Eculizumab Biosimilar, Human C5 Monoclonal Antibody

Recombinant Humanized IgG2 Monoclonal Antibody.
Isotype: Human IgG2/4 kappa.
Source: The monoclonal antibody Eculizumab biosimilar was produced in the Eculizumab biosimilar CHO stable cell line.
Specificity/Sensitivity: The monoclonal antibody Eculizumab biosimilar specifically binds to the human C5, the terminal complement component 5.
Applications: ELISA, functional assays such as bioanalytical PK and ADA assays.
Form of Antibody: 0.2 uM filtered solution, pH 6.0, no stabilizers or preservatives.
Endotoxin: < 1 EU per 1 mg of the protein by the LAL method.
Purity: >95% by SDS-PAGE under reducing conditions and HPLC.

Shipping: The monoclonal antibody Eculizumab is shipped with ice pack. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70°C as supplied.
1 month from date of receipt, 2 to 8°C as supplied.

Background

Eculizumab, a recombinant humanized anti-C5 (the terminal Complement component 5) monoclonal antibody, selectively targets and inhibits the terminal portion of the complement cascade. Eculizumab is a first-in-class terminal complement inhibitor to treat paroxysmal nocturnal hemoglobinuria (PNH) with excessive destruction of red blood cells (hemolysis). Eculizumab is also the first agent to treat atypical hemolytic uremic syndrome (aHUS) with abnormal blood clots to form in small blood vessels throughout the body, leading to kidney failure, damage to other vital organs and premature death.

The complement immune system destroys and removes foreign particles by the complement cascade triggered by foreign particles. The complement proteins activiated in order create holes or pores in the invading organisms, leading to their destruction. The complement immune system in patients can also destroy healthy cells and tissue, resulting in excessive destruction of red blood cells (hemolysis) or abnormal blood clots to form in small blood vessels throughout the body.

When activated, C5 at a late stage in the complement cascade is involved in activating host cells, thereby attracting pro-inflammatory immune cells, while also destroying cells by triggering pore formation. Eculizumab specifically binds to C5 and inhibits the cleavage of C5 to C5a (a potent anaphylatoxin with prothrombotic and proinflammatory properties) and C5b by the C5 convertase, preventing the generation of the terminal complement complex C5b-9 (which also has prothrombotic and proinflammatory effects). Both C5a and C5b-9 cause the terminal complement-mediated events that are characteristic of PNH and aHUS. By doing so, the normal, disease-preventing functions of proximal complement system are largely preserved, while the properties of C5 that promote inflammation and cell destruction are impeded.