LPS-SM (LPS from S. minnesota R595)

LPS-SM Ultrapure Unit size Cat. code Docs Qty Price
Ultrapure LPS, Salmonella minnesota
5 mg

Ultrapure Lipopolysaccharide from Salmonella minnesota R595

Lipopolysaccharide (LPS) is the principal component of Gram negative bacteria that activates the innate immune system. LPS is recognized by Toll-like receptor 4 (TLR4) which interacts with three different extracellular proteins: LPS binding protein (LBP), CD14 and, myeloid differentiation protein 2 (MD-2), leading to the activation of NF-κB and the production of proinflammatory cytokines. However, most LPS preparations on the market are contaminated by other bacterial components, such as lipoproteins, thus activating TLR2 signaling as well as TLR4 signaling.

Ultra-pure LPS-SM is a preparation of a rough (r)-form lipopolysaccharide (LPS) purified from Salmonella minnesota R595. It was extracted by successive enzymatic hydrolysis steps and purified by the phenol-TEA-DOC extraction protocol. This process removes contaminating lipoproteins, and therefore LPS-B5 Ultrapure only activates TLR4. 

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Species : Salmonella enterica serovar minnesota mutant R595

Specificity: TLR4 agonist

Working concentration: 10 ng- 10 μg/ml

Endotoxin level: 1  x 105 EU/mg

Solubility: 5 mg/ml in water

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  • 5 mg ultra pure LPS from S. minnesota (LPS-SM Ultrapure)
  • 1.5 ml endotoxin-free water

room temperature LPS-SM Ultrapure is shipped at room temperature.

store Upon receipt, store at -20 °C.

Resuspended LPS-SM Ultrapure may be stored at -20 °C for 6 months.

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LPS-SM Ultrapure is an ultrapure preparation of lipopolysaccharide from S. minnesota. LPS is the principal component of Gram negative bacteria that activates the innate immune system. LPS recognition is predominantly mediated by TLR4 [1]. This recognition involves the binding of LPS with lipopolysaccharide-binding protein (LBP) and subsequently with CD14 which physically associates with a complex including TLR4 and MD2 [2]. Formation of the TLR4-centered LPS receptor complex induces the production of proinflammatory cytokines through the MyD88 pathway. LPS signaling also involves a MyD88-independent cascade that mediates the expression of IFN-inducible genes. Furthermore, the shape of lipid A, the component responsible for the immunostimulatory activity of LPS, has been shown to direct the interaction of LPS with TLRs. LPS with conical shape (e.g. from E. coli) induce cytokine production through TLR4, whereas more cylindrical LPS (e.g. from P. gingivalis) induce expression of a different set of cytokines through TLR2 [3].


1. Poltorak A. et al., 1998. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in TLR4 gene. Science, 282(5396): 2085-8.
2. Shimazu R. et al., 1999. MD-2, a molecule that confers lipopolysaccharide responsiveness on Toll-like receptor 4. J Exp Med, 189(11):1777-82.
3. Netea MG. et al., 2002. Does the shape of lipid A determine the interaction of LPS with Toll-like receptors? Trends Immunol, 23(3):135-9.

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