The Basics

How do biosimilars work?

Different types of biologicals have different mechanisms of action. They do, however, share a basic mechanism of action in that they are similar to naturally occurring or existing proteins or molecules in the body and therefore share the same actions. Alternatively, they may be able to block the action of the naturally occurring substance.


The different biologics (and therefore biosimilars) can be classified as follows:3

  • Low-molecular weight heparins, e.g. enoxaparin sodium
  • Growth factors: Erythropoietin (EPO), Filgrastim, Pegfilgrastim
  • Hormones: Follitropin alfa, Insulin glargine, Somatropin (growth hormone), Teriparatide, Insulin lispro
  • Fusion proteins: Etanercept
  • Monoclonal antibodies: Infliximab, Rituximab, Bevacizumab, Trastuzumab

As an example of how biological medicines work, let us focus on monoclonal antibodies. Antibodies are normally produced by the body’s immune system in response to a foreign protein – the antigen. Such foreign proteins can be bacteria, viruses or even cancer cells that are different to normal, healthy cells.

Monoclonal antibodies

Once an antibody binds to an antigen, it helps the immune system to “neutralise” the threat(s) from the foreign protein, such as bacterial or viral infection. Similarly, monoclonal antibodies are developed with a specific target in mind and are produced with the help of recombinant DNA technology. While naturally produced antibodies are polyclonal, monoclonal antibodies are produced by a single (= mono) clone of cells but, like polyclonal antibodies, they enlist the natural immune system to fight cancer or autoimmune disorders. All monoclonal antibodies are given names that end with the suffix -mab, i.e., infliximab, trastuzumab, etc.6,7

Cipla biosimilar commitment

Infliximab is an example of a monoclonal antibody against TNF-alpha that is used in the treatment of a wide variety of inflammatory conditions such as rheumatoid arthritis, Crohn’s disease, and ankylosing spondylitis. By binding to TNF-alpha, infliximab disrupts its interaction with its receptors and may also cause lysis (cell death) of cells that produce TNF-alpha. It was first approved by the FDA in 1998.8