Ragazzi facendo un giro nella rete ho trovato questo. In pratica si tratta di un inibitore duale (credo quindi simile alla dutasteride) che è stato studiato nel 2000 e di cui, almeno apparentemente, non si sono avute più notizie.
Ecco l'articolo con traduzione a seguito e un'interessante tabella con i risultati della sperimentazione:
Summary : The local conversion of testosterone (T) to the more potent androgen dihydrotestosterone (DHT) by 5alpha-reductase (5aR) is implicated in the pathogenesis of androgenetic alopecia (AGA). Recently, the clinical effectiveness of finasteride, a selective type II 5aR inhibitor, in treating AGA has been documented, and these clinical studies have shown that circulating DHT is lowered by 60-70% in men taking finasteride. The source of the residual circulating DHT is presumed to be due to type I 5aR activity which is not affected by finasteride. Several novel compounds with potent dual inhibitory activity on both isoenzymes have been described and CS-891 is one of them. This compound may be likewise effective in the prevention or treatment of AGA. As a prerequisite for such an action CS-891 should be able to inhibit 5aR activity in its target tissue: the hair follicles (HF). Here we report on the capability of CS-891 to inhibit 5aR activity in dermal papillae (DP) of human HF.
Keywords : androgen, androgenetic alopecia, hair, hair loss.
Pictures
ARTICLE
The local conversion of testosterone (T) to the more potent androgen dihydrotestosterone (DHT) by 5alpha-reductase (5aR) plays a pivotal role in the development of androgenetic alopecia (AGA) and hirsutism [1-3].
There are at least two isoforms of 5aR, namely type I and II, characterized by distinct molecular, structural and biochemical properties and by different tissue localization [4, 5]. Early studies have shown that individuals lacking 5aR activity have only sparse beard growth and do not develop AGA [6]. It is clear that a mutation within the gene encoding type II 5aR is responsible for this phenotype [7]. These findings plus better experimental evidence that local overexpression of type II 5aR in human hair follicles (HF) might be involved in androgen-mediated effects on susceptible HF [8, 9] suggest that type II 5aR is involved in the development of AGA. Thus the association of DHT with these disorders has generated great interest in 5aR as a therapeutic target.
Recently, the effectiveness of finasteride, a type II 5aR inhibitor, in tre
Ecco l'articolo con traduzione a seguito e un'interessante tabella con i risultati della sperimentazione:
Summary : The local conversion of testosterone (T) to the more potent androgen dihydrotestosterone (DHT) by 5alpha-reductase (5aR) is implicated in the pathogenesis of androgenetic alopecia (AGA). Recently, the clinical effectiveness of finasteride, a selective type II 5aR inhibitor, in treating AGA has been documented, and these clinical studies have shown that circulating DHT is lowered by 60-70% in men taking finasteride. The source of the residual circulating DHT is presumed to be due to type I 5aR activity which is not affected by finasteride. Several novel compounds with potent dual inhibitory activity on both isoenzymes have been described and CS-891 is one of them. This compound may be likewise effective in the prevention or treatment of AGA. As a prerequisite for such an action CS-891 should be able to inhibit 5aR activity in its target tissue: the hair follicles (HF). Here we report on the capability of CS-891 to inhibit 5aR activity in dermal papillae (DP) of human HF.
Keywords : androgen, androgenetic alopecia, hair, hair loss.
Pictures
ARTICLE
The local conversion of testosterone (T) to the more potent androgen dihydrotestosterone (DHT) by 5alpha-reductase (5aR) plays a pivotal role in the development of androgenetic alopecia (AGA) and hirsutism [1-3].
There are at least two isoforms of 5aR, namely type I and II, characterized by distinct molecular, structural and biochemical properties and by different tissue localization [4, 5]. Early studies have shown that individuals lacking 5aR activity have only sparse beard growth and do not develop AGA [6]. It is clear that a mutation within the gene encoding type II 5aR is responsible for this phenotype [7]. These findings plus better experimental evidence that local overexpression of type II 5aR in human hair follicles (HF) might be involved in androgen-mediated effects on susceptible HF [8, 9] suggest that type II 5aR is involved in the development of AGA. Thus the association of DHT with these disorders has generated great interest in 5aR as a therapeutic target.
Recently, the effectiveness of finasteride, a type II 5aR inhibitor, in tre
]...teoricamente dovrebbe essere molto simile alla dutasteride.