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Therefore, specific targeting of complement inhibitors to the site of complement activation is a potential therapeutic strategy for treatment of MG. Methods: We assessed expression of single\u2010chain antibody fragment\u2013decay accelerating factor (scFv\u2010DAF), comprising a single\u2010chain fragment scFv1956 based on the rat complement inhibitor DAF in prokaryotic systems, and studied its inhibitory effect on complement deposition <jats:italic>in vitro<\/jats:italic>. Results: The recombinant conjugate scFv\u2010DAF completely retained the wild\u2010type binding activity of scFv1956 to AChR and inhibited complement activation of DAF <jats:italic>in vitro<\/jats:italic>. Conclusions: We found that scFv\u2010DAF could bind specifically to TE671 cells, and it is significantly more potent at inhibiting complement deposition than the untargeted parent molecule DAF. scFv\u2010DAF may be a candidate for <jats:italic>in vivo<\/jats:italic> protection of the AChR in MG. 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