Single domain antibody-scFv conjugate targeting amyloid β and TfR penetrates the blood-brain barrier and interacts with amyloid β

MAbs. 2024 Jan-Dec;16(1):2410968. doi: 10.1080/19420862.2024.2410968. Epub 2024 Oct 2.

Abstract

Neurodegenerative diseases such as Alzheimer's disease (AD) pose substantial challenges to patients and health-care systems, particularly in countries with aging populations. Immunotherapies, including the marketed antibodies lecanemab (Leqembi®) and donanemab (KisunlaTM), offer promise but face hurdles due to limited delivery across the blood-brain barrier (BBB). This limitation necessitates high doses, resulting in increased costs and a higher risk of side effects. This study explores transferrin receptor (TfR)-binding camelid single-domain antibodies (VHHs) for facilitated brain delivery. We developed and evaluated fusion proteins (FPs) combining VHHs with human IgG Fc domains or single-chain variable fragments (scFvs) of the anti-amyloid-beta (Aβ) antibody 3D6. In vitro assessments showed varying affinities of the FPs for TfR. In vivo evaluations indicated that specific VHH-Fc and VHH-scFv fusions reached significant brain concentrations, emphasizing the importance of optimal TfR binding affinities. The VHH-scFv fusions were further investigated in mouse models with Aβ pathology, showing higher retention compared to wild-type mice without Aβ pathology. Our findings suggest that these novel VHH-based FPs hold potential for therapeutic and diagnostic applications in AD, providing a strategy to overcome BBB limitations and enhance brain targeting of antibody-based treatments. Furthermore, our results suggest that a given bispecific TfR-binding fusion format has a window of "optimal" affinity where parenchymal delivery is adequate, while blood pharmacokinetics aligns with the desired application of the fusion protein.

Keywords: Blood-brain barrier; VHH; brain delivery; camelid antibody; fusion protein; transferrin receptor.

MeSH terms

  • Alzheimer Disease* / drug therapy
  • Alzheimer Disease* / immunology
  • Alzheimer Disease* / metabolism
  • Amyloid beta-Peptides* / immunology
  • Amyloid beta-Peptides* / metabolism
  • Animals
  • Blood-Brain Barrier* / metabolism
  • Brain / immunology
  • Brain / metabolism
  • Humans
  • Immunoconjugates / immunology
  • Immunoconjugates / pharmacokinetics
  • Immunoconjugates / pharmacology
  • Mice
  • Receptors, Transferrin* / immunology
  • Receptors, Transferrin* / metabolism
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / immunology
  • Single-Chain Antibodies* / immunology
  • Single-Domain Antibodies* / immunology

Substances

  • Amyloid beta-Peptides
  • Receptors, Transferrin
  • Single-Chain Antibodies
  • Single-Domain Antibodies
  • Recombinant Fusion Proteins
  • Immunoconjugates

Grants and funding

Open access funding provided by Uppsala University. This work was supported by Hans-Gabriel och Alice Trolle-Wachtmeisters stiftelse för medicinsk forskning, Grants from the Swedish Research Council (2021-01083 and 2021-03524), the Swedish Innovation Agency, Alzheimerfonden, Hjärnfonden, Torsten Söderbergs stiftelse, Åhlenstiftelsen, Stiftelsen för gamla tjänarinnor, Stohnes stiftelse, Magnus Bergvalls stiftelse, Konung Gustaf V:s och Drottning Victorias frimurarestiftelse and Åke Wibergs stiftelse. The funding bodies did not take part in design of the study, in collection, analysis, or interpretation of data, nor in writing the manuscript.