Colony Stimulating Factor (CSF) Drugs

Colony-Stimulating Factor Function

Colony-stimulating factors (CSFs) activate intracellular signaling pathways that can cause the cells to proliferate and differentiate into a specific kind of blood cell (usually white blood cells. For red blood cell formation, see erythropoietin).

Colony stimulating factors circulate in the blood, acting as hormones, and are also secreted locally. An example is erythropoietin, which is produced in the kidney and regulates the formation of red blood cells from progenitor cells in the bone marrow.

G-CSF Drug

As a hormone produced by the body that stimulates the bone marrow to produce more white blood cells, G-CSF can be taken as a drug that can reduce the severity and duration of neutropenia in patients with some types of cancer.

Chemotherapy drugs can kill cancer cells. However, they also damage the bone marrow's ability to produce white blood cells. Chemotherapy can cause myelosuppression and unacceptably low levels of white blood cells, making patients susceptible to infections and sepsis. Low level of white blood cells is also known as neutropenia, it increases the patient's risk of contracting an infection. Neutropenia usually comes along with fever. Patients receiving chemotherapy are likely to suffer this complication – called febrile neutropenia. But when they also receive drugs that stimulate white blood cell production, this complication can be relieved.

G-CSF may be used to stimulate the production of white blood cells, thereby reducing the risk of infection, and helping to ensure chemotherapy treatments are given on time and at the planned dose. G-CSF isn't needed with all types of chemotherapy, as white blood cells usually recover on their own.

GM-CSF Therapy

GM-CSF can be used as a medication to stimulate the production of white blood cells following chemotherapy. GM-CSF is found in high levels in joints with rheumatoid arthritis and blocking GM-CSF may reduce the inflammation or damage. Some drugs (e.g. MOR103) are being developed to block GM-CSF.

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