rowekyle

Anyone hear anything lately on the above drug? I have heard it is suppose to be pretty crazy and actually work.

Hopefully that doesn't mean bye to our salons?! What do you think?

Info below:

Alpha-Melanocyte stimulating hormone (-MSH) is a naturally occurring peptide hormone which is released by cells in the skin in response to the stimulation of ultraviolet radiation (UVR) from the sun. MSH has a very short half life (seconds) in the blood stream but does reach and stimulate other skin cells (melanocytes) which in turn produce and release melanin, a dark brown pigment. Melanin is considered to be photoprotective.
CUV1647 is a chemical analogue of -MSH. CUV1647 is a linear peptide with 13 amino acids. Two amino acids present in -MSH have been changed to produce CUV1647. This small change creates a molecule with the same but more potent biologic effects and a much longer half life (minutes). These changes allow CUV1647 to increase melanin content of the skin even when delivered at a remote location and without exposure of the skin to the damaging effects of UVR.
The peptide acts as a "super-signal" that produces prolonged effects (versus natural -MSH) intra-cellularly.
In-vitro studies demonstrated that CUV1647 is between 10 to 1000 more potent1 than our endogenous (natural) peptide, -MSH. In fact, clinical studies conducted by Clinuvel have confirmed the increased effects by CUV1647.
CUV1647 has or will be tested for efficacy in a number of photodermatoses. These are diseases of the skin which are exacerbated by exposure to UVR. Some of these diseases are caused by what the unaffected would consider trivial doses of UVR. Others result only from chronic exposure. The common factor appears to be melanin compromised skin. All treatments are prophylactic and not therapeutic.
* Polymorphous Light eruption (PLE/PMLE) is a term used to describe a recurrent skin disorder of which there is no known cause. Although PLE symptoms can vary from individual to individual, it is monomorphous (i.e. the symptoms are the same) for an individual sufferer for each outbreak. It appears after exposure to ultraviolet radiation and is characterised by the appearance of red severe rash, papules (lumps), vesicles (bumps) and pruritus (itching) and burning sensations.
Clinuvel has shown in two pilot studies that CUV1647 prevents or reduces the signs and symptoms of the disease and substantially improves quality of life. Management of this disease will be one of the primary indications to be pursued. It is intended that Phase III studies be initiated in 2006.

* Actinic Keratosis (AK's)(or solar keratosis) is a term derived from Actinism meaning the property of radiant energy especially in the visible and ultraviolet spectral regions by which chemical changes are produced and keratosis meaning excessive growth of horny tissue of the skin. In short, actinic keratosis is a precancerous skin growth that is discrete, dry, rough adherent scaly lesions usually caused by sun exposure.
Approximately 50% of the world's population have problems with AK's. The major clinical consequences of AK's is that these lesions may transition into skin cancer. It is not expected that CUV1647 will totally eliminate the effects of previous long term exposure to UVR but that it will reduce, eliminate or mitigate the effects of future continued exposure. This will be the second major indication to be developed for CUV1647. We plan to initiate Phase III in late 2006.
A subset of this program will be a study to determine the effects of CUV1647 in immune-compromised individuals. These subjects will be chosen from a population of organ transplant patients who are particularly prone to develop AK's and skin cancer after only minimal exposure to UVR.
CUV1647's ability to regulate melanin production and release may be utilised to assist in alleviating UV-related skin disorders which are exacerbated by UVR.
Current literature shows evidence that subjects without protective eumelanin (pigmentation) are far more susceptible to skin cancer (squamous cell carcinoma, basal cell carcinoma, melanoma) than are African Americans.
Epidemiological data indicates indeed that light from the ultra-violet spectrum (290 to 420 nanometres) through its mutagenic activity is the most likely cause of skin cancer in Caucasians (people with light coloured skin).
In the US, incidence rates of melanoma (pigmented malignancies of the skin) in white males amount to 25:100,000 compared to black males where the rate is much lower in 1.4:100,000.? In comparison, for white females vs. black females the incidence rate is 17.9:100,000 vs. 1.1:100,0002.
Another illustration of the photo-protective properties of eumalenin is shown in a South African study where only 1.2:100,000 indigenous Africans suffered from malignant melanoma3 ; while the rate of malignant melanoma for Caucasians living in Cape Town was found to be 24.4:100,0004. The rate of other prominent skin cancers (squamous cell carcinoma and basal cell carcinoma) in albinos (people with non-pigmented skin) belonging to the black indigenous population was found to be 23.4%5. This equates to incidences of approximately 25% in white South Africans seen in dermatology practices over a span of 7 years6.
In a population based study in Australia, it was calculated that men with fair skin had a 6.2 times more chance of developing skin cancer in their lifetime than men with naturally high levels of melanin7.
Intellectual Property
Clinuvel Pharmaceuticals has the worldwide licence to intellectual property covering the use of analogues of -MSH invented by scientists at the University of Arizona. In total there are 34 patents in the licence's patent schedule. The patents contain within their scope the use of numerous analogues of -MSH for the induction of melanogenesis, in particular CUV1647. Expiry dates for the allowed claims for the analogues range from September 2006 until October 2015 in the various jurisdictions.
In addition to the licensed patents, Clinuvel Pharmaceuticals has filed three full international patent applications under the Patent Cooperation Treaty (PCT) since September 2005. Currently, Clinuvel is filing additional patents under the same scheme.
The first patent application was filed on 23 November 2004 and contained within its scope the use of numerous analogues of -MSH for the induction of melanogenesis in subjects who do not normally respond to -MSH due to genetic variations of the receptors on the melanin-producing cells, melanocytes.
The second patent was filed on 11 February 2005 and contained within its scope the use of numerous analogues of -MSH for the induction of melanogenesis using any sustained release dosage that results in a low controlled level of drug in the blood for at least a period of twenty four hours.

The third patent was filed on 7 October 2005 and contained within its scope the use of numerous analogues of -MSH for the induction of melanogenesis using a unique topically applied formulation.
Typically, granting of patents under the PCT can take up to five years in each of the individual countries covered under the treaty.
In the major marketing jurisdictions around the world, in order to protect originator pharmaceutical companies from generic pharmaceutical companies following approval of their new drug, a period of data exclusivity is established. This basically affords market exclusivity for a period of 5 years in the US and Australia/New Zealand and 6-10 years (plus a further 1 to 3 years for the generic registration process) in Europe irrespective of the originator pharmaceutical company's patent position.
Together with its extensive data on CUV1647 and clinical trials, Clinuvel is in a strong position to capitalise on CUV1647.

References
1. Hadley, et al. The Proopiomelanocortin system. An. N.Y. Acad. Sci. 1999, 885:1-21.
2. Tsai, et al. Cutaneous, ocular and visceral melanoma in African Americans and Caucasians. Melanoma Res. 2005, 15:213-217.
3. Giraud, et al. Malignant melanoma of the skin in Black Africans. S Afr Med J. 1975, 16:665-8.
4. Hoffman et al. Malignant melanoma in Cape Town, South Africa. Br J Dermatol. 1998, 138:998-1002.
5. Kromberg et al. Albinism and skin cancer in Southern Africa. Clin. Genet. 1989, 36:43-52.
6. Whiting. Skin tumours in White South Africans. Part I. Patients, methods and incidence. S Afr Med J. 1978, 53:98-102.
7. Dwyer et al. Cutaneous Melanin Density of Caucasians measured by spectrophotometry and risk of malignant melanoma, basal cell carcinoma and squamous cell carcinoma of the skin. Am J Epidemiol. 2002 155:614-21.