Initiated September 2019
Completed 2017
TRPV6 plays a key role in cancer pathogenesis. SOR-C13 disrupts the function of TRPV6.
(e.g. Soricimed Peptide
Which introduces specificity, enabling cytotoxic drug delivery to TRPV6 over expressed by tumors, while minimizing unwanted toxicities from non-specific distribution and death of healthy cells
Linking the targeting ligand (Soricimed Peptide) to a cytotoxic drug
For tumor destruction
Peptide Receptor Radionuclide Therapy (“PRRT”), involves targeted delivery of isotopes that emit highly energetic particles to cancer cells leading to their destruction, while minimizing collateral damage to healthy surrounding cells.
PRRT is attracting interest as therapeutic oncology class due to increasing availability of wide range of radionuclides, and recent advances in targeting therapies such as mAbs -> “Weaponized Targeted Therapy”.
SOR-C13, is a novel, short, synthetic peptide developed from the C-terminal region of soricidin, a proprietary 54 amino acid peptide, discovered by Soricimed Biopharma found in the saliva of the Northern Short-tailed Shrew. SOR-C13 binds with high affinity and selectivity - and disrupts the function of - TRPV6, a calcium channel over-expressed in solid tumor cancers. TRPV6 plays a central role in a biochemical cascade that results in the upregulation of an array of pro-cancerous genes. TRPV6 is considered to be an important target for novel anticancer therapy. SOR-C13 is the first highly specific TRPV6 inhibitor to be identified and to be taken into clinical development.
SOR-C13 was effective in inhibition of tumors in animal xenograft models of human ovarian and breast cancer. Studies with fluorescently tagged SOR-C13 injected intravenously (IV) showed rapid uptake by ovarian and prostate xenograft tumors with signals becoming well visible in about 20–30 min, maximizing at about 1 h and maintaining for at least 72 hours. This indicates that SOR-C13 rapidly accumulates within tumors and resides there for several days where its TRPV6 inhibition is exerted.
In rat and dog GLP toxicology studies (required by regulatory bodies to support human clinical trials), where SOR-C13 was injected as a daily IV bolus for 28 days, there was minimal toxicity and no immunogenicity. Importantly there were no toxic effects on the heart in either species. The lack of cardiotoxicity was further substantiated by studies of other channels where there was no modulation of channel activity by SOR-C13. In addition, SOR-C13 could be administered at high doses before any signs of anatomical pathology. The pre-clinical data was submitted to the FDA as an Investigational New Drug Application (IND) and to Health Canada as a Clinical Trial Application (CTA) to support moving SOR-C13 into human clinical trials in cancer patients.
This was a ‘first-in-human’ Phase 1 clinical dose escalation safety study evaluating SOR-C13 in adults with advanced solid tumors of epithelial origin non-responsive to all standard-of-care treatments (NCT01578564). We enrolled 23 patients - 22 stage 4 cancer and one patient with stage 3 cancer. In total, there were 14 different solid tumor cancers represented. The study took place at the University of Texas MD Anderson Cancer Center in Houston, Texas, the Juravinski Cancer Center in Hamilton, Ontario, and the London Health Sciences Centre in London, Ontario.
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