JMW-3B3
JMW-3B3 is a humanized IgG1λ monoclonal antibody targeting CTLA-4. JMW-3B3 selectively binds the unique C-terminal sequence of sCTLA-4 to block its immunoregulatory and immunosuppressive activity without cross-reacting with full-length CTLA-4 receptor. JMW-3B3 enhances cytokine profiles in PBMC cultures responding to lupus autoantigen-derived peptides. JMW-3B3 enhances IFN-γ production in anti-CD3 stimulated PBMC from melanoma patients at low anti-CD3 doses. JMW-3B3 can be used for the research of systemic lupus erythematosus and malignant melanoma.
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.
Biological Activity
Description
Species Reactivity
Human
In Vitro
Biotinylated JMW-3B3 (10 μg/mL) specifically detects sCTLA-4 in PBMC cell culture supernatants, and reveals no population-level difference in sCTLA-4 production between SLE patient and healthy donor PBMC stimulated with lupus-associated autoantigenic peptides[1].
JMW-3B3 (10 μg/mL; 5 days) blocks sCTLA-4 activity in PBMC from both healthy donors and SLE patients, with effects that vary by stimulant: it suppresses some pro-inflammatory and proliferative responses in healthy donors, while enhancing IL-10 production (and altering proliferation/cytokine profiles) in SLE patient PBMC, accentuating the inherent cytokine response differences between the two groups[1].
JMW-3B3 (20 μg/mL; overnight at 4°C) selectively binds intracellular sCTLA-4 in G-361 human malignant melanoma epithelial cells, but does not detect sCTLA-4 in A-375 human malignant melanoma epithelial cells[2].
JMW-3B3 (10 μg/mL; 5 days) enhances IFN-γ production from melanoma patient PBMC stimulated with a low dose (0.02 μg/mL) of anti-CD3 mAb for 5 days, relative to ipilimumab treatment[2].
JMW-3B3 (10 μg/mL; 5 days) enhances IL-17A production from healthy donor PBMC stimulated with a high dose (1 μg/mL) of anti-CD3 mAb for 5 days, relative to ipilimumab treatment[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Gene ID
Accession
Target
CTLA4
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Application
ELISA, FACS, Functional assay
Chemical Information
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SMILES
[JMW-3B3]
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
[1]. Dahal LN, et al. Immunoregulatory soluble CTLA-4 modifies effector T-cell responses in systemic lupus erythematosus. Arthritis Res Ther. 2016;18:180. Published 2016 Aug 4. [Content Brief]
[2]. Khanolkar RC, et al. TGFβ2 Induces the Soluble Isoform of CTLA-4 - Implications for CTLA-4 Based Checkpoint Inhibitor Antibodies in Malignant Melanoma. Front Immunol. 2022;12:763877. Published 2022 Jan 5. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)