You Searched For: MPLA

Supplier: Enzo Life Sciences

Description: TLR4 activator.

Supplier: Enzo Life Sciences

Description: TLR4 activator.

Supplier: Adipogen

Description: Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4), a member of the highly conserved protein family of TLRs, which are specialised in the recognition of microbial components. In mice, defects in TLR4 result in LPS unresponsiveness. For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). This mechanism is believed to be generally true for LPS signaling. Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. Monophosphoryl Lipid A (MPLA) represents a detoxified derivative of Lipid A and constitutes an important adjuvant in prophylactic and therapeutic vaccines.

Supplier: Adipogen

Description: Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4), a member of the highly conserved protein family of TLRs, which are specialised in the recognition of microbial components. In mice, defects in TLR4 result in LPS unresponsiveness. For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). This mechanism is believed to be generally true for LPS signaling. Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. Monophosphoryl Lipid A (MPLA) represents a detoxified derivative of Lipid A and constitutes an important adjuvant in prophylactic and therapeutic vaccines.

Catalog Number: (102987-458)

Supplier: Adipogen

Description: Toll-like receptor 4 (TLR4) activator. Activates TLR4 but does not activate TLR2 even at high concentrations. Defined structure of MPLA. Synthetic lipid A is structurally very similar to natural MPLA but does not exist in nature.
Formula: C96H184N3O22P
MW: 1763.47
CAS: 1246298-63-4
Source/Host Chemicals: Synthetic. Does not contain RNA, DNA or protein fragments.
Purity: No detectable TLR4 independent activity: standardised TLR4-specific agonist.
Appearance: Colourless opaque aqueous solution.
Formulation: Liquid.
Concentration: 0.5mg/ml stabilized in sterile, double-distilled water (ddWater), without any additives.
Other Product Data: Preparation of Stock Solution: To yield a 50µg/ml (500-50x) stock solution add 100µl of MPLA to 900µl endotoxin-free and sterile ddWater (Cat. No.: IAX-900-002) (not PBS) and mix well.

Catalog Number: (76002-224)

Supplier: Enzo Life Sciences

Description: TLR4 activator.

Supplier: Adipogen

Description: Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4), a member of the highly conserved protein family of TLRs, which are specialised in the recognition of microbial components. In mice, defects in TLR4 result in LPS unresponsiveness. For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). This mechanism is believed to be generally true for LPS signaling. Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. Monophosphoryl Lipid A (MPLA) represents a detoxified derivative of Lipid A and constitutes an important adjuvant in prophylactic and therapeutic vaccines.

Supplier: Adipogen

Description: Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4), a member of the highly conserved protein family of TLRs, which are specialised in the recognition of microbial components. In mice, defects in TLR4 result in LPS unresponsiveness. For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). This mechanism is believed to be generally true for LPS signaling. Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. Monophosphoryl Lipid A (MPLA) represents a detoxified derivative of Lipid A and constitutes an important adjuvant in prophylactic and therapeutic vaccines.

Catalog Number: (102991-274)

Supplier: Adipogen

Description: The mycobacterial glycolipid trehalose-6,6'-dimycolate (TDM), also named Cord Factor (CF), is an important regulator of immune responses during Mycobacterium tuberculosis (Mtb) infections. Macrophages recognize TDM through the Mincle receptor and initiate TDM-induced inflammatory responses, leading to lung granuloma formation. Controlled use of its cell wall activates macrophages in ways that can be harnessed for therapy. For example, M. bovis Bacille Calmette-Guerin (BCG) is one of the most widely used antitumor adjuvant therapies in humans. Freund's adjuvant, an emulsion of mycobacterial cell wall components in paraffin oil, is mixed with antigens to optimize memory T and B cell responses in mice. TDM along with a detoxified derivative of Lipid A (MPLA) and cell wall skeleton make up a formulation also known under the name of Ribi adjuvant. Recent studies suggest that Mincle is a pivotal receptor for the mycobacterial cord factor. However, additional receptors may bind TDM independently or in cooperation with Mincle. Candidates include other CLEC proteins, such as Dectin-2, which also associates with FcRg, is expressed in macrophages, and binds to Mtb. The scavenger receptor MARCO interacts with TDM, yet lacks an intracellular domain for signal initiation. In contrast, Mincle can directly trigger Syk-Card9 signaling via its association with FcRg. Whereas in the absence of Mincle macrophages did not respond to TDM, a recent report found Mincle-deficient mice capable of mounting an efficient granulomatous and protective immune response after low and high doseinfections with Mtb. Mutant mice generated a normal T helper (TH)1 and TH17 immune response followed by the induction of efficient macrophage effector mechanisms and control of mycobacterial growth identical to wildtype mice. The absence of the innate receptor Mincle may be fully compensated for in vivo in terms of sensing Mtb and mounting a protective inflammatory immune response.

Catalog Number: (103783-368)

Supplier: Avanti Polar Lipids Inc

Description: 3A-MPLA POWDER FORM 1MG

Catalog Number: (103783-362)

Supplier: Avanti Polar Lipids Inc

Description: MPLA (PHAD) PURITY >99% POWDER 1MG

Catalog Number: (MSPP-699800P5)

Supplier: Avanti Polar Lipids Inc

Description: MPLA PHAD MONOPHOSPHORYL LIPID A 5MG

Catalog Number: (MSPP-TLRL-MPLA)

Supplier: Invivogen

Description: MONOPHOSPHORYL LIPID FROM SMINNESOTA 1MG

Catalog Number: (MSPP-VAC-MPLA)

Supplier: Invivogen

Description: MONOPHOSPHORYL LIPID VACCIGRADE TLR4 1MG