What is the mechanism of action of filgrastim?

What is the mechanism of action of filgrastim?

Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils.

How is G-CSF regulated?

G-CSF can be regulated by transcriptional and post-transcriptional mechanisms. (Center) The increase in G-CSF synthesis stimulates neutrophil production in the bone marrow (anatomical details are not shown).

What does G-CSF bind?

Each receptor is activated by their cognate cytokine, colony stimulating factor (CSF), and the incidence of cross-talk among these cytokine receptors is largely unknown. CSFs are smaller molecular weight secreted glycoproteins which bind to the cell surface receptors of hematopoietic stem cells.

Is GM CSF a cytokine?

Multiple studies have demonstrated that GM-CSF is also an immune-modulatory cytokine, capable of affecting not only the phenotype of myeloid lineage cells, but also T-cell activation through various myeloid intermediaries.

Is G-CSF a cytokine?

Mammalian granulocyte colony-stimulating factor (G-CSF; CSF3) is a primary cytokine that promotes the development, mobilization, and activation of neutrophils and their precursors.

Where is granulocyte colony-stimulating factor?

Granulocyte colony-stimulating factor is injected into the fatty portion of the skin, usually in the upper arm, thigh, or abdomen. To avoid infection, you should wash your hands before and after the injection and clean the injection site. Each needle should be used only once and disposed of properly.

Does G-CSF increase neutrophils?

Further, G-CSF influences the function of mature neutrophils. These actions underpin its rapid uptake into clinical medicine as a drug that increases the production of neutrophils in patients with chemotherapy-induced neutropenia.

Why is G-CSF given 24 hours after chemo?

G-CSFs are administered between 24-72 hours after receiving chemotherapy. The reason for this minimum 24-hour delay is to allow the body time to metabolize and excrete the cytotoxic drugs.

Is GM-CSF proinflammatory?

GM-CSF was first characterized as a pro-inflammatory cytokine due to its ability to stimulate plasminogen-dependent fibrinolysis activity in mouse macrophages (Hamilton and others 1980).

What does GM-CSF do to dendritic cells?

GM-CSF (Csf-2) is a critical cytokine for the in vitro generation of dendritic cells (DCs) and is thought to control the development of inflammatory DCs and resident CD103+ DCs in some tissues.

Does G-CSF increase platelet count?

G-CSF administration induces an inflammatory process with endothelial cell activation. This is probably the reason why platelet volume increases after G-CSF use.

Why is filgrastim given after chemotherapy?

Filgrastim is used to stimulate the production of granulocytes (a type of white blood cell) in patients undergoing therapy that will cause low white blood cell counts. This medication is used to prevent infection and neutropenic (low white blood cells) fevers caused by chemotherapy.

What is protein G-CSF?

Granulocyte colony-stimulating factor (G-CSF or GCSF), also known as colony-stimulating factor 3 (CSF 3), is a glycoprotein that stimulates the bone marrow to produce granulocytes and stem cells and release them into the bloodstream.

Does G-CSF increase lymphocytes?

Our data showed that G-CSF treatment induces an increase in peripheral blood lymphocyte counts and a significant reduction in the proliferative response of PBMC to mitogenic stimulation which reverted 14 days after the end of treatment with G-CSF.

Where is granulocyte colony stimulating factor?

G-CSF is produced by endothelium, macrophages, and a number of other immune cells.

Does G-CSF increase hemoglobin?

In cancer patients, it has been reported that G-CSF does not affect the Hb value when administered before,19 during,20 or after chemotherapy. Our results clearly showed that, with a comparable dose intensity, the rate of grade 2 or worse anemia was higher in the G-CSF arm (38.8%) than in control arm (26.2%; P = .