| Identification | Back Directory | [Name]
FILGRASTIM | [CAS]
121181-53-1 | [Synonyms]
Figrastim
FILGRASTIM
Filgrastim CRS
FILGRASTIM USP/EP/BP
Filgrastim
DISCONTINUED
filgrastimconcentratedSolution
n-l-methionyl-colony-stimulatingfactor(humanclone1034
Filgrastim for Bioassay (96,815 IU) (COLD SHIPMENT REQUIRED)
Filgrastim System Suitability (COLD SHIPMENT REQUIRED) (1 mg)
Colony-stiMulating factor (huMan clone 1034), N-L-Methionyl- (9CI) | [Molecular Formula]
W99 | [MDL Number]
MFCD01771574 |
| Hazard Information | Back Directory | [Chemical Properties]
Clear, colourless or slightly yellowish liquid | [Uses]
Antineutropenic; hematopoietic stimulant. | [Brand name]
Neupogen (Amgen). | [Description]
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. | [Originator]
Amgen (U.S.A.) | [Indications]
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. | [Clinical Use]
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. | [Clinical Use]
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. | [Side effects]
The drug is generally well tolerated, with the major
adverse reaction being mild to moderate bone pain secondary
to stimulation of bone marrow proliferation. | [Veterinary Drugs and Treatments]
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. | [Drug interactions]
Potentially hazardous interactions with other drugs
Cytotoxics: neutropenia possibly exacerbated with
capecitabine, fluorouracil and tegafur. | [Metabolism]
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 |
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