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
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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.
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