Autoimmune Addison’s disease (AAD) is an autoimmune endocrine disorder with limited therapeutic options and no established disease-modifying treatment. We aimed to identify drug repurposing candidates for AAD based on its genetic architecture. We analyzed six autoimmune diseases clinically related to AAD using genomic structural equation modeling (GSEM) to derive latent factors reflecting shared genetic architecture. Drug-target Mendelian randomization (DTMR) was used to screen protein quantitative traits with putative causal effects on these latent factors and to narrow the candidate protein pool. Candidate proteins were analyzed by DTMR against AAD to confirm the final target proteins. Protein–protein interaction (PPI) network analysis was performed to identify interacting proteins and derive drug repurposing candidates. Two latent factors, an endocrine axis and a non-endocrine axis, were identified, and both showed significant genetic covariance with AAD. A total of 36 proteins were screened by DTMR, and five final target proteins were identified in confirmatory DTMR. IFNGR1 showed genetic evidence of a putative causal effect on AAD. Interferon-gamma, interferon-alpha, and their receptors were identified as proteins directly interacting with IFNGR1, and related repurposing candidates included emapalumab, anifrolumab, rontalizumab, and sifalimumab. Our findings highlight interferon-targeting agents as potential repurposing candidates for AAD.