For attendees flying to Washington for the 65th annual meeting of the American Academy of Dermatology last week, the Skymall catalog made bringing a dermatology product to market look easy. A company called Hollywood Gadgets promised wrinkle-free skin with the help of a $59.95 gene therapy machine that it claims can electronically restore "what dermatologists call the S Complex Gene' . . . via a copy sound wave.'"

At Sunday's session on Translational Research in Dermatology, the speakers shared tales of their experiences with the opposite problem: how to get dermatologic treatments to market if you have sound science but nothing else yet.

Barbara Gilchrest, professor and chair of dermatology at Boston University, suggested that one way to bring a dermatology drug to market is to pretend it's something else - she suggested "piggybacking" dermatology drugs onto other indications.

The rationale behind that approach, she explained, is that several factors make drug developers more likely to spend their money elsewhere rather than on dermatology products. For one thing, though cosmetics are obviously a huge business, the medical dermatology market for most diseases is comparatively small. And most skin diseases are chronic but not life threatening.

In terms of regulatory scrutiny, that means "the FDA is going to insist on a huge amount of safety data," Gilchrest said. "And the fact that there is a small market on the other end is not their problem. It is yours."

Gilchrest's academic research is on t-oligos, which are short artificial analogues of telomeres (See BioWorld Today, Sept 13, 2004.)

Originally, Gilchrest's plan was to develop t-oligos as skin protection. When she published data showing a specific t-oligo can protect skin from ultraviolet light damage in 1994, "we thought that we would have a protective agent for human skin within 12 months," she told the audience.

These days, her outlook is more sober, thanks to her experiences with a technology transfer office that was "overwhelmed and underfunded," a pharma company that changed its focus and a biotech that went belly-up after a late-stage clinical failure. She is the co-founder of Boston University spinout SemaCo Inc., and hopes that t-oligos can be developed as cancer therapeutics.

Cancer basically has the opposite constellation of factors that dermatology has. It generally is a life-threatening disease, which makes it easier to obtain FDA approval. And for the same reasons, therapeutics that Gilchrest termed "marginally useful" in terms of their therapeutic benefits have been very successful in the market place.

SemaCo is pursuing the development of t-oligos, which interact with telomeres to selectively kill cancer cells, as an oncology product. Cash flow and accumulated safety data from product approval in the oncology arena could be used in furthering their approval as protective dermatology agents. Gilchrest noted, though, that the newest try may not pan out any more than earlier ones did. Developing t-oligos as cancer therapeutics "is just the next in a long line of pathways that we are exploring," she told her audience. "But it is the hoped-for path now."

While there is a perception in the business community that academics suffer from founderitis - a belief by scientists that they are qualified to run a business based on their discoveries - all three speakers founded their companies only after outlicensing efforts had failed. All three noted that finding a high-caliber business executive had been both one of their primary goals and one of their greatest challenges.

Kenneth Cooper, professor of dermatology at Case Western University, said that co-founding is "effective, if you have the time," but noted that in his experience, "executives need close watching."

Despite their tales of woe - one scientific co-founder who spoke at the panel was fired from the company by his CEO - each of the researchers noted that trying to bring a product to market is rewarding, and can prevent a laboratory from getting bogged down in what one panelist termed "mechaniostic questions with no relevance to therapeutic success."

All speakers on the panel could back up their science with sound experiments published in top-flight journals. Sadly, at times, the top-flight science at the conference seemed thin on the ground, though. Medical education credits were available, among other things, for attending a focus session about the purported "failure" of safer sex campaigns to impact the spread of sexually transmitted diseases. It also promised that "following this focus session, the attendee will be able to recognize the need for dermatologists to . . . incorporate the abstinence message into routine office visits" of teenagers - a goal that is definitely not based on the scientific knowledge of the effects of either condom use or abstinence campaigns on the spread of sexually transmitted diseases.

And the session began with a moment of silence for Aaron Lerner; the only dermatologist member of the National Academy of Sciences, who passed away Saturday.

The conference ends today.

AAD Scientific Presentations

Among the scientific presentations at the AAD meeting:

• Anacor Pharmaceuticals, of Palo Alto, Calif., presented four posters on the results of studies of AN2690, a topical antifungal therapy for onychomycosis. Results of a two-dose, multicenter phase II study showed that patients who received the drug had considerably clear nail growth and were unlikely to show evidence of fungal infection. On Friday, Anacor had announced a deal with Schering-Plough to commercialize AN2690. Schering-Plough, of Kenilworth, N.J., will pay all development costs, and Anacor will receive $40 million up front and milestone payments potentially exceeding $575 million. (See BioWorld Today, Feb. 5, 2007.)

Anacor also presented posters on AN2728, which is entering human trials as a topical treatment for psoriasis. Early results suggested the compound inhibits cytokines that play a key role in inflammation of psoriasis, the company said.

The company also said phase IIa study of AN0128, its lead atopic dermatitis compound, showed it was well tolerated with clinically meaningful efficacy trends. It is now undergoing a phase IIb study in children with the disease.

• AGI Dermatics, of Freeport, N.Y., also presented a poster showing clinic data it said suggested that treatment of UVB-induced DNA damage with the T4 Endonuclease V (T4N5) enzyme significantly decreases MMP-1 secretion and increases repair of corresponding UVB-induced DNA damage. The current study examined the premise of T4N5's ability to simultaneously increase repair of cyclobutane pyrimidine dimmers (CPD) in irradiated keratinocytes (NHEK) and reduce MMP-1 secretion from fibroblasts (NHDF) exposed to irradiated NHEK media.

In another poster session, AGI unveiled data that indicated a novel compound of 4 percent hydroquinone and L-ergothioneine (HQ/EGT) reduces melanin significantly faster (twice as much) and with less irritation than traditional HQ formulation with steroids and a retinoid. The study compared the findings of test patches of Melanoderm-B tissues from MatTek treated daily with 2ul/cm(2) of an HQ/EGT compound cream and patches treated with an equal amount of a cream containing 4 percent HQ, 0.01 percent fluocinolone acetonide, (a steroid) and 0.05 percent tretinoin, a retin-a (HA/F+T). After seven days of treatment, both HQ/EGT and HQ/F+T treated tissues lacked melanin, while the melanocytes in the untreated tissues exhibited a high level of melanin and dendritic (immune) cells. The HQ/EGT treated tissue showed the inhibitory effect on melanin two times faster than the tissue treated with HQ/F+T.