DNP-BSA
DNP-BSA is a multivalent antigen and protein-binding reagent. DNP-BSA binds to subdomain IIA (Site I) of bovine serum albumin via predominantly hydrophobic forces, with spontaneous complex formation via combined dynamic and static quenching. DNP-BSA induces cross-linking of IgE-bound FceRI, triggering tyrosine phosphorylation of FceRI β and γ subunits. DNP-BSA binds to anti-DNP IgE via its DNP groups, forming cross-links between IgE-FceRI complexes, with most DNP groups initially unavailable but transiently exposed for binding. DNP-BSA induces FITC fluorescence quenching in FITC-labeled anti-DNP IgE, proportional to occupied IgE Fab binding sites. DNP-BSA can be used for the research of allergy, inflammation, and contact sensitivity (allergic contact dermatitis).
For research use only. We do not sell to patients.
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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
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- References
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Help & FAQs
Biological Activity
DNP-BSA forms spontaneously under physiological pH, with hydrophobic forces as the dominant driving force, as evidenced by positive ΔH° (46.22 kJ mol-1) and ΔS° (237.2 J mol-1 K-1) values and negative ΔG° values ranging from -24.46 to -29.21 kJ mol-1[1].
DNP-BSA forms at site I of BSA's subdomain IIA, forming stable interactions with Trp213, Leu197, Arg217, Asp450, and Leu480, with a docking score of -8.71 kcal/mol[1].
Stimulates FceRI β subunit tyrosine phosphorylation in RBL-2H3 cells that correlates directly with the kinetics of DNP-BSA-mediated IgE-FceRI cross-linking at 15°C, but shows a biphasic decline while cross-linking increases at 35°C[2].
DNP-BSA potently stimulates degranulation of adherent RBL-2H3 cells, inducing ~50% β-hexosaminidase release at concentrations of 0.2 nM and 1.1 nM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
DNP-BSA (100 µg per animal; epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days) suppresses DNFB-induced contact sensitivity and induces TCRab+ CD4+ CD25+ FoxP3+ regulatory T cells in C57BL/6 mice[3].
DNP-BSA (100 µg per animal; epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days) induces regulatory lymph node cells that potently suppress DNFB-induced contact sensitivity in B10.PL and related knockout mice, with suppression efficacy ranging from 80-92%[3].
DNP-BSA (100 µg per animal; epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days) induces regulatory T cells that distribute equally across peripheral lymphoid tissues and suppress DNFB-induced contact sensitivity in NOD mice[3].
DNP-BSA (100 µg per animal; epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days) suppresses DNFB-induced lymph node cell proliferation by 43-56% and reduces proinflammatory cytokine production in BALB/c mice[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (H-2d) (female, 6-10 weeks of age)[3]
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Dosage:100 µg per animal; 3 µg per animal
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Administration:epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days
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Result:Reduced DNFB-induced ear swelling to 26% of the positive control, vascular permeability to 19% of the positive control, ear weight to 46% of the positive control, myeloperoxidase activity to 50% of the positive control, and IFN-γ concentration in ear extracts to 50% of the positive control.
Significantly inhibited ear swelling (3 µg dose).
Increased the absolute number of TCRab+ CD4+ CD25+ FoxP3+ regulatory T cells in auxiliary and inguinal lymph nodes compared to PBS-treated mice.
Reduced ear swelling to 50% of the positive control when 5×107 lymph node cells from DNP-BSA-patched mice were transferred 2 hours before DNFB sensitization.
Reduced ear swelling to 56% of the positive control when 5×107 lymph node cells from DNP-BSA-patched mice were transferred 2 hours before challenge.
Reduced ear swelling to 40% of the positive control at 24 hours and 28% at 48 hours when 5×107 lymph node cells from DNP-BSA-patched mice were transferred 4 hours after DNFB challenge.
Reduced ear swelling to 38% of the positive control when administered 1 day after DNFB sensitization.
Reduced ear swelling after rechallenge to 13% of the positive control when administered 1 day after the first DNFB challenge.
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Animal Model:C57BL/6 (H-2b) (female, 6-10 weeks of age)[3]
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Dosage:100 µg per animal
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Administration:epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days
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Result:Significantly suppressed DNFB-induced ear swelling compared to PBS-treated mice.
Increased the absolute number of TCRab+ CD4+ CD25+ FoxP3+ regulatory T cells in auxiliary and inguinal lymph nodes.
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Animal Model:B10.PL (H-2u), β2m-/-, TCRδ-/-, CD1d-/- (6-10 weeks of age)[3]
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Dosage:100 µg per animal
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Administration:epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days
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Result:Reduced DNFB-induced ear swelling to 32% of the positive control when lymph node cells from DNP-BSA-patched B10.PL mice were transferred.
Reduced DNFB-induced ear swelling to 13% of the positive control when lymph node cells from DNP-BSA-patched β2m-/- mice were transferred.
Reduced DNFB-induced ear swelling to 20% of the positive control when lymph node cells from DNP-BSA-patched TCRδ-/- mice were transferred.
Reduced DNFB-induced ear swelling to 8% of the positive control when lymph node cells from DNP-BSA-patched CD1d-/- mice were transferred.
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Animal Model:NOD, FoxP3-FIR NOD (6-10 weeks of age)[3]
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Dosage:100 µg per animal
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Administration:epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days
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Result:Resulted in a higher percentage of FoxP3+ regulatory T cells in auricular lymph nodes, auxiliary/inguinal lymph nodes, and spleens of DNFB-sensitized recipients compared to recipients receiving cells from PBS-treated donors.
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Animal Model:BALB/c (H-2d) (female, 6-10 weeks of age)[3]
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Dosage:100 µg per animal
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Administration:epicutaneous, via occlusive patch; days 0 and 4, each patch left in place for 3 days
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Result:Reduced lymph node cell proliferation (measured by [3H]-thymidine uptake) to 44-57% of the positive control across DNP-BSA concentrations of 30, 100, and 300 µg/mL.
Reduced production of IL-12 to ~57% of the positive control, TNF-α to ~68% of the positive control, and IFN-γ to ~64% of the positive control in lymph node cell cultures.
Chemical Information
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SMILES
[DNP-BSA]
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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.
Purity & Documentation
References
[1]. El Gammal RN, et al. Insights on the in-vitro binding interaction between donepezil and bovine serum albumin. BMC chemistry. 2023 Apr 06;17(1):31. [Content Brief]
[2]. Xu K, et al. Kinetics of multivalent antigen DNP-BSA binding to IgE-Fc epsilon RI in relationship to the stimulated tyrosine phosphorylation of Fc epsilon RI. J Immunol. 1998 Apr 1;160(7):3225-35. [Content Brief]
[3]. Majewska-Szczepanik M, et al. Epicutaneous immunization with DNP-BSA induces CD4+ CD25+ Treg cells that inhibit Tc1-mediated CS. Immunology and cell biology. 2012 Sep;90(8):784-95. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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