INTRODUCTION
Minoxidil is a widely accepted medication for hair loss, with extensive regional coverage and various application methods, including solutions and foam formulations that are available over the counter in the United States. These formulations primarily range in concentration from 2% to 5%, with custom compounded formulations available at concentrations of up to 8% to 10%. Research on various forms of minoxidil, including topical, oral, and injectable options, is expanding the treatment possibilities for dermatologists, with significant potential for nonsurgical and minimally invasive approaches to hair loss.
Approximately 1.4% of topical minoxidil can be absorbed through the scalp. Oral minoxidil, typically prescribed by dermatologists in doses ranging from 0.625 to 2.5 mg daily, has a bioavailability of 0.27 to 0.55%.1 In comparison, intradermal injection of minoxidil (0.5% dosage) has 100% bioavailability when properly injected into the scalp in an insulin syringe with a 30-gauge needle. As a prodrug, topical minoxidil efficacy requires bio-activation into minoxidil sulfate by sulfotransferase in hair follicle outer root sheath cells (ORS), whose activity predicts topical minoxidil therapeutic response. Interestingly, hair growth associated with oral minoxidil is also predicted by sulfotransferase activity as opposed to the liver, the primary absorption site of oral minoxidil. The exact bioavailability and accumulated concentration of low-dose oral minoxidil within the scalp is yet to be elucidated.
Minoxidil functions as a potent vasodilator that induces hyperpolarization by stimulating the opening of potassium channels, essential for the transition into the G1 stage of the cell cycle. At a cellular level, Minoxidil plays a crucial role in cell proliferation at an early stage. In animal studies, minoxidil thus increases cellular DNA synthesis and enhances cell proliferation. The enzyme responsible to convert minoxidil into its metabolite minoxidil sulfate is sulfotransferase, located in hair follicles and varying in concentration among individuals. Minoxidil-treated hair follicles have a reduced telogen phase and an extended anagen phase, which stimulates follicular proliferation and differentiation, further increasing both follicular size and percentage of anagen follicle.
Approximately 1.4% of topical minoxidil can be absorbed through the scalp. Oral minoxidil, typically prescribed by dermatologists in doses ranging from 0.625 to 2.5 mg daily, has a bioavailability of 0.27 to 0.55%.1 In comparison, intradermal injection of minoxidil (0.5% dosage) has 100% bioavailability when properly injected into the scalp in an insulin syringe with a 30-gauge needle. As a prodrug, topical minoxidil efficacy requires bio-activation into minoxidil sulfate by sulfotransferase in hair follicle outer root sheath cells (ORS), whose activity predicts topical minoxidil therapeutic response. Interestingly, hair growth associated with oral minoxidil is also predicted by sulfotransferase activity as opposed to the liver, the primary absorption site of oral minoxidil. The exact bioavailability and accumulated concentration of low-dose oral minoxidil within the scalp is yet to be elucidated.
Minoxidil functions as a potent vasodilator that induces hyperpolarization by stimulating the opening of potassium channels, essential for the transition into the G1 stage of the cell cycle. At a cellular level, Minoxidil plays a crucial role in cell proliferation at an early stage. In animal studies, minoxidil thus increases cellular DNA synthesis and enhances cell proliferation. The enzyme responsible to convert minoxidil into its metabolite minoxidil sulfate is sulfotransferase, located in hair follicles and varying in concentration among individuals. Minoxidil-treated hair follicles have a reduced telogen phase and an extended anagen phase, which stimulates follicular proliferation and differentiation, further increasing both follicular size and percentage of anagen follicle.
