26-SNP Panel Aids Guiding Androgenetic Alopecia Therapy and Provides Insight into Mechanisms of Action

Inter-individual variability in response to androgenetic alopecia (AGA) therapies remains a therapeutic challenge. This study evaluated the clinical and mechanistic utility of a 26-SNP pharmacogenetic panel in guiding treatment decisions. By using a database containing data from 252 individuals stratified by genotype, overall response rates were high (85.6–91.0%), exceeding published benchmarks for minoxidil, finasteride, and dutasteride. SNP association analysis identified rs1042028 in SULT1A1 as a robust predictor of poor response across all three drugs (minoxidil: p = 2.4 × 10−8, OR = 0.09; dutasteride: p = 0.023, OR = 0.21; finasteride: p = 0.025, OR = 0.11). For dutasteride, the TT genotype of rs39848 in SRD5A1 was also associated with reduced efficacy (p = 0.018, OR = 0.02). SNP–SNP interaction analysis revealed significant epistatic effects between genes involved in prostaglandin signalling and oxidative stress response, including PTGFR × MUC1 (p = 5.38 × 10−6) and GPR44 × FUT2 (p = 9.4 × 10−5). Network enrichment analyses further supported drug-specific mechanistic clusters. Importantly, no statistically significant differences in response were observed between pharmacogenetically guided treatment groups (p > 0.1), suggesting successful genotype-based alignment. Together, these findings demonstrate that SNP-informed therapy can enhance efficacy, clarify drug mechanisms, and provide a foundation for precision treatment in AGA.