If you've ever wondered why topical minoxidil produces visible regrowth in one person and almost nothing in another, the answer has been hiding in plain sight for a decade. Minoxidil itself isn't pharmacologically active, it's a prodrug that requires conversion to minoxidil sulfate to actually affect hair follicles. That conversion is performed by the enzyme sulfotransferase SULT1A1, which is expressed at variable levels in scalp tissue.

Work from the Goren lab and others published between 2014 and 2020 established that scalp SULT1A1 activity follows a roughly trimodal distribution: low, intermediate, and high expressors. Low expressors, estimated at 30–45% of the population in some samples, convert insufficient minoxidil to sulfate to achieve a clinical response, regardless of how religiously they apply the drug. A commercial test for scalp SULT1A1 activity (Minoxidil Response Test) has been available for several years but remains niche in clinical practice.

The practical implication: if you've used 5% minoxidil twice daily for six months with no visible benefit, your scalp may genuinely lack the enzymatic capacity to activate it. Switching to oral minoxidil bypasses the scalp sulfotransferase requirement because the liver performs the conversion systemically. Alternatively, formulations that include adjuvants designed to upregulate SULT1A1 expression, including topical retinoic acid co-application, have a mechanistic basis even if the clinical evidence is thin. This is one of the few areas in hair loss therapeutics where a simple test could meaningfully personalise treatment selection.