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Preclinical findings demonstrate that a fusion protein reduces complement levels in C3 glomerulopathy, suggesting a new treatment strategy.
Taken together, the FHR51-9FH1-5 protein reduced glomerular C3 in experimental models of C3 glomerulopathy driven by either factor H deficiency or mutated FHR5. These preclinical data indicate that FHR51-9FH1-5 protein represents a novel treatment strategy for complement-mediated kidney disease.
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Malik et al. (2026) studied this question.
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