Our Platform

SOR-C13 TRPV6 Inhibitor

University of Texas MD Anderson Cancer Center investigator-initiated Phase 1b clinical trial in progress for the treatment of solid tumor cancer

TRPV6 MOA SOR C-13

SOR-C13, is a novel, short, synthetic peptide developed from the C-terminal region of Soricidin, our proprietary 54 amino acid peptide. SOR-C13 binds with affinity and selectivity to - 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 currently being studied at the University of Texas MD Anderson Cancer Center in an investigator-initiated Phase 1b clinical trial and has been granted orphan drug status by the U.S. Food and Drug Administration for the treatment of pancreatic and ovarian cancers. It is the first highly specific TRPV6 inhibitor to be identified and to be taken into clinical development.


MD Anderson Logo

Investigator Initiated Phase 1b Clinical Trial – University of Texas MD Anderson Cancer Center

In August 2019, the University of Texas MD Anderson Cancer Center (MDACC) activated an Investigator Initiated Clinical trial of SOR-C13 with the aim to refine dosing and further explore safety and efficacy of SOR-C13 in late-stage solid tumor cancers. The study’s primary objective is to define a maximum tolerated dose (MTD) for SOR-C13 and further define its safety profile.  Secondary objectives include the evaluation of clinical response to SOR-C13 and to determine predictive biomarkers in patients who have achieved objective responses.

MDACC has completed the first and second cohort of the dose escalation phase of the trial, which focuses on late-stage pancreatic cancer patients and results to date show that SOR-C13 is safe and well-tolerated, with no drug-related adverse events and promising anti-tumour activity.  Currently MDACC is enrolling patients for the third cohort which is expected to be completed within the next few months.

SOR-C13 Phase 1 Clinical Trial – Safe with Indications of Efficacy

Our prior study 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 patients with 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 Centre in Houston, Texas, the Juravinski Cancer Center in Hamilton, Ontario, and the London Health Sciences Centre in London, Ontario.

MD Anderson Cancer Center

Juravinski Cancer Centre

London Health Sciences Centre

Patients were treated on a set schedule of IV dosing for two 21-day cycles. At the end of the second cycle if their physician felt the patient was receiving a treatment benefit without unacceptable side effects, the duration of treatment could be expanded using the same 21-day treatment cycles.

55 Percent of patient icon

2 patients icon

The results showed SOR-C13 was safe and generally well tolerated in the FIH trial patients, without evidence of the hematological, cardiac, neurological or other significant toxicities often observed with cytotoxic chemotherapy.  Because of the expanded treatment duration, a total of 486 IV infusions were given in the Phase 1 trial.  With this, there were no drug related serious adverse events reported.

The FDA has awarded orphan drug status to SOR-C13 for the treatment of ovarian cancer and for the treatment of pancreatic cancer.

The study also provided preliminary indications of anticancer activity for SOR-C13. After the first two cycles of treatment, 55% of patients had stable disease. One patient that came into the study with progressive disease was stable for more than one year. Promising anti-tumor activity was seen in both patients with pancreatic ductal adenocarcinoma, who had each failed three prior regimens of anticancer therapy. One of these patients showed a 27% reduction in tumor size after four treatment cycles which correlated with a validated blood biomarker for pancreatic cancer. The FDA has awarded orphan drug status to SOR-C13 for the treatment of ovarian cancer and for the treatment of pancreatic cancer.

For a comprehensive description of our Phase 1 clinical trial please see the attached paper published in the journal Investigational New Drugs.

SOR-C13 provides a unique mechanism for anticancer activity, through the inhibition of the TRPV6 calcium channel activity. Based on a favorable safety profile, coupled with promising anti-tumor activity observed from the first clinical trial, further studies to investigate SOR-C13 as an anti-cancer agent were initiated.

The absence of toxicity commonly observed with cytotoxic agents provides a rationale for the investigation of SOR-C13 with standard of care antineoplastic agents (i.e., combination with other cancer drugs) to improve anticancer efficacy with reduced risk of cumulative or overlapping toxicities.


Pre-clinical Studies

SOR-C13 was effective in inhibiting tumor growth 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 minutes, maximizing at about one hour 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.

Powered by Innovasium