Gaucher disease type 1 (GD1) is caused by mutations in the GBA1 gene, which result in deficient enzyme β-glucocerebrosidase (GCase) activity and production with the harmful accumulation of the lipid substrate glucocerebroside. Replacement of GCase is current standard of care for GD1; however, GCase has a relatively short active half-life at both physiological and lysosomal pH and biweekly intravenous administration does not provide a consistent exposure to active enzyme. FLT201 is the first adeno-associated virus (AAV) gene therapy in clinical trials for treatment of GD1. FLT201 consists of a rationally designed AAV capsid (AAVS3) containing an expression cassette with an engineered GBA1 transgene that encodes a unique glucocerebrosidase variant (GCase85). GCase85 includes an engineered disulfide, which results in a >6-fold increase in active half-life in human serum and a >21-fold increase in active half-life at lysosomal pH conditions, with similar catalytic properties to those of wild-type and exogenous GCase. Preclinical data indicate that FLT201 could offer a durable treatment for Gaucher disease type 1, addressing unmet needs related to substrate accumulation in tissues poorly treated by current enzyme replacement therapy. The improved stability of the engineered GCase85 variant is predicted to be crucial for FLT201's therapeutic effectiveness.
FLT201, a novel liver-directed AAV gene therapy candidate for Gaucher disease type 1.
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作者:Comper Fabrizio, Miranda Carlos J, Liou Benjamin, Dodev Tihomir, Jeyakumar Jey M, Canavese Miriam, Cocita Clement, Khoshrou Khashayar, Tiscornia Gustavo, Chisari Elisa, Stotter Emmaline, Shehu Erald, Sridharan Sudharsan, Yu I-Mei, Pandya Jalpa, Khinder Jaminder, Northcott Natalie, Kalcheva Petya, Correia Samantha, Sun Ying, Dane Allison P, Sheridan Rose, Nathwani Amit C, Corbau Romuald
| 期刊: | Molecular Therapy | 影响因子: | 12.000 |
| 时间: | 2025 | 起止号: | 2025 Aug 6; 33(8):3789-3807 |
| doi: | 10.1016/j.ymthe.2025.05.003 | ||
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