C5 antibody | Eculizumab

For Research Use Only. Not for use in diagnostic procedures.

Monoclonal

IgG2 Kappa

Human

>98% by SDS PAGE
Purified IgG prepared by affinity chromatography on Protein A

Liquid; Phosphate Buffered Saline

1.0 mg/ml (lot specific)

Store at 4 degree C or at -20 degree C if preferred.
Storage in frost-free freezers is not recommended. This product should be stored undiluted. Avoid repeated freezing and thawing as this may denature the antibody.
Should this product contain a precipitate we recommend microcentrifugation before use.

Small volumes of anti-C5 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Description: Anti-C5 Antibody is a non-therapeutic biosimilar of the monoclonal antibody drug eculizumab (Soliris) for research use. It can be used in bioanalytical assays and for studying biological pathways affected by the drug.

Summary: Human Anti-C5 Antibody is a research grade biosimilar of the monoclonal antibody drug eculizumab. It is a recombinant human IgG2/4 kappa antibody with variable regions from the therapeutic antibody eculizumab.
Human Anti-C5 Antibody is for research use only. It is suitable as a reference standard in a pharmacokinetic (PK) bridging ELISA with anti-eculizumab antibodies. It can also be used as capture and detection reagent in an anti-drug antibody (ADA) bridging ELISA, with an anti-eculizumab antibody in IgG1 format as reference standard.
Eculizumab (Soliris) is a humanized IgG2/4 kappa antibody. The heavy chains are comprised of human IgG2 sequences in CH1, the hinge and the adjacent portion CH2, and human IgG4 sequences in the remaining part of CH2 and CH3. The drug is used to treat paroxysmal nocturnal hemoglobinuria (PNH), a rare acquired life-threatening disease of the blood characterized by destruction of red blood cells by the complement system. It also has approval as an orphan drug for treatment of atypical hemolytic uremic syndrome (aHUS). Eculizumab specifically binds to the terminal complement component 5 (C5) and inhibits the cleavage of C5 to C5a and C5b by the C5 convertase, which prevents the generation of the terminal complement complex C5b-9. Both C5a and C5b-9 cause the terminal complement-mediated events that are characteristic of PNH and aHUS. A 1: 1 molar ratio of eculizumab to C5 is sufficient for C5 inhibition.

ELISA (EIA)

Purity Assessment by SDS-PAGE
0.5 mug of Human Anti-C5 Antibody, MCA6103 (eculizumab biosimilar, research grade) was denatured and analyzed under reducing (R) and non-reducing (NR) conditions. Bands were visualized using Coomassie Blue staining. Full IgG (H2L2), heavy (H) and light chains (L) are indicated.

Monodispersity assessment by HPLC-SEC
Size exclusion chromatography (SEC) of Human Anti-C5 Antibody, MCA6103 (eculizumab biosimilar, research grade) was performed on an analytical HPLC instrument. Shown is the monomer peak (H2L2), calculated relative monomer portion and aggregates. Column: MAbPac SEC-1, 5 mum; dimension: 4.0 x 150 mm; mobile phase: 50 mM sodium phosphate, pH 6.8, 300 mM NaCl, 200 mM Arginine; flow rate: 200 mul/min; inj. volume [mul]: 3; temp.: 25 degree C; detection: 280 nm; sample: mAb (1 mg/ml).

complement C5

complement C5

Complement C5

CPAMD4??[Similar Products]

CO5_HUMAN

This gene encodes a component of the complement system, a part of the innate immune system that plays an important role in inflammation, host homeostasis, and host defense against pathogens. The encoded preproprotein is proteolytically processed to generate multiple protein products, including the C5 alpha chain, C5 beta chain, C5a anaphylatoxin and C5b. The C5 protein is comprised of the C5 alpha and beta chains, which are linked by a disulfide bridge. Cleavage of the alpha chain by a convertase enzyme results in the formation of the C5a anaphylatoxin, which possesses potent spasmogenic and chemotactic activity, and the C5b macromolecular cleavage product, a subunit of the membrane attack complex (MAC). Mutations in this gene cause complement component 5 deficiency, a disease characterized by recurrent bacterial infections. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Nov 2015]

C5: Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient for C6. The C5b-C6 complex is the foundation upon which the lytic complex is assembled. Defects in C5 are the cause of complement component 5 deficiency (C5D). A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria meningitidis. An association study of C5 haplotypes and genotypes in individuals with chronic hepatitis C virus infection shows that individuals homozygous for the C5_1 haplotype have a significantly higher stage of liver fibrosis than individuals carrying at least 1 other allele (PubMed:15995705).

Protein type: Secreted, signal peptide; Secreted

Chromosomal Location of Human Ortholog: 9q33-q34

Cellular Component: membrane attack complex; extracellular space; extracellular region

Molecular Function: protein binding; chemokine activity; endopeptidase inhibitor activity; receptor binding; C5a anaphylatoxin chemotactic receptor binding

Biological Process: activation of MAPK activity; positive regulation of chemotaxis; in utero embryonic development; cytolysis; complement activation, alternative pathway; chemotaxis; glucose homeostasis; leukocyte migration during inflammatory response; complement activation; cellular calcium ion homeostasis; G-protein coupled receptor protein signaling pathway; positive regulation of angiogenesis; cell surface receptor linked signal transduction; regulation of complement activation; response to stress; innate immune response; negative regulation of dopamine secretion; inflammatory response; complement activation, classical pathway

Disease: Complement Component 5 Deficiency; Eculizumab, Poor Response To

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