[5][6] Functionally, it is a cytokine and hormone, a type of colony-stimulating factor, and is produced by a number of different tissues.

The more-abundant and more-active 174-amino acid form has been used in the development of pharmaceutical products by recombinant DNA (rDNA) technology.

[citation needed] Chemotherapy can cause myelosuppression and unacceptably low levels of white blood cells (leukopenia), making patients susceptible to infections and sepsis.

In oncology and hematology, a recombinant form of G-CSF is used with certain cancer patients to accelerate recovery and reduce mortality from neutropenia after chemotherapy, allowing higher-intensity treatment regimens.

[22] Two research teams independently identified mouse colony stimulating factors in the 1960s: Ray Bradley at University of Melbourne and Donald Metcalf at Walter and Eliza Hall Institute, from Australia, and Yasuo Ichikawa, Dov Pluznik and Leo Sachs at the Weizmann Institute of Science, Israel.

[23][24][7] In 1980 Antony Burgess and Donald Metcalf discovered that mouse lung conditioned medium contained at least two different CSFs [25] - GM-CSF, which they had purified in 1977 and a G-CSF which stimulated the production of colonies of neutrophils.

In 1983, Donald Metcalf's research team, led by Nicos Nicola, isolated the murine cytokine from medium conditioned with lung tissue obtained from endotoxin-treated mice.

[26][27][7] In 1985, Karl Welte, Erich Platzer, Janice Gabrilove, Roland Mertelsmann and Malcolm Moore at the Memorial Sloan Kettering Cancer Center (MSK) purified human G-CSF produced by bladder cancer cell line 5637 from conditioned medium.

[citation needed] The Food and Drugs Administration (FDA) first approved filgrastim on February 20, 1991 marketed by Amgen with the brand name Neupogen.

[31] It was innitially approved to reduce the risk of infection in patients with non-myeloid malignancies who are taking myelosuppressive anti-cancer drugs associated with febrile neutropenia with fever.

[38] Due to its neuroprotective properties, G-CSF is currently under investigation for cerebral ischemia in a clinical phase IIb [39] and several clinical pilot studies are published for other neurological disease such as amyotrophic lateral sclerosis[40] A combination of human G-CSF and cord blood cells has been shown to reduce impairment from chronic traumatic brain injury in rats.