No observations pointing to interference with CYP-metabolism of other drugs. Not listed as CYP-inducer. Found to be weak CYP-inhibitor in in-vitro studies, but the concentration needed to inhibit is much higher than reached during therapy. However, side effects such as anorexia, nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Vinorelbine is a semisynthetic derivative of vinblastine, structuturally modified in the catharantine part of the molecule. Administered as tartrate salt, hygroscopic and freely soluble in water.

Vinorelbine is used in the treatment of advanced breast cancer and non-small cell lung cancers, and has been tried in other malignancies including lymphomas and tumours of ovary and prostate. It can be administered by intravenous injection or orally. Common adverse reactions of vinorelbine that can be confused with an acute porphyric attack are nausea, vomiting, diarrhoea or obstipation, neuromotor disturbances, peripherel neuropathy or peripheral numbness and loss of deep tendon refelexes. Side effects such as anorexia, nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Metabolism of vinorelbine is mediated by CYP3A4. The main active metabolite is 4-O-deacetyl vinorelbine. Metabolites mainly excreted via bile. Kajita (2000) found that vinorelbine is a substrate and an inhibitor of CYP 3A4 in-vitro, however the plasmakoncentrations of vinorelbine needed for inhibition are much higher than those reached during therapy. Listed as an inhibitor of CYP 2D6 and as a substrate and a weak inhibitor of CYP 3A4 by Rendic (2002) and Zhou (2007). Metabolites excreted mainly via bile. No observations of interferences with CYP-metabolism of other drugs. Not listed as CYP-inducer.

Reports of uneventful use: Kristiansen (2006) reported uneventful use of vinorelbine in the treatment of breast cancer in a 42 year old female AIP-patient.

No.