Archives for: December 2009

Treatments for hair loss

12/30/09 | by druggscom [mail] | Categories: Announcements [A]

Drugs. 2001;61:53.

Treatments for male pattern hair loss and alopecia areata: current options and future prospects.
Meidan VM, Touitou E.

Male pattern hair loss and alopecia areata are common disorders of the hair follicle which may heavily influence self esteem and self image. Androgenetic alopecia is caused by the heightened sensitivity of scalp follicles to dihydro- testosterone whereas alopecia areata is induced by an autoimmune reaction. Current drug treatment approaches include the use of hair regrowth stimulators such as topical minoxidil and oral finasteride for androgenetic alopecia, as well as topical minoxidil, dithranol (anthralin), corticosteroids, contact sensitisers, and psoralen plus ultraviolet A irradiation (PUVA) therapy for alopecia areata. Combination regimens are also proposed. However, extreme cases of either type of hair loss do not generally respond well to these existing treatments. For this reason, new therapeutic strategies are directed towards both improving the targeting of existing agents, as well as the development of novel hypertrichotic modalities.

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The hair regrowth and loss cycle-- modulators

12/02/09 | by druggscom [mail] | Categories: Announcements [A]

…Our results demonstrate that caspases are expressed in discrete areas of the hair follicle and may control the hair loss andhair regrowth cycle. It appears that all the caspase family members are expressed in normal cells in an enzymatically inactive pro-form, and that upon the onset of apoptosis they are converted to an enzymatically active processed form via a poorly understood mechanism involving either oligomerization, self-proteolysis or cleavage by another family member or both. All members of the protease family show an extremely high prefe-rence for cleavage of their substrates after an aspartyl residue at the P1 position. Once activated, caspases are sensitive to inhibition by the viral products CrmA and p35, and perhaps more significantly from the point of normal regulation, by endogenous inhibitors, X-linked inhibitor of apoptosis (XIAP).

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