Archive for December, 2009

Antiandrogens for hair loss treatment

Wednesday, December 30th, 2009

J Steroid Biochem.1986;25:885

Edited for hair loss treatment blog

Pharmacology of antiandrogens.
Neumann F, Töpert M.

Principally, antiandrogens affect all androgen-dependent organs and functions as for instance accessory sexual glands, spermatogenesis, skin and skin appendages, libido and potency, male sexual differentiation, longitudinal bone growth and bone maturation. Pharmacologically, it is important to distinguish between the steroidal antiandrogens of the cyproterone acetate type and the nonsteroidal pure antiandrogens. For the clinical use of cyproterone acetate and similar antiandrogens in both men and women the three main properties are important: Cyproterone acetate is antiandrogenic, it is a quite potent progestogen and it is antigonadotrophic. Based on pharmacological and biochemical backgrounds cyproterone acetate is used in the following indications: Androgen mediated disorders of the skin such as acne, seborrhoea, hirsutism, hair loss treatment, prostatic carcinoma, precocious puberty and male hypersexuality. In order to avoid undesired systemic side effects local application of antiandrogens, e.g. of cyproterone acetate, has been tried several times.snip.. 17 alpha-propylmesterolone is active when given topically (hamster ear model) and has no systemic antiandrogenic effects. This antiandrogen is highly lipophilic and does penetrate preferentially through the hair follicle as has been shown by autoradiography.

The hair regrowth cycle

Wednesday, December 2nd, 2009

“..Recent reports have shown that apoptosis contributes to the hair cycle of regrowth and loss. It is now firmly established that apoptosis is regulated by an intracellular proteolytic cascade, primarily mediated by members of the caspase family of cysteine proteases, which cleave one another and various key intracellular target proteins to destroy the cell. Two prototypical signalling pathways for the induction of apoptosis have been described. One pathway involves ligation of death receptors that activate procaspase 8 and possibly other initiator caspases. The other pathway is controlled by the mitochondrion and involves the apoptosis protease inducing factor-1. Once activated by cytochrome c,, together with cofactor nucleotide triphosphates, they then bind and activate procaspase 9, which in turn cleaves and activates caspase 3 and other downstream caspases. Therefore, caspase 8 and 9 represent the pinnical caspases in the death receptors and cytochrome c/Apap-1 pathways respectively….”