotoxemia.  Crit Care Med 37:1024-30.
 
Nacira, S., F. Meziani, O. Dessebe, V. Cattan, S. Collin, C. Montemont, S. Gibot, P. Asfar, A. Ramaroson, V. Regnault, M. Slama, T. Lecompte, P. Lacolley, and B. Levy. (2009). Activated protein C improves lipopolysaccharide-induced cardiovascular dysfunction by decreasing tissular inflammation and oxidative stress.  Crit Care Med 37:246-55.