SurModics Inc (SRDX)

[aslan2772]

re: Lucentis I-vation musings

The surprise to me is that Avastin, which does not efficiently penetrate the retina, seems to work well in AMD (although to my knowledge this is not yet conclusive). Thus after some consideration, I am softening my mental position that VEGF-binding therapies must penetrate deeply into the retina in order to impact CNV. It might be possible that lowering the concentration of VEGF in the vitreous by "mopping it up" has a beneficial lowering effect on VEGF concentration in the retina. If this is the case, your rusty nail approach might actually have clinical benefit. I am keeping in mind that under normal physiological conditions, VEGF signaling is primarily paracrine (local gradients), but under pathological conditions VEGF action may in fact become more long-distance.

In summary, I am open to the idea that immobilizing Lucentis or Avastin, for example, on a device in the vitreous (even in the absense of release) could have clinical benefit in AMD/DME. However, I still think putting a given drug- or antibody-containing device closer to the macula (for example with a translucent, biodegradible, thermoplastic polymer such as polycarbonate or amorphous polyarylate http://www.corporate-ir.net/ireye/ir_site.zhtml?ticker=SRDX&script=410&layout=-6&item_id... )would have the highest efficacy. Note, the polyarylates are biodegradable and can be used to deliver both large proteins and small molecules, whereas the polycarbonates are better suited to deliver small hydrophobic drugs. With the Rutgers and Octoplus licenses, SDRX is positioned to pursue biodegradible subretinal implants (eg. http://www.touchbriefings.com/pdf/17/pt031_t_octoplus.pdf) and could also test polyarylate/Lucentis on the screw, I think.

BTW, protein release from hydrogels is controlled by bulk degradation rather than by surface erosion.