Anti-Mouse CD120α (TNFR1) [Clone 55R-170] — Purified in vivo GOLD™ Functional Grade

Clone 55R-170 is most commonly used in vivo in mice to block or neutralize the bioactivity of mouse TNF Receptor I (TNFRI, CD120a), enabling investigation into TNFRI-mediated pathways, particularly in the context of inflammation, infection, and TNF-related diseases.

Key in vivo applications include:

• Blocking TNFRI Signaling: 55R-170 antibody specifically inhibits TNFRI by blocking ligand binding, thus preventing TNF-alpha–initiated inflammatory signaling.
• Neutralization of TNF Bioactivity: Used to assess the role of TNF-alpha in pathophysiological processes by disrupting TNFRI-mediated responses.
• Protection from Endotoxin Shock: In mouse models, anti-TNFRI antibodies like 55R-170 have been shown to confer protection against lethal endotoxin shock, highlighting its utility in acute inflammatory challenge studies.
• Infection Models: 55R-170 blocks development of protective immune responses, such as those against Listeria monocytogenes, allowing researchers to dissect TNFRI’s crucial function in infection and immunoregulation.
• Modeling TNF-Related Pathology: Widely used to understand TNFRI's role in autoimmunity, neurodegenerative diseases, and other inflammatory disorders by selectively inhibiting receptor signaling in vivo.
• Skin Necrosis Models: Shown to block TNF-alpha-induced skin necrosis—this anti-inflammatory effect is part of its utility for studying tissue damage and repair.

Additional relevant uses:

• Used in combination with other receptor-specific antibodies to distinguish the roles of TNFRI vs. TNFRII in complex disease models.
• Applied in chronic and acute settings to analyze TNFRI’s contribution to cytokine networks and cell death pathways.

In sum, 55R-170 is a functional blocking antibody deployed in vivo to dissect the physiological, immunological, and pathophysiological roles of TNFRI in mouse models. Its specific applications involve analysis of inflammation, immune defense, and TNF-mediated disease mechanisms.

Commonly used antibodies or proteins in the literature alongside 55R-170 (an anti-mouse TNF receptor type I/TNFRI/p55 monoclonal antibody) include:

• Anti-p75 (TNFRII) antibodies: These are frequently used to distinguish the roles of the two main TNF receptors by comparing TNFRI (p55) blockade with TNFRII (p75) blockade.
• Anti-TNF-α antibodies: Targeting the ligand (tumor necrosis factor-alpha) itself is common in mechanistic and inhibition studies.
• Anti-LT-α/TNF-β antibodies: As lymphotoxin-α (TNF-β) is also a ligand for TNFRI, studies often include antibodies that detect or neutralize LT-α/TNF-β.
• 55R-286: This is another anti-CD120a/TNFRI antibody from a different clone and is frequently paired with 55R-170 in ELISA detection formats for sandwich assays or ligand/receptor quantification.
• 55R-176: This clone is also cited as used in functional or comparative TNFRI blockade assays alongside 55R-170.

Additional context:

• Functional assays and detection protocols sometimes combine biotinylated 55R-170 with purified 55R-286 for ELISA, highlighting their complementary use in quantitative detection.
• In broader TNF signaling studies, researchers also monitor downstream molecules or adapters (such as TRADD, TRAF2, and BAG4/SODD proteins), though antibodies against these adapters are less commonly cited specifically with 55R-170.

In summary, Anti-p75 (TNFRII) antibodies, anti-TNF-α, anti-LT-α/TNF-β, 55R-286, and 55R-176 are among the most commonly reported antibodies/proteins used in conjunction with 55R-170 for studying TNF signaling in mouse models.

Clone 55R-170 is a widely cited monoclonal antibody that specifically targets mouse TNFR1 (CD120a), serving as a potent and selective antagonist in both in vitro and in vivo studies.

Key findings and applications from scientific literature using clone 55R-170 include:

• Selective Blockade of TNFR1 Signaling: 55R-170 is used to selectively block TNFR1, enabling researchers to dissect the distinct biological functions of TNFR1 versus TNFR2 in mouse models of inflammation, infection, autoimmune disease, and cytokine storm.
• Elucidation of TNF Receptor Roles: The antibody has demonstrated that TNFR1 and TNFR2 play different roles in immune responses. Neutralization of TNFR1 with 55R-170, for example, protected mice from lethal endotoxin shock and disrupted the development of protective responses against Listeria monocytogenes infection, which was not observed with anti-TNFR2 antibodies.
• Mechanistic Insights: 55R-170 inhibits the biological activity of TNF-alpha, including suppression of TNF-induced cytotoxicity and downstream signaling (such as NF-κB and ERK pathways). This antagonism has enabled mechanistic dissection of individual TNF functions in various models.
• Therapeutic Hypotheses: Its use supports hypotheses for developing TNFR1-selective therapies for human diseases characterized by pathological TNF signaling, such as autoimmune and inflammatory disorders.
• Combination Immunotherapy Research: 55R-170 has been employed to assess the combined effect of TNFR1 blockade with immune checkpoint inhibitors (e.g., anti-PD-1) in enhancing anti-tumor responses in preclinical cancer models.
• Functional Validation: The antibody is validated for several applications, including ELISA, flow cytometry, and functional in vitro and in vivo blockade of TNFR1. Specifically, at 25 μg/mL, it inhibits 50% of the biological effects of 1 ng/mL mouse TNF-alpha in cytotoxicity assays.
• Insights Into Dendritic Cell Maturation: Studies using 55R-170 have shown its role in modulating and clarifying TNF-α–mediated effects on dendritic cell populations and related immune maturation phenomena.

Overall, clone 55R-170 is regarded as an essential research tool for dissecting TNF/TNFR1-mediated signaling and pathology in murine models, advancing understanding of TNF biology and informing therapeutic strategies for inflammatory and immune-mediated diseases.

Dosing regimens of clone 55R-170 (anti-mouse TNFR1/CD120a) vary by mouse model, disease context, and experimental goal, and there is currently no universal standard. However, most published protocols for in vivo studies in mice typically use doses in the range of 100–250 μg per mouse per injection, with administration routes usually intraperitoneal (i.p.) or intravenous (i.v.) as appropriate for the chosen disease model.

Key details:

• In vitro, 25 μg/mL of clone 55R-170 antibody can inhibit by 50% the biological effects of 1 ng/mL mouse TNF alpha.
• For in vivo applications, 100–250 μg per mouse is the commonly reported starting range, often administered as single or repeated doses, adapted empirically based on outcomes observed in pilot studies.
• Regimen frequency and timing (for example, weekly vs. every 2–3 days) may vary according to the disease model (e.g., acute inflammation, chronic autoimmune disease, colitis, etc.) and the half-life of the antibody in mice. Some protocols report single injections, while others use multiple doses over days to weeks.
• Strain-specific and pathology-specific adjustments are often necessary, as mouse genetic background and immune responses can affect both efficacy and safety, making empirical optimization and pilot titration studies a common practice.
• Sterility and endotoxin control are emphasized in preparation and application, as non-antibody contaminants can confound immunological and pathological outcomes.

Summary of regimens in published literature:

Key recommendations:

• Empirical adaptation is strongly recommended for each new disease model, mouse strain, or study design, given the heterogeneity of published regimens and lack of formal dosing standard.
• Pilot experiments to optimize dose, timing, and route are a common and practical approach, especially if working in less-characterized disease models or novel therapeutic settings.

No published studies directly compare clone 55R-170 dosing regimens across a wide range of mouse models in a systematic fashion; most information derives from protocol notes by suppliers and scattered literature reports.

If you have a specific disease model or mouse strain in mind, dosing nuances may be further tailored according to previous work in that area or pilot optimization.