However, the first alpha decay of Ac225 generated enough recoil for the daughter nucleus to break its bond to the conjugate. This is doubly bad since not only are alphas removed from the target site, but the long-lived daughter is now free to travel throughout the body causing damage to healthy tissue. Maximum tolerated dose and therapeutic gain are other comparison endpoints. Cost considerations for preclinical and clinical trials as well as clinical use are relevant.
Considering all these factors, Ac225 is still found to have better or equal performance to Bi213 at much lower cost.
Presented By: Barry Allen from Faculty of Medicine, University of Western Sydney, NSW Australia
Written By: William Carithers, Lawrence Berkeley National Laboratory
at the 10th International Symposium on Targeted Alpha Therapy (TAT-10) May 31 - June 1, 2017 - Kanazawa, Japan.