Jim, The shaved mouse market may not be huge, but the shaved face is.
Maybe Gillette will move into Biotechs. The estrogen receptor is
very well conserved evelutionarily, so I would be EXTREMELY surprised
if a similar mechanism didn't apply to humans. In fact the receptor
is so well conserved, that related receptors include the androgen,
retinoic acid, glucocorticoid, minerocorticoid, and many others.
LGND has used these structural similarities to screen a wide range
of compounds for non-polypeptide activity. Large pharmaceuticals have
many approved drugs on the market (Retin-A, Renova, Vassanoid, various
glucocorticoids, estrogens, and androgen analogs including Tamoxifin.
I found the PNAS article and it was a ZEN anti-estrogen that was used.
I have posted in the past on anti-estrogens. The WSJ had a comprehensive
article about a year and a half ago. The leaders at that time included
LLY, SBH, PFE, AHP, ZEN, and LGND. Interestingly, LGND was the
only Biotech and it was the only company to have alliances with
two of the leaders (PFE and AHP - LGND also has an alliance with SBE
but its for hematopoetic growth factors). LGND has since expanded its
activities and is a clear leader in the area of 2nd and 3rd generation
sex hormones (as well as many other non-polypeptide hormones).
Proceedings of the National Academy of Sciences
Volume 93, Number 22; Pages: 12525-12530
Medical Sciences
An estrogen receptor pathway regulates the telogen-anagen hair follicle
transition and influences epidermal cell proliferation
Hye-Sun Oh, Robert C. Smart
c 1996 by the National Academy of Sciences
ABSTRACT The hair follicle is a cyclic, self renewing epidermal structure which is thought to be controlled by signals from the dermal papilla, a specialized cluster of mesenchymal cells within the dermis. Topical treatments with 17-beta-estradiol to the clipped dorsal skin of mice arrested hair follicles in telogen and produced a profound and prolonged inhibition of hair growth while treatment with the biologically inactive stereoisomer, 17-alpha-estradiol, did not inhibit hair growth. Topical treatments with ICI 182,780, a pure estrogen receptor antagonist, caused the hair follicles to exit telogen and enter anagen, thereby initiating hair growth. Immunohistochemical staining for the estrogen receptor in skin revealed intense and specific staining of the nuclei of the cells of the dermal papilla. The expression of the estrogen receptor in the dermal papilla was hair cycle-dependent with the highest levels of expression associated with the telogen follicle. 17-beta-Estradiol-treated epidermis demonstrated a similar number of 5-bromo-2'-deoxyuridine (BrdUrd) S-phase cells as the control epidermis above telogen follicles; however, the number of BrdUrd S-phase basal cells in the control epidermis varied according to the phase of the cycle of the underlying hair follicles and ranged from 2.6% above telogen follicles to 7.0% above early anagen follicles. These findings indicate an estrogen receptor pathway within the dermal papilla regulates the telogen-anagen follicle transition and suggest that diffusible factors associated with the anagen follicle influence cell proliferation in the epidermis. |
