地拉罗司的疗效好吗？

It is a tridentate iron chelator that combines with ferric iron ions at a ratio of 2:1 to form a complex, which is excreted in the feces, thereby reducing iron storage in the body. Due to the continued presence of deferasirox in plasma, plasma non-transferrin-bound iron can be continuously reduced and the iron formed by toxicity in the body can be directly removed. Today let’s take a look at the efficacy of deferasirox?

Severe aplastic anemia has an acute onset and rapid progression, with fever and bleeding. Especially in extremely severe aplastic anemia, the granulocytes are very low, the natural survival period is short, and the mortality rate is high. This disease means that the hematopoietic function has been severely damaged and cannot produce normal hematopoiesis. Therefore, during routine blood tests, you will find that white blood cells are low, red blood cells are low, platelets are low, and whole blood cell values ​​are all declining. The result is that patients will have varying degrees of bleeding. Deferasirox dispersible tablets (Enrige) are commonly used drugs for the treatment of such diseases.

The pharmacokinetics of deferasirox were studied. Five adult patients with thalassemia took 20 mg of deferasirox orally daily. After 7 days, the pharmacokinetics reached a stable state. Blood, plasma, feces, and urine samples were collected to analyze the concentrations of radioactive deferasirox, Fe-deferasirox complex, and deferasirox metabolites, and study the absorption, distribution, metabolism, and excretion processes of deferasirox. Studies have shown that deferasirox is well absorbed, with radioactive deferasirox and its Fe complex accounting for 87% and 10% of plasma concentrations, respectively, and most of them are excreted in the feces (84%), of which 60% is radioactive deferasirox. Unaltered deferasirox in the feces is partly due to incomplete intestinal absorption and partly due to hepatobiliary elimination of deferasirox and its glucuronide (including first-pass elimination), with renal excretion of only 8%, the main component being glucuronide M6. CYP450 enzymes catalyze deferasirox, and the products are M1 (5-OH deferasirox) (CYP1A) and M4 (5-OH deferasirox) (CYP2D6). Their contents are very small, accounting for only 6% and 2%. Direct and indirect results show that the main metabolic pathway of deferasirox is through glucuronidation to generate the metabolites M3 (acyl glucuronide) and M6 (2-O-glucuronide).

The above is the content of the efficacy, I hope it can help you!