4A-MPLA ammonium
4A-MPLA ammonium is an orally active TLR4 agonist. 4A-MPLA ammonium induces TLR4 endocytosis dependent on Cdc42 and galectin-3, triggering TRIF-mediated signaling and sustained IFN-β production. 4A-MPLA ammonium promotes lipid droplet formation, upregulates interferon-stimulated genes and type I IFN signaling genes, downregulates lysosome/phagosome function genes, and modulates tolerogenic dendritic cell function. 4A-MPLA ammonium can be used for the research of colitis.
For research use only. We do not sell to patients.
- CAS No.: 2260669-09-6
- Formula: C68H132N3O19P
- Molecular Weight:1326.76
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Biological Activity
Description
IC50 & Target
[1]|
TLR4 |
Galectin-3 |
In Vitro
4A-MPLA (1.0 μg/mL; 24 h) ammonium induces a distinct cytokine profile in mouse bone-marrow-derived dendritic cells, with lower overall cytokine induction than 6A-DPLA but enhanced IFN-β production in MyD88-deficient mBMDCs[1].
4A-MPLA (10-1000 nM) ammonium binds to the human TLR4-MD2 complex with high affinity, comparable to 6A-DPLA and significantly stronger than 3A-MPLA (HY-N16231) and 5A-MPLA[1].
4A-MPLA ammonium drives a distinct transcriptomic signature in mouse bone-marrow-derived dendritic cells, strongly upregulating type I IFN and interferon-stimulated gene pathways[1].
4A-MPLA (3-48 h post-treatment) ammonium induces a sustained Ifnb mRNA response in mouse bone-marrow-derived dendritic cells, with elevated expression remaining through 36 h post-treatment[1].
4A-MPLA (15-90 min post-treatment) ammonium promotes robust TLR4 endocytosis in mouse bone-marrow-derived dendritic cells, inducing a ~30% loss of monomeric surface TLR4 by 30 min post-treatment[1].
4A-MPLA (3-24 h post-treatment) ammonium induces sustained intracellular lipid droplet formation in mouse bone-marrow-derived dendritic cells; this formation is dependent on TLR4 and TRIF signaling and persists up to 24 h post-treatment[1].
4A-MPLA ammonium-induced IFN-β production and TLR4 endocytosis in mouse bone-marrow-derived dendritic cells are dependent on Cdc42 and galectin-3 activity, as shown by dose-dependent inhibition with CASIN (HY-12874) (5-1000 nM) and anti-mGal-3 mAb (0.5-10 μg/mL)[1].
4A-MPLA ammonium preferentially engages endosomal TLR4 in mouse bone marrow-derived dendritic cells, signals through TRIF, and induces a sustained IFNβ response[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
4A-MPLA (100 μg/mouse; p.o.; single dose) ammonium induces a sustained IFN-β response in colonic pDCs, with elevated production persisting for at least 18 hours in naive B6 SPF IFNβ1-EYFP reporter mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:B6 SPF WT C57BL/6J mice (male or female, 6-8 weeks old)[1]
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Dosage:20 μg/day; 80 μg/mouse total
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Administration:p.o.; daily; 4 days
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Result:Reduced weight loss relative to control.
Reduced the proportion of IL-17A+ colonic lamina propria CD4+ T cells from 11% (control) to 3%.
Reduced the proportion of IFN-γ+ colonic lamina propria CD4+ T cells from 6% (control) to 3%.
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Animal Model:Naive B6 SPF IFNβ1-EYFP reporter mice (male or female, 6-8 weeks old)[1]
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Dosage:100 μg/mouse
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Administration:p.o.; single dose
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Result:Increased IFN-β-producing colonic pDC proportions from a baseline of 25% to 35% at 6 hours post-treatment.
Peaked at 40% at 12 hours post-treatment.
Remained elevated at 38% at 18 hours post-treatment.
Chemical Information
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CAS No. 2260669-09-6
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Molecular Weight 1326.76
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Formula C68H132N3O19P
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SMILES
O[C@@H]([C@@H]([C@H]([C@H](O1)O)NC(C[C@@H](CCCCCCCCCCC)O)=O)OC(C[C@H](O)CCCCCCCCCCC)=O)[C@H]1CO[C@H]2[C@@H]([C@H]([C@@H]([C@H](O2)CO)OP(O)(O)=O)O)NC(C[C@@H](CCCCCCCCCCC)OC(CCCCCCCCCCCCC)=O)=O.N
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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DSS-Induced Colitis
Dextran sulfate sodium (DSS)-induced colitis is generated by administering DSS in mouse drinking water, producing epithelial injury, barrier disruption, weight loss, diarrhea, fecal blood, colon shortening, histologic mucosal damage, and inflammatory mediator changes; the model is mainly used to study acute or chronic intestinal inflammation resembling selected features of ulcerative colitis. DSS injury is interpreted through clinical and tissue readouts rather than a single molecular endpoint: daily body weight, stool consistency, and bleeding are combined into a disease activity index, while colon length, histology, cytokines, myeloperoxidase activity, intestinal permeability, and tight-junction markers provide complementary measures of inflammation and barrier damage.
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TNBS-Induced Colitis
TNBS-induced colitis is produced by intrarectal delivery of 2,4,6-trinitrobenzene sulfonic acid in ethanol, where ethanol disrupts the mucosal barrier and TNBS haptenates colonic proteins, generating immune-mediated colonic inflammation with weight loss, diarrhea, ulceration, transmural injury, inflammatory-cell infiltration, and cytokine responses. The model is used as an experimental intestinal inflammation model with Crohn’s disease–like features, especially when Th1-type responses, IL-12–dependent inflammation, chronic relapsing inflammation, or fibrosis-related endpoints are studied.
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Lysosome and acidic-vesicle live-cell staining
Lysosome and acidic-vesicle live-cell staining detects acidic intracellular compartments by using membrane-permeant acidotropic probes that accumulate in low-pH vesicles, including lysosomes, late endosomes, autolysosomes, and acidic phagosomes. LysoTracker staining is commonly used as an intensity-based readout of acidic lysosomal compartment abundance or enlargement, while acridine orange produces green fluorescence in less concentrated compartments and red fluorescence after concentration-dependent accumulation in acidic vesicular organelles. Loss or reduction of acridine-orange red signal can be used as a readout of lysosomal membrane permeabilization or reduced acidic-vesicle integrity. This protocol is designed for live cultured cells and can be adapted for fluorescence microscopy, high-content imaging, plate-reader readout, or flow cytometry when the selected literature supports the readout. Because these dyes report acidotropic accumulation rather than lysosome identity alone,
Purity & Documentation
References
[1]. Cho HS, et al. Structure of gut microbial glycolipid modulates host inflammatory response. Cell. 2025;188(19):5295-5312.e18. [Content Brief]
[2]. Starling S. Commensal glycolipid structure shapes gut immunity. Nat Rev Microbiol. 2025 Oct;23(10):617. [Content Brief]
[3]. Zhang Y, et al. Diversity of oligosaccharides in lipooligosaccharides of Akkermansia muciniphila and its anti-atherosclerotic activity. Nat Prod Bioprospect. 2026;16(1):58. Published 2026 May 2. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
4A-MPLA ammonium Related Classifications
HY-N16021 Related Classifications
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