Capricor Therapeutics, Inc. (NASDAQ:CAPR) Q3 2018 Earnings Conference Call - Final Transcript
Nov 13, 2018 • 04:30 pm ET
Welcome to Capricor Therapeutics' Third Quarter 2018 Conference Call. My name is Latif and I will be your operator for today's call. (Operator Instructions).
I will now turn the call over to Capricor's CFO, AJ Bergmann.
Thank you. Good afternoon everyone. (Forward-Looking Cautionary Statements)
With that, I would like to turn the call over to Linda Marban, CEO.
Thank you, AJ and good afternoon. Thank you for joining us for our third quarter update and conference call. These are busy days at Capricor and we continue to strive forward in our DMD program as well as in the development of our exosome platform technology. We are making good progress in both, so I am delighted to provide you with some color on both of our programs today. As you know we are actively enrolling HOPE-2 our potential registration clinical trial in Duchenne muscular dystrophy. In that trial, we will be dosing up to 84 DMD patients with either CAP-1002 or placebo every three months, but the primary efficacy end point being the middle level performance of the upper limb otherwise known as the mid-level pull out one year after four doses. We currently have 11 sites across United States recruiting participants.
Patients and families are eager to get into the trial, so we are doing our very best to continue the momentum in enrolling so that the sites can quickly treat as many patients as possible. What I can tell you is that the response by the patients in the DMD community to this trial has been overwhelmingly positive. Recently, we have had over 100 inquiries by prospective patients as to whether they may be eligible for HOPE-2. One of the reasons for the overwhelming response is that as you may remember we are focusing on those later stage patients that are nearly or are already non-ambulatory and while we are looking to improve skeletal muscle function using the performance of the upper limb as an indicator. We are also focusing on potential improvements in cardiac structure and functions, which is an important and heretofore unaddressed complication of DMD.
In fact, one of the most common causes of death in patients with DMD is the cardiomyopathy or scar in the heart, which leads to heart failure. In addition, our thought leaders tell us that if the gene therapy is successful in keeping patients with DMD on their feet longer, the load on their hearts will increase substantially and there is likely to be further exacerbation of the cardiomyopathy. We believe that CAP-1002 could be important and perhaps necessary to counteract the worsening of the heart disease associated with DMD in the face of gene therapy. In HOPE-2, we will get an idea of how the cells can ameliorate skeletal and cardiac muscle function. One of our goals is to build CAP-1002 to be used in conjunction with gene therapy and some of our key opinion leaders believe that reduction in fibrosis prior to gene therapy in later stage patients may be