Filgrastim

Neutrophils are critical granulocytes involved in the acute inflammatory response and host defences against bacterial infections. They also contribute to long-term adaptive immunity by promoting immediate host immune response and attracting other cells, such as macrophages and dendritic cells. As neutrophils promote both the initiation and the maintenance of inflammation at sites of infection, suppressed neutrophil responses lead to extreme susceptibility to infection. Low neutrophil levels, or neutropenia, caused by chronic neutropenia, myelosuppressive chemotherapy, and radiation therapy increases the risk of infection and related events. Neutropenia caused by chemotherapy or radiation therapy can further progress into febrile neutropenia, which is associated with an elevated risk for life-threatening systemic infections and chemotherapy-associated morbidity and mortality.

The production and release of functional neutrophils from the bone marrow are normally regulated by granulocyte colony-stimulating factors (G-CSF), which are major cytokine regulators of neutrophilic granulocytes. G-CSFs act on hematopoietic cells by binding to specific cell surface receptors to stimulate the proliferation‚ differentiation‚ and maturation of neutrophil progenitors. G-CSF also induces some end-cell functional activation of neutrophils, including enhanced phagocytic ability‚ priming of the cellular metabolism associated with respiratory burst‚ antibody-dependent killing, and the increased expression of some cell surface antigens. Filgrastim is a short-acting recombinant G-CSF that mimics the biological actions of endogenous G-CSF. It also facilitates the release of neutrophils from the bone marrow into the blood to reduce the incidence of infection and manage neutropenia.