Filgrastim is a glycoprotein with no hormonal effects of relevance for porphyrogenicity, and no effects on the mechanisms behind hepatic xenobiotic metabolism. However, side effects such as nausea, anorexia and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Filgrastim is a single-chain polypeptide containing 175 amino acids. It is identical to that of endogenous human G-CSF, but differs from the endogenous glycoprotein by the addition of an N-terminal methionine and the absence of glycosylation.

Filgrastim is a haematopoietic growth factor that stimulates the development of granulocytes used to treat or prevent neutropenia. It is also used to mobilise peripheral blood progenitor cells for collection and subsequent use in autologous or allogeneic peripheral blood stem cell transplantation. Filgrastim may be given intravenously or subcutaneously. Common adverse reactions of filgrastim that can be confused with an acute porphyric attack are nausea, vomiting, constipation, diarrhoea, and musculoskeletal pain. Side effects such as nausea, anorexia and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

The metabolic fate of filgrastim has not been fully determined and it is not known whether the drug is metabolized or how it is eliminated from the body. While it has been suggested that receptor-mediated mechanisms of filgrastim clearance (e.g., neutrophilic endocytosis and degradation) may be involved, this hypothesis remains to be established, and other mechanisms may be involved or principally responsible for such neutrophil-associated alterations in elimination.