<0.001 EU per 1 μg of the protein by the LAL method
This drug is a leucocyte growth factor indicated to:Decrease the incidence of infection‚ as manifested by febrile neutropenia‚in patients with nonmyeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a significant incidence of severe neutropenia with fever. Reduce the time to neutrophil recovery and the duration of fever, following induction or consolidation chemotherapy treatment in patients with acute myeloid leukemia (AML)Reduce the duration of neutropenia and neutropenia-related clinical sequelae‚ e.g.‚ febrile neutropenia, in patients with nonmyeloid malignancies undergoing myeloablative chemotherapy followed by bone marrow transplantation (BMT)Mobilize autologous hematopoietic progenitor cells into the peripheral blood for collection by leukapheresisReduce the incidence and duration of sequelae of severe neutropenia (e.g.‚ fever‚ infections‚ oropharyngeal ulcers) in symptomatic patients with congenital neutropenia‚ cyclic neutropenia‚ or idiopathic neutropenia.Neupogen is approved for treatment of patients with radiation-induced myelosuppression following a radiological/nuclear incident.
Examples of Clinical Use:
The product binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow.Colony-stimulating factors are glycoproteins which act on hematopoietic cells by binding to specific cell surface receptors, in turn, stimulating proliferation and differentiation.G-CSF and its receptor are necessary for basal and stress-induced granulopoiesis, which forms neutrophils. Mice deficient in G-CSF or G-CSFR have severe neutropenia and reduced levels (~50%) of late-stage neutrophil precursors in the bone marrow under normal, resting conditions.Endogenous G-CSF is a lineage-specific colony-stimulating factor that is produced by monocytes‚ fibroblasts, and endothelial cells. G-CSF regulates the production of neutrophils within the bone marrow and enhances neutrophil progenitor proliferation‚ differentiation, and selected end-cell functions (including enhanced phagocytic ability‚ priming of the cellular metabolism associated with respiratory burst‚ antibody-dependent killing, and enhanced expression of certain cell surface antigens). G-CSF is not species-specific and has demonstrated to have negligible direct in vivo or in vitro effects on the production or action of hematopoietic cell types other than the neutrophil and its lineage.
Mechanism of action:
As a G-CSF analog, this drug controls the proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and decreases their time to maturation. Filgrastim acts to increase the phagocytic activity of mature neutrophils, thus allowing them to prevent infection. In patients receiving cytotoxic chemotherapy, filgrastim may accelerate neutrophil recovery, leading to a reduction in the duration of the neutropenic phase post chemotherapy.
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