Dyne Therapeutics has patented a method for reducing DMPK expression in muscle cells by administering a complex with an anti-transferrin receptor antibody linked to an oligonucleotide targeting DMPK RNA. The oligonucleotide degrades DMPK RNA via RNase H mediated degradation, offering a potential treatment for diseases associated with DMPK alleles. GlobalData’s report on Dyne Therapeutics gives a 360-degree view of the company including its patenting strategy. Buy the report here.
According to GlobalData’s company profile on Dyne Therapeutics, Antibody-conjugate nanoparticles was a key innovation area identified from patents. Dyne Therapeutics's grant share as of February 2024 was 8%. Grant share is based on the ratio of number of grants to total number of patents.
Patent granted for method of reducing dmpk expression in muscle
A recently granted patent (Publication Number: US11911484B2) discloses a method for reducing the expression level of DMPK in muscle cells of a subject. The method involves administering a complex intravenously to the subject, comprising an anti-transferrin receptor antibody covalently linked to an oligonucleotide targeting a DMPK RNA. The oligonucleotide, 15-18 nucleotides in length, is designed to degrade the DMPK RNA via RNase H mediated degradation. The complex is configured to deliver the oligonucleotide into muscle cells, with the antibody binding to the transferrin receptor protein 1 (TfR1) of the subject.
Furthermore, the patent claims detail various aspects of the method, including the specific structure of the oligonucleotide, the protease-sensitive linker connecting it to the antibody, and the role of lysosomal and/or endosomal proteases in cleaving the linker. The method aims to reduce DMPK RNA levels by at least 50% in muscle cells, potentially rescuing splicing defects. The application of the complex is specified for skeletal, cardiac, or smooth muscle cells in human or cynomolgus subjects, particularly targeting disease-associated repeat sequences linked to myotonic dystrophy type 1 (DM1). The administration of the complex through intravenous infusion highlights the potential therapeutic implications of this method in addressing muscle-related disorders.
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