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MPLA-SM VacciGrade™

MPLA-SM VacciGrade™ Unit size Cat. code Docs Qty Price
Monophosphoryl Lipid A from S. minnesota R595 - TLR4-based adjuvant
1 mg
vac-mpla
+-
$359.00

Monophosphoryl Lipid A from Salmonella minnesota R595 - TLR4-based adjuvant

The TLR4 agonist, MPLA (monophosphoryl lipid A) is a derivative of lipid A from Salmonella minnesota R595 lipopolysaccharide (LPS or endotoxin).

MPLA is considerably less toxic than LPS whilst maintaining the immunostimulatory activity.

When tested in animal models as a vaccine adjuvant, MPLA induces a strong Th1 response.

MPLA-SM VacciGrade™ is suitable for preclinical studies. It is prepared under strict aseptic conditions. It is guaranteed sterile.

MPLA-SM VacciGrade™ is for research use only, not for use in humans.

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Specifications

Species: Salmonella enterica serovar minnesota mutant R595.

Specificity: Th1 response.

Working concentration: 2- 20 μg/mouse.

Quality: Sterile.

Solubility: 1 mg/ml in DMSO.

Quality control:

  • MPLA-SM VacciGrade™ is a preclinical grade preparation of monophosphoryl lipid A (MPLA) derived from Salmonella enterica serovar Minnesota R595 LPS.
  • It is prepared under strict aseptic conditions.
  • MPLAs VacciGrade™ is guaranteed sterile.
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Contents

  • 1 mg of lyophilized MPLA-SM VacciGrade™
  • 10 ml sterile endotoxin-free physiological water (NaCl 0.9%)

MPLA-SM VacciGrade™ is shipped at room temperature.

Upon receipt it should be stored at -20°C.

Product is stable 1 year when properly stored.
Upon resuspension, prepare aliquots of MPLA-SM VacciGrade™ and store at -20°C. Product is stable 6 months when properly stored.

Avoid repeated freeze-thaw cycles.

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Description

Monophosphoryl lipid A (MPLA) is a low-toxicity derivative of the lipid A region of lipopolysaccharide (LPS), that retains the immunologically active lipid A portion of the parent molecule [1]. While the toxicity associated with LPS prohibits its potential clinical use, MPLA is being developed as a vaccine adjuvant  [2].

Both LPS and MPLA are TLR4 agonists, but they signal through different adaptors, MyD88 and TRIF, respectively. The reduced toxicity of MPLA is attributed to the preferential recruitment of TRIF upon TLR4 activation, resulting in decreased induction of inflammatory cytokines [3].

MPLA has been tested as an adjuvant in mice and reported to induce a strong Th1 response [4-6]. Although the mechanism of action of MPLA has not been fully eludicated, it has been suggested that MPLA improves vaccine immunogenicity by enhancing antigen presenting cell maturation [5].

1. Okemoto K. et al., 2006. A potent adjuvant monophosphoryl lipid A triggers various immune responses, but not secretion of IL-1beta or activation of caspase-1. J Immunol. 176(2):1203-8.
2. Casella CR. et al., 2008. Putting endotoxin to work for us: monophosphoryl lipid A as a safe and effective vaccine adjuvant. Cell Mol Life Sci. 65(20):3231-40.
3. Mata-Haro V. et al., 2007. The vaccine adjuvant monophosphoryl lipid A as a TRIF-biased agonist of TLR4. Science. 316(5831):1628-32.
4. Fransen F. et al., 2007. Agonists of Toll-like receptors 3, 4, 7, and 9 are candidates for use as adjuvants in an outer membrane vaccine against Neisseria meningitidis serogroup. Infect Immun. 75(12) :5939-46.
5. Rhee eG. et al., 2010. TLR4 Ligands Augment Antigen-Specific CD8+ T Lymphocyte Responses Elicited by a Viral Vaccine Vector. J. Virol. 84: 10413 - 10419.
6. Didierlaurent A. et al., 2009.AS04, an aluminum salt- and TLR4 agonist-based adjuvant system, induces a transient localized innate immune response leading to enhanced adaptive immunity. J Immunol 183(10): 6186-97.

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Citations

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