RFK antibodies target riboflavin kinase (RFK), an enzyme critical for converting riboflavin (vitamin B2) into flavin mononucleotide (FMN), a precursor of flavin adenine dinucleotide (FAD). Both FMN and FAD serve as essential cofactors in redox reactions, energy production, and cellular metabolism. RFK dysfunction has been linked to mitochondrial disorders, neurodegenerative diseases, and certain cancers, making it a subject of interest in metabolic and autoimmune research.
The discovery of RFK antibodies stems from studies on autoimmune conditions where the immune system mistakenly targets self-proteins. While RFK itself is not a common autoantigen, its antibodies have been identified in niche contexts, such as paraneoplastic syndromes or rare autoimmune disorders. These antibodies may disrupt flavin metabolism, impairing energy-dependent processes and contributing to symptoms like fatigue, neuropathy, or mitochondrial dysfunction. Research also explores their potential as diagnostic biomarkers in specific cancers or metabolic syndromes.
Structurally, RFK antibodies often recognize epitopes in the enzyme’s active or regulatory sites, inhibiting FMN synthesis. This inhibition can exacerbate cellular oxidative stress, linking RFK autoimmunity to pathologies involving redox imbalance. Current studies focus on elucidating their role in disease mechanisms and therapeutic targeting, though clinical relevance remains limited to case reports or small cohorts. Further investigation is needed to clarify their pathogenic significance and utility in personalized medicine.