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R. Formica, J. Shen, Y. Gong, C. P. Seidel, S. F. Hackett, K. Kesavan, D. B. Jacoby, P. A. Campochiaro; TM601, a Peptide That Binds Annexin A2, Causes Regression of Choroidal Neovascularization (CNV). Invest. Ophthalmol. Vis. Sci. 2009;50(13):1164.
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TM601 is a synthetic polypeptide with sequence derived from the venom of the scorpion Leiurus quinquestriatus that has anti-neoplastic activity. In this study, we investigated the effects of TM601 in mice with laser-induced CNV.
The effect of intraocular and periocular TM601 on CNV and its localization was investigated.
Intraocular injection of 50 µg of TM601 at the time of and 1 week after rupture of Bruch’s membrane resulted in a 50.4% reduction in CNV area compared to vehicle-injected eyes. When 50 µg of TM601 was injected one week after Bruch’s membrane rupture, the area of CNV regressed by 62.4% due to apoptosis of endothelial cells in CNV lesions compared to a 9.6% reduction of CNV size with no apoptosis in vehicle-injected eyes. Daily periocular injections of 10 µg of TM601 did not cause a statistically significant reduction in CNV size, but injections of 50, 250, or 1000 µg each caused reductions of 65-70%. Immunohistochemistry of ocular sections with an antibody directed against TM601 after intraocular or periocular injection of TM601 in eyes with CNV showed selective localization of TM601 to new vessels. On tumor cells, TM601 has been shown to bind annexin A2 at the cell surface.
TM601 selectively binds to vascular cells in CNV lesions, induces apoptosis, and causes regression of CNV making it a good therapeutic candidate for further testing.
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