FILGRASTIM

Filgrastim is a recombinant human granulocyte colony stimulating factor (G-CSF) indicated as an adjunct to cancer chemotherapy for patients with non-myeloid malignancies. It reduces the duration of chemotherapy-induced neutropenia by forcing immature leucocytes to differentiate into neutrophils, thereby decreasing the incidence and length of infections.Bone pain is the most significant side effect.Chugai launched the second G-CSF, lenograstim, in December 1991. Other potential uses include bone marrow transplants, myelodysplastic syndromes and febrilelchronic neutropenia.

Clear, colourless or slightly yellowish liquid

Amgen (U.S.A.)

Filgrastim is a human granulocyte colony stimulating factor (G-CSF) used to treat neutropenia.

Antineutropenic; hematopoietic stimulant.

Filgrastim (Neupogen) is a human recombinant granulocyte colony–stimulating factor (rG-CSF) produced using recombinant DNA technology. It acts on precursor hematopoietic cells in the bone marrow by binding to specific receptors that stimulate cellular proliferation and differentiation into neutrophils. It also enhances some neutrophil functions, including phagocytosis and antibody-dependent killing.

Neupogen (Amgen).

Filgrastim is used to accelerate recovery of neutrophils after chemotherapy, both to prevent infections and to shorten the duration of neutropenia in patients in whom infections have developed.

Filgrastim, G-CSF, Neupogen, stimulates the proliferation ofgranulocytes (especially neutrophils) by mobilizinghematopoietic stem cells in the bone marrow. The native protein is glycosylated.Filgrastim selectively stimulates proliferation and differentiationof neutrophil precursors in the bone marrow. Thisleads to the release of mature neutrophils into the circulationfrom the bone marrow. Filgrastim also affects mature neutrophilsby enhancing phagocytic activity, priming the cellularmetabolic pathways associated with the respiratoryburst, enhancing antibody-dependent killing, and increasingthe expression of some functions associated with cell surfaceantigens.
In patients receiving chemotherapy with drugs such ascyclophosphamide, doxorubicin, and etoposide, the incidenceof neutropenia accompanied by fever is rather high.Administration of G-CSF reduces the time of neutrophilrecovery and duration of fever in adults with acute myelogenousleukemia. The number of infections, days thatantibiotics are required, and duration of hospitalization arealso reduced.

The drug is generally well tolerated, with the major adverse reaction being mild to moderate bone pain secondary to stimulation of bone marrow proliferation.

Filgrastim may be of benefit in treating neutropenias in dogs or cats when the intrinsic response to endogenously produced cytokines is thought to be inadequate and there is evidence that there are precursors in the bone marrow available. Because of the drug’s cost and lack of good evidence for its efficacy in reducing mortality versus using antibiotic therapy alone, its use in small animal medicine is somewhat controversial.

Potentially hazardous interactions with other drugs
Cytotoxics: neutropenia possibly exacerbated with capecitabine, fluorouracil and tegafur.

Filgrastim is primarily eliminated by the kidney and neutrophils/neutrophil precursors; the latter presumably involves binding of the growth factor to the G-CSF receptor on the cell surface, internalisation of the growth factor-receptor complexes via endocytosis, and subsequent degradation inside the cells