Rosacea Blog

Clinuvel (was Epitan) has completed a small Phase II trial with patients suffering from Polymorphous Light Eruption (PLE). This is part of their strategy of ensuring targeting relevant dermatological diseases that benefit from increased sun protection via melanin.


"We have made a significant step forward in the development of CUV1647, but there are ample challenges ahead” said Clinuvel’s CEO, Dr Philippe Wolgen."

There is also an update on when Phase III trials are to start (they haven't yet), and complete (now slated for 2009...).

"Clinuvel is preparing to start Phase III clinical trials in Europe, Australia and the United States and remains on target to complete these by 2009. Following completion of the clinical development program, Clinuvel’s next steps will be to continue to work with regulators to facilitate the regulatory evaluation process."

Phase III trials in Australia have been cancelled and will now go ahead in Europe instead, they are planning to start them in 2007.

"CEO Philippe Wolgen


We’ve scheduled to begin PLE Phase III trials in Europe in early 2007. We’ve
already finalised the protocols and agreed trials with nine European sites and
are pressing for medical/ethical approval in EU countries. We are well on
target to start Phase III trials in early 2007. The PLE Phase III trials in
Australia are no longer planned. Focussing on one continent to do the Phase III
trial rather than spreading over two continents made more sense from an
organisational point of view." (source)

Worth noting that recently a rosacea sufferer posted about his positive experiments with the peptide Melanotan II (not Melanotan, which is the drug Clinuvel is developing). See the melanotan forums for more information on these drugs (note: I would assume that experimenting with unapproved peptides is potentially very dangerous -- please wait for the licensed version after 2009!).

See also the 28th August Q&A session with the CEO

An interesting laboratory study that speculates on the possible treatment of rhyinophyma (red, bulbous nose of rosacea, often with excess tissue) with the "breast cancer" drug, tamoxifen (also rarely used to treat retroperitoneal fibrosis).

A number of studies appear to have suggested that fibrosis (caused by overexpression of the fibrogenic protein TGF-beta 2?) is implicated in the development and progression of advanced rhinophyma.

Down-regulating causes of fibrosis with tamoxifen: a possible cellular/molecular approach to treat rhinophyma.

Ann Plast Surg. 2006 Mar;56(3):301-5.

Payne WG, Ko F, Anspaugh S, Wheeler CK, Wright TE, Robson MC.

Institute for Tissue Regeneration, Repair, and Rehabilitation, Department of Veterans Administration Medical Center, Bay Pines, FL, USA.

Fibrosis and proliferative scarring are prominent features of the severe forms of rhinophyma. Up-regulation of growth and fibroblast kinetics are hallmarks of fibrosis. Persistent overexpression or dysregulated activation of the fibrogenic isoforms of transforming growth factor beta (TGF-beta) is associated with the increased fibroblast function leading to fibrotic conditions such as rhinophyma. Tamoxifen, a synthetic nonsteroidal antiestrogen, can neutralize or down-regulate TGF-beta. Fibroblast-populated collagen lattices (FPCLs) were constructed from fibroblasts cultured from rhinophyma or normal nasal skin. One-half of each set of FPCLs was treated with Tamoxifen. Lattice contraction was serially measured over 5 days, and the supernatants of the cultures were analyzed for TGF-beta-2 by immunoassay. Tamoxifen significantly decreased fibroblast activity by decreasing contraction of the treated lattices.