Optimization of Lu-labelling of DOTA-TOC, PSMA-I&T and FAPI-46 for clinical application.

EJNMMI Radiopharm Chem

Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Nuclear Medicine, Augustenburger Platz 1, 13353, Berlin, Germany.

Published: May 2023

Background: Lu-radiopharmaceuticals are routinely used for the treatment of various tumor entities. The productions of radiopharmaceuticals follow strict good-manufacturing practice guidelines and synthesis optimizations thereof have a strong impact on e.g. the quality of the product, radiation safety and costs. The purpose of this study is to optimize the precursor load of three radiopharmaceuticals. For that, different precursor loads were evaluated and compared to previously reported findings.

Results: All three radiopharmaceuticals were successfully synthesized in high radiochemical purities and yields on the ML Eazy. The precursor load was optimized for [Lu]Lu-FAPI-46 from 27.0 to 9.7 µg/GBq, for [Lu]Lu-DOTATOC from 11 to 10 µg/GBq and for [Lu]Lu-PSMA-I&T from 16.3 to 11.6 µg/GBq.

Conclusions: We successfully reduced the precursor load for all three radiopharmaceuticals while maintaining their quality.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10219910PMC
http://dx.doi.org/10.1186/s41181-023-00196-1DOI Listing

Publication Analysis

Top Keywords

precursor load
12
three radiopharmaceuticals
12
load three
8
optimization lu-labelling
4
lu-labelling dota-toc
4
dota-toc psma-i&t
4
psma-i&t fapi-46
4
fapi-46 clinical
4
clinical application
4
application background
4

Similar Publications

Background: Autosomal dominant Alzheimer's Disease (ADAD) represents around 0.5% of all AD cases, and is caused by mutations in PSEN1, PSEN2 and APP genes. Gene expression studies can be useful for unravelling the physiopathology of AD and identifying potential biomarkers.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

The Jackson Laboratory, Bar Harbor, ME, USA.

Background: Late-onset Alzheimer's disease (LOAD) is the leading cause of dementia and a major contributor to increased mortality. Recent human datasets have revealed many LOAD genetic risk factors that are correlated with the degree of AD burden. Further, the complexity and heterogeneity of LOAD appears to be promoted by interactions between genetics and environmental factors such as diet, sedentary behavior, and exposure to toxicants, like lead (Pb), cadmium (Cd), and arsenic (As).

View Article and Find Full Text PDF

Background: While social and medical debate about the efficacy and safety of anti-Aβ immunotherapy is ongoing, one thing that emerged is that we have little understanding of the working mechanisms of these antibodies and this lack of knowledge complicates the interpretation of the clinical results. Here, we aimed to establish if microglia are required for the efficacy of Lecanemab, one of the most promising FDA-approved disease-modifying therapy for AD (Van Dyck et al. N Engl J Med 2023).

View Article and Find Full Text PDF

Background: Chronic heavy alcohol drinking may be a modifiable risk factor for Alzheimer's disease (AD), but studies in rodent AD models more closely mimic chronic moderate alcohol drinking in humans and largely focus on the brain. The role of the liver, which is significantly impacted by chronic heavy alcohol intake, in driving brain changes in alcohol-dependent AD remains unexplored. Our study using intragastric-ethanol feeding, which mimics chronic heavy alcohol intake in humans, in C57BL/6J mice showed significant AD-relevant changes in the brain and liver.

View Article and Find Full Text PDF

Background: Late-onset Alzheimer's disease (LOAD) represents the majority of human AD cases, yet the availability of animal models that accurately reflect LOAD progression and pathology is limited. Traditional transgenic mouse models including 3xTg-AD and 5xFAD rely on supraphysiological overexpression of familial AD risk genes, failing to adequately replicate the disease progression observed in LOAD. Here, we present the first characterization of MODEL-AD1 (MAD1), a platform mouse developed by the Model Organism Development and Evaluation for Late-onset Alzheimer's Disease (MODEL-AD) Consortium.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!