Anagrelid is not a substrate, inhibitor or inducer of CYP3A4 or 2C9. Probably only insignificant hepatic exposure. No signs of autoinduction or induction of CYP-metabolism of other drugs. Side effects such as nausea, anorexia and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Anagrelide is an imidazoquinazoline-derivative.

Anagrelide is an antineoplastic agent used in essential thromocytemia for reduction of blood platelet number. It is administered orally. Common adverse reactions of anagrelide that can be confused with an acute porphyric attack are nausea, vomiting, diarrhoea, abdominal pain, and tachycardia. Side effects such as nausea, anorexia and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Probably insignificant.

Metabolized by CYPA2, less than 1 per cent recovered in urine as unchanged drug. When using various expressed human cytochrome systems only CYP1A2 appeared to metabolise the drug. Weak inhibitor of CYPA2. Effects on CYP metabolism of other drugs not noted. There is no evidence of auto-induction of the anagrelide clearance. In vivo interaction studies in humans have demonstrated that anagrelide does not affect the pharmacokinetic properties of digoxin or warfarin, a known substrate of CYP3A4 and 2C9, therefore not strong inhibitor or inducer of CYP3A4 or 2C9.