Hi Wayne,
Thanks for your post.
You wrote...
Efficacy doesn't appear to have been an issue in previous antibody trials. Rather an unfortunate side effect - thromboembolic complications - appears to have torpedoed trials.
From Dr. Paul Watt back in 2007...
Our hits not only block the activity of CD40L, but they also bind this target with sufficient affinity to compete with well characterised antibodies specific for that target. This has important implications for dosing and cost of goods of any subsequent drug, since these non-optimised Phylomer® hits show encouraging biological efficacy. We have now confirmed the RA hits announced in May are biologically active in cell based assays, clearing the way for progression into animal disease model testing.
http://www.asx.com.au/asxpdf/20071010/pdf/31516w48lx96v3.pdf
Comments from management recently..
Be assured there is plenty of big Pharma interest in CD40L. Prospective Pharma partners for CD40L want in vitro data rather than anything more extensive in animal models. We envisage 6-12 months for the data.
I found this old presentation of Phylogica's that touched on managements comments too.
February 2009, Technical Presentation...
http://www.phylogica.com/webbox/media/PYCtechFeb09.pdf
Regards,
Tony
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