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Monophosphoryl Lipid A (synthetic) (Ready-to-Use)

TLR4 activator
 
ALX-581-205-C100 100 µg 269.00 USD
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Product Specification

Alternative Name:MPL-A, Glucopyranosyl lipid adjuvant, GLA
 
Formula:C96H184N3O22P
 
MW:1763.47
 
Source:Synthetic.
 
CAS:1246298-63-4
 
Concentration:0.5mg/ml
 
Formulation:Liquid. Sterile, ready-to-use solution in pyrogen free double distilled water.
 
Activity:Activates Toll-like receptor 4 (TLR4) about 10-fold less (100ng/ml) compared to the endotoxic lipid A molecule.
Synthetic lipid A does not activate TLR2 as determined with splenocytes and macrophages from TLR4 deficient mice. Exhibits reduced endotoxic and pyrogenic activity compared to lipid A and LPS.
 
Shipping:Ambient
 
Long Term Storage:+4°C
 
Handling:Keep sterile.
 
Scientific Background:Lipopolysaccharides (LPS), which constitute the major components on the cell surface of Gram-negative bacteria, have been proved to be particularly endotoxic and cause septicemia. It has been further demonstrated that the LPS anchor part, namely, lipid A, is primarily responsible for the endotoxicity of LPS. Lipid A binds to Toll-like receptor 4 (TLR4) to activate a cascade of immunological responses, including the production of a number of cytokines and chemokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and interferon-β (IFN-β). Thus, lipid A has become a valuable molecular template in the discovery of new immunostimulants, for example vaccine adjuvant, and in the design and development of novel conjugate vaccines.
Lipid A is a highly hydrophobic glycolipid, consisting of a β1,6-linked di-glucosamine with two phosphate or pyrophosphate groups and 4–8 long lipid chains attached to the 1,4'-O-and 2,2'-N-3,3'-O-positions, respectively. The structures of lipid A derived from different bacteria can vary significantly in terms of the number, structures and locations of their lipids. In order to understand and eventually mitigate the endotoxicity of lipid A for the development of useful immunostimulant, numerous lipid A derivatives have been designed, synthesized, and biologically assayed. The structure-activity relationship studies of natural lipid A and various synthetic analogs have shown that both the number and lengths of acyl chains and the phosphorylation state of lipid A have a significant impact on its endotoxicity. It appears that the diphosphorylated  hexa-acyl form of lipid A, such as Escherichia coli Lipid A, is optimally recognized by TLR4 to exhibit the full spectrum of endotoxicity. Most importantly, it was observed that the endotoxic activity of Lipid A could be significantly reduced after the removal of its anomeric phosphate group, Monophosphoryl Lipid A (MPL-A) while its immunostimulatory property remained unaffected.
 
ALX-581-205
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ALX-581-205

Product Literature References

Caspase-11 cleaves gasdermin D for non-canonical inflammasome signaling: N. Kayagaki, et al.; Nature (2015), Application(s): Caspase-11 signaling, Abstract;
Noncanonical inflammasome activation by intracellular LPS independent of TLR4.: N. Kayagaki, et al.; Science 341, 1246 (2013), Abstract;
CD14 and TRIF govern distinct responsiveness and responses in mouse microglial TLR4 challenges by structural variants of LPS: T. Regen, et al.; Brain Behav. Immun. 25, 957 (2011), Abstract;

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