Insignificant hepatic exposure. Little is known about the metabolism of cladribine, but as there is no data supporting CYP-affinity or capacity for CYP-induction or inhibition, probably non-CYP metabolism. However, side effects such as nausea, vomiting and loss of appetite may be potentially porphyrinogenic through reduction in caloric intake.

Cladribine is a chlorinated purine nucleoside analogue (chemical name: 2-chloro-2-deoxy-adenosine).

Cladribine is used to treat active hairy cell leukemia, and is being tested for use in multiple sclerosis. Administered as an infusion. Common adverse reactions of cladribine that can be confused with an acute porphyric attack are nausea, vomiting, obstipation or diarrhoes, abdominal pain, tachycardia and myalgia. Side effects such as nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Insignificant hepatic exposure. The recommended intravenous dose of cladribine is a single course of 0,1 mg/kg daily for 7 days by continuous infusion. Piro et al (1988) found that 0.05 to 0.2 mg/kg/daily via continuous infusion for 7 days resulted in daily drug levels of less than 10 nanomoles/liter during therapy, well below the 1 micromolar limit.

Plasma concentration of cladribine declines multiexponentially with time; terminal half life 3-20 h. Steady state plasma concentration is about 5.7 ng/ml. Accumulates in cells deficient in deoxynucleotidas (lymphocytes, monocytes) and undergoes consecutive phosphorlylations to the active triphosphate nucleotid (CdATP). Limited information on metabolism and elimination. No observations of interactions with CYP-metabolized drugs. Not listed by Rendic as having CYP-affinity or capable of CYP-induction or inhibition.

No.