G-CSF

G-CSF acts on hematopoietic stem and progenitor cells, binding to the G-CSF receptor (CSF3R) to stimulate proliferation, differentiation, and survival of neutrophil precursors in the bone marrow, and promotes their release into circulation. Endogenously, it is produced by macrophages, endothelial cells, and fibroblasts in response to infection or inflammation, forming part of the acute response to increase neutrophil counts.

Clinically, recombinant forms—filgrastim (short-acting) and pegfilgrastim (long-acting, PEGylated)—are used to: (1) reduce the duration and severity of neutropenia following myelosuppressive chemotherapy, lowering risk of febrile neutropenia; (2) treat congenital neutropenia (e.g., Kostmann syndrome) and cyclic neutropenia; (3) mobilize CD34+ hematopoietic stem cells from bone marrow into peripheral blood for collection prior to autologous or allogeneic stem cell transplantation; and (4) manage neutropenia in aplastic anemia or myelodysplastic syndromes in select cases.

Key adverse effects include bone pain (due to marrow expansion), splenomegaly/rare splenic rupture, and theoretical concern for stimulating growth of myeloid malignancies. Leukocytosis is an expected pharmacologic effect, not toxicity. Important to distinguish from GM-CSF (sargramostim), which stimulates a broader range of myeloid lineages (granulocytes, macrophages, eosinophils) and has a different side effect profile.

High-yield test points: recognize filgrastim/pegfilgrastim as G-CSF analogs, understand the mechanism of neutrophil production stimulation, and recall bone pain as a classic side effect. Differentiate G-CSF (neutrophil-specific) from GM-CSF (broader myeloid stimulation) and erythropoietin (RBC-specific) and thrombopoietin (platelet-specific) growth factors in the hematopoietic growth factor family.