Filgrastim(granulocytecolony)

Base Information

• Chemical Name: Filgrastim(granulocytecolony)
• CAS No.: 143011-72-7
• Molecular Weight: 0
• Mol file: 143011-72-7.mol

Synonyms:CSF-b;Colony-stimulating factor 3;G-CSF;GM-DF;Granocyte;Granulocyte colony-stimulating factor;Hebervital;MGI 2;Pluripoietin;

Chemical Property of Filgrastim(granulocytecolony)

Chemical Property:

• PSA: 0.00000
• LogP: 0.00000

Purity/Quality:

98%,99%, ^*data from raw suppliers

Granulocyte Colony Stimulating Factor ^*data from reagent suppliers

Safty Information:

• Pictogram(s):  
• Hazard Codes: 

MSDS Files:

Useful:

• Biological functions: G-CSF stimulates the proliferation, differentiation, and survival of neutrophil precursors in the bone marrow to promote their maturation process. G-CSF exerts minimal direct effects on the production of hematopoietic cell types other than the neutrophil lineage, as obtained in white blood cell differentials during clinical trials. The G-CSF-G-CSFR signaling in mature neutrophils activates multiple effector functions in response to bacterial infections, such as superoxide anion generation, the release of arachidonic acid, and the production of leukocyte alkaline phosphatase and myeloperoxidase. Neurons of the CNS express both G-CSF and G-CSF-R, suggesting an autocrine neuroprotection system, as a nonhematopoietic function
• Description: Granulocyte colony-stimulating factor is the primary regulator of proliferation and differentiation, maturation, survival, and functions of neutrophils/ granulocytes to exert biological defense mechanisms via neutrophil progenitors in the bone marrow. The bone marrow colony-forming activity of maturing granulocytes was recognized in various cell and tissue cultures. Murine G-CSF was first purified from a lungconditioned medium from mice injected with bacterial endotoxin. The human G-CSF was purified from the conditioned media of tumor cell lines, and the cDNA was independently cloned in 1986 by two groups.
• Clinical Use: Recombinant G-CSF therapies by filgrastim and lenograstim have been established in several indications. Primarily, G-CSF is administered to patients with severe congenital or chronic neutropenia caused by a myeloid maturation arrest in the bone marrow. G-CSF is also applicable to therapy-induced neutropenia developed in cancer patients receiving myelosuppressive chemotherapy and bone marrow transplant and in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. In addition, G-CSF induces the release of hematopoietic stem and progenitor cells from the bone marrow into the peripheral blood. Therefore, G-CSF is used in transplantation therapy for the mobilization and isolation of peripheral hematopoietic stem cells. The stem cell mobilization by G-CSF is supported by multiple mechanisms, including proteolytic enzyme release, the modulation of adhesion molecules, and the activation of CXCR4 chemokine receptors. Recently, the nonhemopoietic role of G-CSF has been evaluated in clinical trials including spinal cord injury by the ability of G-CSF for neuroprotective and neuroregenerative actions.