Deferasirox

Absorption

The absolute bioavailability (AUC) of deferasirox tablets for oral suspension is 70% compared to an intravenous dose.

Description

Linagliptin was originally discovered at Boehringer Ingelheim as an orally active dipeptidyl peptidase-IV (DPP-4) inhibitor. Eli Lilly and Boehringer Ingelheim co-developed and launched linagliptin for type II diabetes as an adjunct to diet and exercise for the improvement of adult glycemic control. Linagliptin has a superior DPP-4 IC50 value of 1 nM, compared with 19 nM for sitagliptin, 24 nM for alogliptin, 50 nM for saxagliptin and 62 nM for vildagliptin. In addition, linagliptin exhibited prolonged pharmacodynamic activity with long-lasting DPP-4 inhibition in several preclinical species. Linagliptin showed good efficacy in phase II clinical trials with doses as low as 5 mg and no signs of hypoglycemia with doses as high as 600 mg. The prolonged pharmacological effect of DPP-4 activity and the good safety/tolerability profile provided the basis for linagliptin’s approval.

The Uses of Deferasirox

Labeled Deferasirox, intended for use as an internal standard for the quantification of Deferasirox by GC- or LC-mass spectrometry.

Background

Deferasirox is an iron chelator and the first oral medication FDA approved for chronic iron overload in patients receiving long term blood transfusions.

Indications

For the treatment of chronic iron overload due to blood transfusions (transfusional hemosiderosis) in patients 2 years of age and older.

What are the applications of Application

Deferasirox is a tridentate chelator that binds iron with high affinity, while having low affinity for zinc and copper.

Pharmacokinetics

Deferasirox is an orally active chelator that is selective for iron (as Fe3+). It is a tridentate ligand that binds iron with high affinity in a 2:1 ratio. Although deferasirox has very low affinity for zinc and copper there are variable decreases in the serum concentration of these trace metals after the administration of deferasirox. The clinical significance of these decreases is uncertain.

Metabolism

Hepatic. CYP450-catalyzed (oxidative) metabolism of deferasirox appears to be minor in humans (about 8%). Glucuronidation is the main metabolic pathway for deferasirox, with subsequent biliary excretion.