Anti-Mouse TNFR2 Antibody (TR75-54.7)
Based on 1 Customer Validation
Anti-Mouse TNFR2 Antibody (TR75-54.7) is an anti-mouse TNFR2 IgG monoclonal antibody. Anti-Mouse TNFR2 Antibody (TR75-54.7) can reduce white blood cell count (WBC) and decrease the expression of some pro-inflammatory cytokines such as CCL2 and CXCL5. Anti-Mouse TNFR2 Antibody (TR75-54.7) can be used for researches on inflammation conditions and cancer such as breast cancer.
For research use only. We do not sell to patients.
- Purity : 98.864%
- Molecular Weight:150 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Isotype
Armenian Hamster IgG
Recommend Isotype Controls
Species Reactivity
Mouse
IC50 & Target
TNFR2
In Vivo
Anti-Mouse TNFR2 Antibody (TR75-54.7) (5 mg/kg, i.p., twice weekly, for 3 weeks) significantly reduces white blood cell count (WBC) and downregulates some pro-inflammatory cytokines in JAK2+/VF knock-in C57BL/6 mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:1×105 4T1 cells injected female wild-type Balb/c mice (8-12 weeks)[1]
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Dosage:200 μg
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Administration:Intraperitoneal injection (i.p.), single dose, 3 days before inoculation of 4T1 tumor cells
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Result:Significantly prolonged the survival period of mice.
Significantly inhibited tumor volume.
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Animal Model:JAK2+/VF knock-in C57BL/6 mice[2]
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Dosage:5 mg/kg
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Administration:Intraperitoneal injection (i.p.), twice weekly, for 3 weeks
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Result:Significantly reduced white blood cell count (WBC), but did not significantly improve hematocrit (HCT), hemoglobin (HGB), and splenomegaly.
Downregulated some pro-inflammatory cytokines such as CCL2 and CXCL5, but upregulated other inflammatory markers such as CXCL2 and IL-12.
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Application
in vivo TNFR2 blockade; in vitro TNFR2 blockade
Chemical Information
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Appearance Liquid
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Molecular Weight 150 kDa
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Color Colorless to light yellow
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SMILES
[Anti-Mouse TNFR2 Antibody (TR75-54.7)]
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Shipping
Shipping with dry ice.
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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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
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
Purity & Documentation
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Data Sheet (261 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
References
[1]. Nie Y, et al. Blockade of TNFR2 signaling enhances the immunotherapeutic effect of CpG ODN in a mouse model of colon cancer. Sci Signal. 2018 Jan 2;11(511):eaan0790. [Content Brief]
[2]. Müller P, et al. Anti-inflammatory treatment in MPN: targeting TNFR1 and TNFR2 in JAK2-V617F-induced disease. Blood Adv. 2021 Dec 14;5(23):5349-5359. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)