A further benefit of directly targeting the transcription factor (Myc protein) product of the MYC gene, rather than using a nucleotide therapeutic (eg RNAi) approach, is that it should allow more straightforward access to a broad range of tissues, rather than being largely restricted to the liver. The additional potency offered by our FPP could also improve efficacy in target tissues.
The most advanced MYC-targeting drug development program of which I am aware uses an RNAi approach.
Dicerna Pharmaceuticals (Cambridge, MA) is currently conducting a Phase 1 Study of its RNAi investigational drug (DCR-MYC-101) in patients with advanced solid tumours, multiple myeloma, or lymphoma who are refractory or unresponsive to standard therapies. This study commenced in April 2014 and is expected to report results before the end of this year. Dicerna is also conducting a Phase 1b/2 study of DCR-MYC-102 in Hepatocellular Carcinoma. Neither program is partnered yet.
Consequently, I'd expect that PYC will not only need to meet all of the listed POC data pack milestones and successfully develop a definitive data pack in order to attract a partner, these data packs will also need to demonstrate that the FPP-iMYC approach is potentially superior (greater efficacy/lower toxicity) to Dicerna’s RNAi approach.
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