iC3b Antibody (Monoclonal - neoantigen)

A murine monoclonal antibody to a neo-epitope expressed on iC3b.


Product Specifications

Citations24
Clonality

Monoclonal

Immnogen

Purified human protein.

Applications

See citations and technical data sheet for application info.

Concentration≥ 1.0 mg/mL
ConjugateUnconjugated
Cross Reactivity

Human

Ordering Information

For Research Use Only in the United States. Not for use in diagnostic procedures.
Catalog NumberA209
Catalog Number (CE)N/A
Size100 µl
Price (USD)$365.00
Price (EURO)330,00 €

Contact us

US Phone+1 (858) 552 1100
EU Phone+353 (91) 412 474
US Emailcontact-us@quidelortho.com
EU Emailcontact-emea@quidelortho.com

Specifications

Description

A murine monoclonal antibody to a neo-epitope expressed on iC3b.

Size

100 µl

Concentration≥ 1.0 mg/mL
ApplicationsSee citations and technical data sheet for application info.
FormLiquid. Borate Buffered Saline (pH 8.4 ± 0.2), with ≤ 0.1% Sodium Azide.
ClonalityMonoclonal
Immunogen

Purified human protein.

ConjugateUnconjugated
Cross ReactivityHuman
Isotype

IgG2bk

Purity

> 95% by SDS PAGE

SourceMouse
Specificity

This monoclonal antibody was raised against purified human iC3b. It is specific for a neo-antigen on iC3b.

Storage

Short term (30 days) 4˚C. Long term at or below –20˚C.

Background

Under normal conditions, activation of either of the complement pathways leads to the formation of C3 convertase enzymes which cleave C3 into two fragments C3a, an anaphylatoxin, and C3b.The C3b fragment has many biologic functions including promotion of phagocytosis and participation as a structural component in both the C3 and C5 convertase enzymes. These processes are under stringent control in vivo. One control mechanism involves a two-site cleavage of C3b by Factor I with the cooperation of Factor H or CR1 as cofactors. When cleaved in this way the biologic functions of C3b are lost. The resulting protein is termed iC3b.This fragment, in turn, has a host of new biologic activities. iC3b fragments, either in fluid phase or bound to biological surfaces, can interact with a variety of cell types expressing complement receptors (either CR2 or CR3). iC3b levels in fluid phase are elevated in a variety of disease states including Systemic Lupus Erythematosis, Rheumatoid Arthritis as well as in a variety of pathologic conditions including sepsis and Myocardial Infarct. Quidel’s monoclonal antibodies to complement antigens were prepared using standard techniques. They are purified from mouse ascites fluid via protein A affinity chromatography. 3 The specificity of the monoclonal antibody was established via a series of immunological techniques including ELISA, hemagglutination and RIA. Firstly, the antibody was shown by ELISA to bind to C3 antigens using highly pure, immobilized C3. Subsequent studies showed that this antibody agglutinates EC3bi but not EC3b or EC3d cells in an indirect hemagglutination assay. Further experiments showed that this antibody bound to radio-labeled purified iC3b but not to similarly labeled C3, C3b, C3d, or C3c.

Citations

TitleYearApplicationsSample SpeciesSampleSample Details

Efficient complement-mediated clearance of immunosuppressed T cells by macrophages.

2023IFHuman

T Cells

Immunosuppressed

Sequential Increase in Complement Factor I, iC3b, and Cells Expressing CD11b or CD14 in Cutaneous Vasculitis.

2022IHCHuman

Skin Tissue

Cutaneous Vasculitis

Heme Interferes With Complement Factor I-Dependent Regulation by Enhancing Alternative Pathway Activation.

2021ELISAHuman

Plasma

Sickel Cell Anemia

Complement receptor 3 mediates Aspergillus fumigatus internalization into alveolar epithelial cells with the increase of intracellular phosphatidic acid by activating FAK.

2021WBHuman

Serum

Aspergillus incubated

A monoclonal antibody targeting amyloid β (Aβ) restores complement factor I bioactivity: Potential implications in age-related macular degeneration and Alzheimer's disease

2018ELISAHuman

Plasma

Age-Related Macular Degeneration

A monoclonal antibody targeting amyloid β (Aβ) restores complement factor I bioactivity: Potential implications in age-related macular degeneration and Alzheimer's disease

2018ELISAHuman

Plasma

Alzheimer's Disease

Inhibition of Immune Complex Complement Activation and Neutrophil Extracellular Trap Formation by Peptide Inhibitor of Complement C1.

2018ELISAHuman

Serum

N/A

Arabinosylation of recombinant human immunoglobulin-based protein therapeutics

2017ELISAHuman

Serum

N/A

Complement Receptor 3 Has Negative Impact on Tumor Surveillance through Suppression of Natural Killer Cell Function

2017FCHuman

NK Cells

N/A

Eculizumab treatment: stochastic occurrence of C3 binding to individual PNH erythrocytes.

2017FCHuman

Red Blood Cells

PNH

Bacillus anthracis Spore Surface Protein BclA Mediates Complement Factor H Binding to Spores and Promotes Spore Persistence.

2016FCHuman

Serum

B. anthracis incubated

Tumor necrosis-initiated complement activation stimulates proliferation of medulloblastoma cells.

2015IHCHuman

Brain Tissue

Medullablastoma

quantitative lateral flow assay to detect complement activation in blood.

2015Lateral Flow AssayHuman

Plasma

N/A

Complement activation by heme as a secondary hit for atypical hemolytic uremic syndrome.

2013FCHuman

HUVEC Cells

aHUS

Control of Entamoeba histolytica adherence involves metallosurface protease 1, an M8 family surface metalloprotease with homology to leishmanolysin.

2012FCParasite

Entamoeba histolytica

N/A

Design and development of TT30, a novel C3d-targeted C3/C5 convertase inhibitor for treatment of human complement alternative pathway-mediated diseases

2011IHCHuman

Lung Tissue

Asthmatic Alzheimer's

Design and development of TT30, a novel C3d-targeted C3/C5 convertase inhibitor for treatment of human complement alternative pathway-mediated diseases

2011IHCHuman

Lung Tissue

N/A

Complement Activation on Platelets Correlates with a Decrease in Circulating Immature Platelets in Patients with Immune Thrombocytopenic Purpura

2009ELISAHuman

Plasma

N/A

Plaque complement activation and cognitive loss in Alzheimer’s disease.

2008ICC, IHCHuman

Brain Tissue

N/A

Pneumolysin, PspA, and PspC Contribute to Pneumococcal Evasion of Early Innate Immune Responses During Bacteremia in Mice.

2007WBBacteria

Pneumococci

N/A

Complement activation in the Parkinson’s disease substantia nigra: an immunocytochemical study.

2006ICC, IHCHuman

Brain Tissue

N/A

Opsonization of apoptotic cells by autologous iC3b facilitates clearance by immature dendritic cells, down-regulates DR and CD86, and up-regulates CC chemokine receptor 7.

2002Confocal MicroscopyCell Culture

Jurkat Cells

N/A

Spontaneous classical pathway activation and deficiency of membrane regulators render human neurons susceptible to complement lysis.

2000IHCHuman

Brain Tissue

Fetal

Complement-dependent proinflammatory properties of the Alzheimer's disease beta-peptide.

1998ELISAHuman

Amyloid-βeta peptides & NHS

N/A