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Mesoblast Cleared to Begin First Phase 2 Clinical Trial for Eye Diseases
Date:10/24/2011

ecurrence and risk of vision loss.

In Asia, wet AMD affects as many as 1.9% of people 65 or older. However, up to 55% of cases of wet AMD in Chinese, Japanese, and Malay populations are caused by Polypoid Choroidal Vasculopathy (PCV), a disorder of eye blood vessel proliferation that is different from the wet form seen in North America and Europe. Anti-VEGF therapy does not result in adequate regression of PCV lesions, and for this reason first line therapy for PCV is photodynamic therapy.

Mesoblast's proprietary adult stem cells may be effective for both forms of wet AMD since they have successfully reduced excessive blood vessel formation and leakiness in several preclinical studies:

1.  Results from a study at the Lions' Eye Institute in Western Australia in 30 rodents with laser-induced excessive blood vessel formation showed that a single intra-ocular injection of human MPC prevented development of leaky blood vessels beyond day 7 after laser-induced damage (eyes treated with MPC had 39% and 32% non-leaky vessels at days 14 and 28, compared with only 7% and 2% non-leaky vessels in the controls at the same time-points, p<0.05).  Moreover, at day 28 only 9% of vessels in eyes treated with a single MPC injection were severely leaking compared with 28% of vessels in control eyes (p<0.05).

2.  Results from a trial at Charles River in Canada in 42 non-human primates with laser-induced excessive blood vessel formation showed that combining a single injection of Mesoblast's allogeneic cells with an injection of the anti-VEGF agent Lucentis resulted in a synergistic, and superior, outcome compared with Lucentis alone in reducing severity of blood vessel leakage within 2 weeks (p<0.05), preventing relapse of severe vessel leakage by days 28-42 (p<0.05), reducing total formation of new blood vessels (p<0.01), and preventing retinal detachment by day 42 (p<0.01).

Mesoblast's randomized, placebo-controlle
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SOURCE Mesoblast Limited
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