DPPE-PEG350
Based on 1 Customer Validation
DPPE-PEG350 (16:0 PEG350 PE) is a CD1d lipid antagonist. DPPE-PEG350 blocks alpha-GalCer-dependent ERK tyrosine kinase phosphorylation in cells. DPPE-PEG350 inhibits cellular IL-4 and IFN-gamma production following alpha-GalCer stimulation. DPPE-PEG350 selectively antagonizes iNKT without affecting MHC class II-dependent OVA-specific Th2 responses. DPPE-PEG350 reduces MCP-1 and VCAM-1 protein expression and necrotic core formation in atherosclerotic lesions. DPPE-PEG350 can be used for research on asthma and atherosclerosis.
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- Pureté : 99%
- CAS No.: 474922-84-4
- Formule: (C2H4O)nC39H76NO10P.H3N
- Masse moléculaire:350(Average)
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Stockage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
IC50 & Target
[1]|
CD1d |
IL-4 |
In Vitro
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:DN32.D3 NKT hybridoma cells
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Concentration:200 µg/mL
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Incubation Time:4 h
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Result:Inhibited IL-2 release from DN32 cells, particularly at suboptimal concentrations of α-GalCer.
In Vivo
DPPE-PEG350 (100 µg; intranasal administration; single dose) completely prevents α-GalCer-induced AHR and lung inflammation in naive mice[1].
DPPE-PEG350 (500 µg; intravenous injection; once weekly) completely eliminates αGalCer-aggravated atherosclerosis in mice, confirming the CD1d-dependent anti-atherosclerotic effect[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/cByj (female, 6-8 weeks old, OVA-induced allergic airway hyperreactivity)[1]
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Dosage:250 µg
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Administration:i.v.; single dose
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Result:Completely prevented the development of airway hyperreactivity upon intranasal OVA challenge.
Inhibited eosinophilic airway inflammation, significantly reducing the number of eosinophils, lymphocytes, and macrophages in the BAL fluid compared to the OVA-immunized control group.
Revealed no significant differences from saline controls in H&E- and PAS-stained lung sections, showing minimal mucus production and negligible cellular infiltration.
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Animal Model:BALB/cByj (female, 6-8 weeks old, α-GalCer-induced airway hyperreactivity)[1]
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Dosage:100 µg
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Administration:i.n.; single dose
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Result:Completely prevented the development of AHR in the group that received DPPE-PEG350 and α-GalCer when compared with α-GalCer alone.
Administration of DPPE-PEG350 alone showed no effect on the induction of AHR or pulmonary inflammation.
Revealed no significant differences between vehicle control and DPPE-PEG350-treated mice in H&E- and PAS-stained lung sections, showing minimal mucus production and minor cellular infiltration.
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Animal Model:ApoE-/- mice on C57BL/6 background (male, 6-8 weeks old)[2]
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Dosage:250 µg
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Administration:i.v.; twice weekly
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Result:Reduced total intimal atherosclerotic lesion size by 45% and ORO-stained lipid accumulation by 52% compared to PBS group.
Reduced CD4+ T cells by 54%, CD8+ T cells by 94%, and CD19+ B cell accumulation by 80% in atherosclerotic lesions.
Reduced MCP-1 and VCAM-1 protein expression by 30% and 57% respectively.
Reduced necrotic core areas by 64%.
Did not affect liver NKT cell populations (NK1.1+TCRβ+), CD4+ T cells, CD8+ T cells, B cells, or NK cells.
Did not affect plasma lipids despite ~10% reduction of body weight.
Did not affect smooth muscle and collagen content in atherosclerotic lesions.
Did not affect IFNγ mRNA expression in arterial and spleen tissues or plasma IFNγ levels.
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Animal Model:ApoE-/- mice on C57BL/6 background (male, 6-8 weeks old)[2]
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Dosage:250 µg
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Administration:i.v.; twice weekly; 6 weeks
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Result:Reduced established atherosclerosis by 49% when assessed by total intimal lesion areas.
Reduced lipid accumulation in aortic sinus lesions by 27%.
Reduced necrotic cores by 59%.
Reduced CD68+ macrophages, CD4+ T cells, CD8+ T cells, and CD19+ B cells in atherosclerotic lesions.
Decreased apoptotic cells in developed atherosclerotic lesions, with macrophages being a major target of apoptosis.
Did not affect the ratio of lipid accumulation to intima area.
Did not affect smooth muscle and collagen content in established atherosclerotic lesions.
Did not affect endothelial cell continuity.
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Animal Model:ApoE-/- mice on C57BL/6 background (male, 6-8 weeks old)[2]
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Dosage:500 µg (DPPE-PEG350); 2 µg (αGalCer)
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Administration:i.v.; once weekly (DPPE-PEG350); i.p.; fortnightly (αGalCer)
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Result:Completely abrogated αGalCer-aggravated atherosclerosis, which increased total intimal lesion by 112% without DPPE-PEG350 treatment.
Similar finding was observed with ORO-stained lipid accumulation; however lipid contents adjusted to lesion area were similar.
FACS analysis of liver lymphocytes showed that αGalCer-injection reduced CD1d-tetramer+ iNKT cells.
Chemical Information
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CAS No. 474922-84-4
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Appearance Solid
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Masse moléculaire 350(Average)
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Formule (C2H4O)nC39H76NO10P.H3N
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Color White to light yellow
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SMILES
O=C(NCCOP(O)(OC[C@@H](COC(CCCCCCCCCCCCCCC)=O)OC(CCCCCCCCCCCCCCC)=O)=O)OCCOC.N.[n]
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Synonyms
16:0 PEG350 PE; 1,2-Dipalmitoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(polyethylene glycol)-350] ammonium
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Pureté et documentation
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Fiche technique (282 KB)
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SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Lombardi V, et al. A CD1d-dependent antagonist inhibits the activation of invariant NKT cells and prevents development of allergen-induced airway hyperreactivity. Journal of immunology (Baltimore, Md. : 1950). 2010 Feb 15;184(4):2107-15. [Content Brief]
[2]. Li Y, et al. A CD1d-dependent lipid antagonist to NKT cells ameliorates atherosclerosis in ApoE-/- mice by reducing lesion necrosis and inflammation. Cardiovasc Res. 2016 Feb 1;109(2):305-17. . [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
DPPE-PEG350 Related Classifications
HY-144012A Related Classifications
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Keywords
- DPPE-PEG350
- 474922-84-4
- 16:0 PEG350 PE
- 1,2-Dipalmitoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(polyethylene glycol)-350]
- CD1
- ERK
- Interleukin Related
- IFNAR
- Extracellular signal regulated kinases
- IL
- Interferon-α/β receptor
- Interferon-alpha/beta receptor
- asthma
- CD1d lipid antagonist
- ApoE-/- mice
- IFN-gamma
- alpha-GalCer
- iNKT cell activation
- IL-4
- atherosclerosis
- invariant TCR signaling
- ERK tyrosine kinase phosphorylation
- Inhibitor
- inhibitor
- inhibit