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About afamelanotide (CUV1647)

Afamelanotide (CUV1647) acts by increasing the levels of melanin in the skin; it appears to shield against subsequent prolonged UV irradiation (UVR). Afamelanotide is delivered from a subcutaneous dissolving implant approximately the size of a grain of rice.  Increased pigmentation of the skin appears after 2 days and lasts up to 2 months. It is proposed that afamelanotide will treat the millions of people world-wide who suffer from UV-related skin disorders.

Alpha-Melanocyte stimulating hormone (α-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. α-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.

Afamelanotide (CUV1647) is a chemical analogue of α-MSH. Afamelanotide is a linear peptide with 13 amino acids. Two amino acids present in α-MSH have been changed to produce afamelanotide. This small change creates a molecule with the same but more potent biologic effects and a much longer half life (minutes). These changes allow afamelanotide 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 α-MSH) intra-cellularly.

In-vitro studies demonstrated that afamelanotide (CUV1647) is between 10 to 1000 more potent than our endogenous (natural) peptide, α-MSH. In fact, clinical studies conducted by Clinuvel have confirmed the increased effects by afamelanotide.

Afamelanotide (CUV1647) is being 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.

2008 Annual Report