Diazoxide is a nondiuretic benzothiazide. This potent and rarely anti-hypertensive agent has diverse pharmacologic effects including:
- Hypertrichosis (hair growth).
- Hyperglycemia associated with suppression of insulin release, which is why it is used to treat idiopathic hypoglycemia of infancy.
- Elevation of serum levels of androgens.
Taking advantage of the hypertrichotic side effects of diazoxide, several authors have examined the effect of topical application of the drug on hair re-growth in androgenetic alopecia. A topical formulation of diazoxide was reported in 1989 to show efficacy in male pattern baldness. Nineteen men with “early to midstage” androgenetic alopecia were treated with 3% diazoxide solution twice daily for 2 to 11 months. Reports indicate that four men had a dense growth of new hair, seven had moderate growth by way of some new terminal hairs, one had vellus hair growth, and seven had no re-growth at all. Local irritation occurred in one patient.
The potential mechanism of action of diazoxide in hair growth may be through inhibition of phosphodiesterase. Phosphodiesterase (PDE) is an enzyme that catalyzes the hydrolysis of phosphodiester bonds. PDEs are responsible for the degradation of the cyclic nucleotides cAMP and cGMP. They are therefore important regulators of signal transduction mediated by these molecules. In all probability, dihydrotestosterone hinders energy production by keeping phosphodiesterase relatively inactive and by suppressing various protein (enzyme) synthetases. A relatively high concentration of cAMP may cause premature termination of the growing stages of hair follicles. Repetition of such processes over several years presumably transforms terminal follicles to vellus – type follicles and ultimately causes baldness. However, this theory on the metamorphosis of terminal hair to vellus hair is not proven as yet.
Research studies provide correlative evidence that the opening of potassium channels is an important regulatory mechanism for hair growth. Diazoxide has also been shown, like Minoxidil, to be a potassium channel opener. Therefore oral diazoxide can induce hypertrichosis in a distribution similar to that caused by oral minoxidil but with far less frequency.