Good morning, ladies and gentlemen, and welcome to the Catabasis Pharmaceuticals third-quarter 2018 earnings conference call. [Operator Instructions]. I would now like to turn the conference over to your host, Ms. Andrea Matthews, Vice President Corporate Affairs. Ma'am, you may begin..

Thank you, Bridget. Welcome to today's Catabasis Pharmaceuticals conference call where we will provide a corporate update and review our third-quarter 2018 financial results.

With me today are Jill Milne, Chief Executive Officer; Joanne Donovan, Chief Medical Officer; Andrew Nichols, Chief Scientific Officer; and Noah Clauser, Vice President of Finance.

We issued a press release this morning summarizing our corporate update and our Q3 2018 financial results, which we will reference on today's call and is available on our website. We are also using slides during today's call that are available within the Events & Presentations section in the Investors part of our website.

I would like to note that during today's call, as mentioned on slide 2, we will make statements related to our business based on the current and future expectations that may be considered forward-looking statements under federal securities laws.

Actual results may differ materially from those indicated by these statements as a result of a variety of risks and uncertainties, including those discussed in our most recent quarterly report on Form 10-Q, which we filed this morning with the SEC and is also available on our website.

Such statements represent our judgment as of today and Catabasis undertakes no obligation to publicly update any forward-looking statements except as required by law. With that let me pass the call over to Jill who will provide our corporate update.

Joanne will review our clinical program for edasalonexent and will be followed by Andy who will discuss our new preclinical cardiac collaboration with UT Southwestern. Noah will then provide the financial update and Jill will wrap things up.

Jill?.

Thank you, Andrea. Good morning, everyone, and thank you for joining us today for our third-quarter 2018 financial results and an update on progress. At Catabasis, we are focusing our efforts on Duchenne Muscular Dystrophy, a debilitating disease that affects tens of thousands of boys and men worldwide.

There's no cure today and, despite tremendous progress in the development of potential new therapies for DMD, there are no products in development that will cure this disease.

This statement was reinforced once again for me this past weekend at the Action Duchenne Conference in Birmingham, England where I listened to 10 other companies, in addition to Catabasis, present their work in Duchenne. It is clear there remains a substantial unmet medical need for new therapies.

Today the goal for new treatments in Duchenne is to preserve muscle function and slow disease progression. We have recently reached important milestones in the development of edasalonexent that I will walk through this morning.

Together these advancements support the potential future value of edasalonexent and get us closer to our goal of making this innovative treatment available to all of those affected by Duchenne to enable individuals to maintain their functional abilities longer.

We believe with edasalonexent that we can slow the progression of this disease in a meaningful way, preserving muscle function and improving quality of life for those affected. While his peers are running around on the soccer field, a typical young boy with Duchenne can struggle to climb a flight of stairs.

Our hope is that boys with Duchenne and will grow and play with their friends and that we can make their tomorrows better. Since our last earnings call we have made great advancements across our edasalonexent program, as outlined on slide 3. We are now in the final stage of clinical development for registration.

Multiple sites for our Phase 3 PolarisDMD trial are now open for enrollment. We are receiving tremendous interest and positive feedback from families and physicians, reflecting the high level of unmet need in Duchenne and enthusiasm for edasalonexent.

We are working diligently to quickly open additional sites for enrollment and connecting the list of patients that have expressed interest in our PolarisDMD trial with clinical sites in the US. Joanne will review the trial design and share more about the feedback we are hearing from physicians and families.

While the Phase 3 trial is underway, our MoveDMD Phase 2 trial open label extension continues. Some of the boys in the study have now been treated with edasalonexent for two years. Last month we presented the latest data showing efficacy following 72 weeks of edasalonexent treatment.

What is exciting to us and others is that these data highlight the consistency and durability of the effects of edasalonexent.

For over a year we have presented additional MoveDMD data and this is now the fifth time point from this trial where we see consistent data across all functional measures and biomarkers of muscle health and inflammation after an extended treatment period.

This reinforces our confidence that edasalonexent preserves muscle health and slows disease progression and that these effects are durable. Joanne will share more details of the recently released 72-week data on today's call.

An additional area of important progress over the last quarter is in the development of meaningful endpoints for clinical outcome in Duchenne. Current assessments of Duchenne rely on physical function tests and invasive procedures. As a community it is in everyone's best interest to execute effective and efficient clinical trials.

We see surrogate biomarkers as a potentially more efficient and effective path forward in Duchenne research. To further this effort we presented data at the World Muscle Society Congress that could potentially contribute to establishing MRI endpoints to support the development of edasalonexent as well as other future products in muscular dystrophy.

Catabasis continues to be a leader in the use of MRI to study therapeutic intervention in Duchenne. Our vision for edasalonexent is summarized on slide 4.

As the Duchenne treatment landscape evolves we believe we are well positioned having designed edasalonexent to inhibit NF-kB, a key link between loss of dystrophin and disease manifestation and progression in DMD. By inhibiting NF-kB we believe that edasa has the potential to have benefits in skeletal and cardiac muscle.

In Duchenne, boys never have functional dystrophin, yet they do not typically present with disease symptoms until ages three to five. Why is this? It is because the lack of dystrophin alone is not enough to drive disease progression. But as boys continue to use their muscles, the absence of dystrophin combined with mechanical stress activates NF-kB.

Chronically activated NF-kB drives muscle damage and functional decline. This is why we believe it is critical to inhibit NF-kB in Duchenne to limit damage, preserve muscle function and slow disease progression.

This is why we believe edasa has great potential as a single agent and why we are developing it as a foundational therapy to treat all of those affected by Duchenne. The landscape is evolving and includes multiple different approaches, so the ability to safely and effectively combine therapies is critical in Duchenne.

Edasa's mechanism of action and safety profile strongly support combination with other agents. For example, edasa could enhance the benefit of dystrophin targeted therapies including exon skipping and gene therapy by limiting NF-kB mediated muscle damage.

In addition, we know that NF-kB regulates dystrophin production and we have already demonstrated preclinically that edasalonexent increased dystrophin production in combination with exon skipping. We are also excited about the promising early data we have shown showing potential beneficial cardiac effects of edasalonexent.

As you may have seen in our press release this morning, we have entered into a new preclinical research collaboration to further explore the potential cardiac benefits of edasalonexent with Dr. Pradeep Mammen at the University of Texas Southwestern Medical Center. Dr. Mammen is a leading muscular dystrophy cardiologist and researcher.

With cardiomyopathy being the leading cause of mortality in both Duchenne and Becker Muscular Dystrophies, improving heart health is critically important in these diseases and Andy will speak more about that shortly. First, Joanne will provide the clinical update.

Joanne?.

Thank you, Jill, and good morning, everyone. Echoing what Jill said, we are excited to have initiated our Phase 3 PolarisDMD trial with clinical trial sites now open for enrollment. As a reminder, on slide 5 PolarisDMD is a randomized double-blind placebo-controlled trial. We are planning to enroll about 125 boys.

As we did in our Phase 2 MoveDMD trial, our Phase 3 PolarisDMD trial will enroll boys aged four to seven up to their eighth birthday. This age range was chosen because we believe that early intervention with edasalonexent has the greatest potential for benefit.

The study will include boys, regardless of mutation type, who have not taken steroids for the past six months. The randomization is two to one such that for every two boys that receive 100 milligrams per kilogram per day of edasa one boy will receive placebo.

The primary efficacy endpoint is change in the North Star Ambulatory Assessment score after 12 months of a treatment with edasa compared to placebo. Key secondary endpoints include the age-appropriate time function tests, time to stand, four stair climb and 10 meter walk/run.

Assessments of growth, cardiac and bone health are also included as important potential differentiators of edasalonexent from the current standard of care.

We believe we have designed a robust trial based on our MoveDMD Phase 2 trial and open label extension in which edasalonexent showed improvement compared to the off-treatment control across all of these same functional measures.

Boys on a stable dose of EXONDYS 51 who are otherwise eligible can enroll in the PolarisDMD trial and we look forward to obtaining additional combination treatment data from their participation. In the PolarisDMD trial these boys will be stratified but will not be included in the primary analysis.

We expect that a small portion of the boys will receive both therapies as a little more than 10% of the Duchenne population are eligible for EXONDYS 51. As you can see on slide 6, we're excited that PolarisDMD trial sites are open for enrollment and we expect several additional sites to open within the next week with more to follow soon after.

The clinical trial sites are currently engaged in screening activities. We are receiving a terrific amount of interest and positive feedback from families and physicians and we expect to have close to 40 sites globally in total for the PolarisDMD trial. We expect the international sites to open for enrollment early next year.

Last month we held our North American PolarisDMD investigator meeting here in Cambridge, Massachusetts. We had fantastic speakers over the two days and thank everyone for participating and making this an incredibly successful experience.

We very much appreciated Pat Furlong, the Founding President and CEO of Parent Project Muscular Dystrophy, who gave the keynote address and stressed the need for safe and effective therapies for all people affected by Duchenne. Thank you to the physicians, coordinators, and large study team that are all deeply motivated to bring edasa to these boys.

We also reviewed with investigators the 72-week edasalonexent results from our MoveDMD trial that we presented at the International Congress of the World Muscle Society last month in Argentina. A summary of the promising clinical study results we'll be seeing with edasa is on slide 7.

We've looked at the effects of edasalonexent at multiple levels from demonstrating that edasalonexent inhibits NF-kB in adults and boys with DMD to confirmatory significant biomarker results and ultimately showing changes in muscle function.

We have seen sustained stabilization of disease progression in all four of the assessments of muscle function - the North Star Ambulatory Assessment, time to stand, four stair climb and 10 meter walk/run - all through 72 weeks of edasalonexent treatment compared to the off-treatment control period.

The North Star results can be seen on slide 8 and the free time function test on slide 9. For all these functional measures we saw a change in the disease trajectory after the boys started edasalonexent at the week zero point.

For biomarkers on slide 10 we also saw a significant decrease in all 4 muscle enzymes, including CK, through 72 weeks supporting the durability of edasalonexent treatment effects and positive effects on muscle integrity. Now cardiomyopathy is the leading cause of mortality in Duchenne.

Boys with Duchenne in this age range typically have resting tachycardia, a heart rate that exceeds the normal resting rate, which is actually the first cardiac manifestation in boys with DMD.

But in boys treated with edasalonexent we observe significantly decreased heart rate towards age normative values, supporting the potential beneficial cardiac effects of edasalonexent. These results are shown on slide 11. Andy will speak more about our research on the cardiac effects of edasalonexent shortly.

Through 72 weeks of treatment edasalonexent continued to be well tolerated with no safety signals observed in the trial. Boys treated with edasa continue to follow age-appropriate growth curves with age-appropriate increases in height and weight.

As you can see on slide 12, their overall BMIs have trended down on a percentage basis to age normative values. We are pleased to see boys on edasa continue to grow and have an appearance similar to their peers and, as expected, the complete lack of typical steroid associated side effects.

We hear frequently from families how important it is to the boys to grow taller as they mature. Thank you to everyone involved in the MoveDMD trial, including the participating boys, their families and the clinical trial sites for their continued dedication to this trial.

As Jill mentioned, we presented MRI data at the World Muscle Society Congress that could potentially contribute to establishing MRI as an endpoint for clinical outcome in Duchenne.

Developing therapies for Duchenne has been focused on physical tests and invasive procedures, whereas MRI represents an objective, sensitive and noninvasive way to assess disease progression in Duchenne.

The potential of MRI T2 to predict disease progression and potential treatment benefit in Duchenne could greatly enhance the ability of investigators to assess clinical effects of investigational agents.

These data represent a promising step forward to better understand MRI endpoints and their utility in Duchenne and to support our work to quickly bring forward hope and life-changing therapies to those affected by Duchenne. Slide 13 provides an introduction to MRI in Duchenne.

As we know, disease progression is characterized by the progressive replacement of muscle with fat, which can be measured in a noninvasive way using MRI. Last month we presented an analysis of data from Imaging DMD, the largest natural history database of MRI assessments in more than 150 boys with Duchenne, as shown on slide 14.

This illustrates the relationship between MRI T2, a measurement of fat and inflammation, and the ability of boys with Duchenne to perform physical function. The imaging DMD data demonstrate a strong correlation between the composite of lower leg MRI T2 and boys' functional abilities.

You can see on the left that the boys with lower MRI T2 can perform all the functional assessments. But for boys with higher MRI T2 values, they progressively lose functional milestones.

Overall the lower leg composite MRI T2 correlated with the ability to complete assessments of physical function with 2 milliseconds, which are the MRI T2 measurement units, corresponding to a clinically relevant difference in function.

These results highlight the clinical importance of the significant improvement observed in our MoveDMD trial with edasalonexent treatment for lower leg MRI T2 compared to the off-treatment control period, as shown on slide 15.

We saw a close to 4 millisecond increase per year in MRI T2 when the boys were off treatment, whereas we saw a significantly smaller 0.3 millisecond per year increase in MRI treatment after 48 weeks of edasalonexent treatment.

These improvements in MRI T2 are consistent with the improvements observed in all assessments of physical function with edasalonexent treatment compared to the off-treatment control period that I reviewed earlier.

These functional improvements are also consistent with the strong correlation between MRI T2 and clinical meaningful changes in function, as demonstrated in the imaging DMD data. We also looked at MRI fat fraction. We know that the amount of fat in the muscles of those affected by Duchenne increases irreversibly over time.

In the imaging DMD natural history data shown on slide 16 you can see that, compared with boys in the same age range not receiving any treatment, boys on steroids had less fat accumulation in both the vastus lateralis, a muscle in the upper leg that is part of the thigh, as well as the soleus, a muscle in the lower leg that's part of the calf.

Now what happened in the Catabasis MoveDMD trial? On slide 17 you can see that before the boys started edasa, the amount of fat in the VL and soleus was increasing, but on edasalonexent the rate of fat accumulation slowed. Again, all the pieces fit together with edasalonexent treatment.

We are seeing preservation of muscle integrity on MRI supported by decreases in muscle enzymes and translating into preserved function, our ultimate goal. I will now pass the call over to Andy Nichols, our CSO, who will tell us more about our collaboration announcement this morning.

Andy?.

Thank you, Joanne, and good morning, everyone. As Jill touched on earlier, we announced this morning that we entered into a preclinical collaboration with Dr. Pradeep Mammen at the University of Texas Southwestern Medical Center to explore the potential benefits of edasalonexent on cardiac function in Duchenne and Becker Muscular Dystrophies.

We are excited to collaborate with Dr. Mammen, a leading cardiologist in muscular dystrophy, and learn from his extensive experience as we build upon the potential beneficial heart effects of edasalonexent in Duchenne and Becker Muscular Dystrophies.

As cardiomyopathy is the leading cause of mortality in both of these muscular dystrophies, it is essential to improve heart health in these diseases. As slide 18 outlines, Dr. Mammen is the Founder and Medical Director of the Neuromuscular Cardiomyopathy Clinic at UT Southwestern Medical Center.

He is also co-director of the NIH Sponsored UT Southwestern Senator Paul D. Wellstone Muscular Dystrophy Cooperative Research Center. The mission of this center is to rapidly translate discoveries at the bench into the clinic and is focused on therapies for Duchenne. He is an ideal partner for this important research.

Inhibiting NF-kB with edasalonexent offers a unique mechanism with the advantage of potentially impacting both skeletal and cardiac muscle disease in those living with Duchenne or Becker Muscular Dystrophies.

The collaboration will build on our previous preclinical and clinical work and is a one-year preclinical study of edasalonexent in animal models of muscular dystrophy to investigate potential improved cardiac function. We expect results in this collaboration in the second half of 2019.

Today, we have our Vice President of Finance, Noah Clauser, joining us to share our financial update.

Noah?.

Thanks, Andy, and good morning, everyone. I'm glad to be joining you today. Turning to our financials, our third-quarter 2018 press release and 10-Q provide the details, so I will give you a brief summary.

We ended the quarter in a strong financial position with $43.2 million of cash, cash equivalents and short-term investments as of September 30, 2018. In the third quarter of 2018 our net cash used in operating activities was $5.8 million.

Based on our current operating plan, we believe we have sufficient capital to fund operations into the second quarter of 2020. We established a credit facility in 2014.

The final principal and interest payments due under that credit facility were paid as of September 30, 2018 and we have now completed all of our payment obligations under the credit facility. Our R&D expense in Q3 2018 was $3.9 million compared to $4.8 million in Q3 2017, a decrease of $900,000.

The decrease in research and development expenses was primarily attributable to a reduction in post-restructuring employee compensation and other non-program costs. We are pleased to share that, as part of our Q2 restructuring, we have now successfully subleased our extra facility space.

Our G&A expense in Q3 2018 was $2.1 million compared to $2.4 million in Q3 2017. Our operating loss was $6 million in Q3 2018, a decrease of $1 million versus Q3 2017. Our net loss was $5.7 million or $0.08 per share in Q3 2018, a decrease of $1.3 million compared to our net loss in Q3 2017.

For the third quarter we had weighted average common shares outstanding of $71 million. Additional financial information is available in our 10-Q, which we filed with the SEC earlier today. I will now pass the call back over to Jill..

Thank you, Noah. The advancements that we've discussed this morning support the potential future value of edasalonexent and get us closer to our goal of making this innovative treatment available to all of those affected by Duchenne. I will close on our vision for edasalonexent on slide 19.

As the Duchenne treatment landscape evolves we are well positioned having designed edasalonexent to inhibit NF-kB, a key link between the loss of dystrophin and disease manifestation and progression in DMD. We believe that inhibition of NF-kB with edasalonexent has broad therapeutic potential in Duchenne and may benefit skeletal and cardiac muscle.

Edasalonexent has great potential as a single agent for all of those affected by Duchenne as well as in combination with other agents that do not themselves target NF-kb. We are excited to have our Phase 3 PolarisDMD trial for edasalonexent underway and to see the 72-week results from our MoveDMD trial show durable beneficial effects.

We are focused on developing a therapy to improve the lives of those affected by Duchenne. And we are grateful to learn from a mother with a son participating in the MoveDMD trial about how, on edasalonexent, he has experienced positive progress with changes in muscle function observed at home.

This boy has stopped using a Gower's maneuver to pick up items from the floor and, for the first time, he started walking up the stairs in their home using both legs alternating each step. The family generously shared a video of their son showing his mother how he could climb the stairs.

It was so inspiring to see the excitement in his mom and incredibly heartwarming to see how proud the young boy was of his new accomplishment. While we recognize that this is an anecdote, experiences like his propel us forward as we look to bring edasalonexent to the broad population of all boys and men that could potentially benefit.

Thank you to the boys, their families and the clinical trial sites in our MoveDMD and now PolarisDMD trials. We truly appreciate their partnership and support of our shared mission. With that I will ask Bridget to open up the call for your questions. Bridget, can you please repeat the instructions and poll for questions? Thank you..

[Operator Instructions]. Our first question comes from the line of Hartaj Singh with Oppenheimer. Your line is open..

So, I've just got a few questions and I will keep them short. One is just talking about PolarisDMD, Jill, Joanne, I know that looking at my notes from a few months ago, and it seems that at that point you were talking of centers in the mid-30s in terms of the total number of centers you have.

Now you have got 40 centers worldwide, 25 I believe just in North America. And then also just our channel checks are indicating that there's a lot of demand at some centers for even additional patients or patients or siblings wanting to come on the trial.

Just what are your thoughts on what you're seeing initially as you're starting to conduct patient screening visits? And then I've just got some follow-up questions. Thank you..

Great, thanks, Hartaj. I will start. So yes, we have indicated that we intend to activate approximately 40 sites around the world to support the PolarisDMD Phase 3 trial. I would say it is exciting to see all of the activity in the Duchenne space. And you are right, there is a lot of activity and, for that matter, a lot of clinical activity.

I think we are in a unique position with regard to edasalonexent and the clinical trial in the Phase 3 Polaris, in particular in that we've had, I would say, a tremendous amount of interest from patients, incoming interest that we've been able to collect and now, as sites begin to open up, can transfer that interest to the appropriate site.

There are other trials that are recruiting in a similar age range. I think edasa has some benefits in terms of the trial design that make it a family-friendly trial. And I will turn over to Joanne to add a little more color to that..

We have gotten a lot of interest from sites and some additional sites as well. And we are the only trial in this age range that is not looking to randomize boys potentially to a steroid or steroid analog. So, I think that's - we are seeing a lot of interest..

Yes, that makes sense. The amount of literature on the long-term side effects of corticosteroids is pretty extensive. Do you have any potential - I know you have got a data monitoring committee.

Is there any potential that if you were to see a fairly significant robust clinical efficacy in the drug that you could actually terminate early? I know that those are always complicated simply because of what the FDA expectations are for the NDA, etc.

But just any thoughts there?.

Yes, we absolutely have a DSMB who will be monitoring the trial. And certainly they will be assessing progress of the trial and, of course, one reason they are there is to make sure the boys - that the safety is clear and there are no untoward effects that we should be aware of. They will be seeing unblinded data.

I will hand it to Joanne to add some more color around that..

They will be taking a look at that. In general they go on the side of completing the study because, of course, FDA wants to see a completed study for registration purposes. But they do have certainly the ability to ask us to make changes..

Yes, no, that makes sense, Joanne. And then the data you keep on collecting on MRI T2, you've got now the data from MoveDMD, you've got the imaging DMD data, which seems to suggest a pretty good correlation between MRI T2 and then functional changes.

You're obviously seeing a correlation - you presented at World Muscle, I believe, on correlation between MRI T2 and functional changes in MoveDMD.

So, how do you feel now about sort of getting this data together and the potential for your Type C meeting, whenever you have it with the FDA? I mean, how are you thinking about your dossier and the strength of this data that you are going to present to them?.

I would say in terms of the MRI data, we've been fortunate in being able to now collect data out following more than a year of treatment with edasalonexent.

And I would say we are quite pleased with the data we've collected to date and the consistency of that data and the concordance of that data with what we are seeing on other measurements that were captured in the MoveDMD trial, including assessments of physical function and also the other biomarkers that we looked at.

So that really, in our opinion, creates a very nice data set that we hope can begin to lay the groundwork to help regulators and others in the field to think about MRI and to consider it as a potential end point in DMD that reflects outcome.

And so, I think we've done a nice job at collecting data and beginning to build the data set and the positioning for that and certainly look forward to more discussions with experts in the field..

Jill, do you have any sense of when you will have that next meeting? I assume it's a Type C meeting, when you could have a discussion with the FDA for potential for accelerated approval..

So, I will give an unsatisfying answer. We can't really speak about our specifics of our regulatory interactions. But I can assure you we are absolutely pursuing all available options for expediting the edasa program to make it available as soon as possible to patients..

Great. Thanks, Jill. And then just a last housekeeping question. We've gotten a little bit of - a couple of questions from folks talking about the reverse split. I believe that's a technical issue with the listing for and the potential vote on that.

Can you just talk to us a little bit about that? Because there seems to be this inordinate concern on that and would love to get any color. And again, thank you so much for everything and all the progress..

Yes, thanks, Hartaj, and thanks for the questions. And so, with regard to the reverse stock split, so yes, we are looking, seeking shareholder approval to give the Board the authority to enact a reverse stock split should it be necessary. And that is for - you can define it as a technical reason to maintain our listing on the NASDAQ.

As you know, if we go more than 180 days trading below $1 then there is the potential for a delisting. And so, we want to have a mechanism in place should we need to address that..

Our next question comes from the line of Joel Beatty with Citi. Your line is open..

Thanks, good morning and thanks for taking the questions. The first one is related to the gene therapies that are in development. It looks like there is potential for them to be on the market in a few years or so for DMD.

In that type of landscape, could you discuss a little bit more about how you see edasalonexent fitting in? Could it be used in combination with patients that have already received a gene therapy?.

Thanks for the question, Joel. I'm going to hand it over to Andy..

Yes, Joel, as you know, the gene therapies are going to deliver a shortened form of the dystrophin, of micro dystrophin, which will most likely lead to a Becker-like phenotype where there is certainly - in Beckers disease there's certainly still inflammation and activation of NF-kB in the muscle.

And importantly, there's also cardiomyopathy which is similar to Duchenne, the leading cause of death in Becker muscular disease.

So we actually see a great potential for a combination of edasalonexent with gene therapy to actually enhance the activity, the efficacy of gene therapies because of that residual activation of NF-kB which occurs in Becker-like diseases and particularly the cardiomyopathy.

There's also the potential possibly of enhancing the activity of gene therapy through mechanisms related to work which other people have published to demonstrate NF-kB has the possible potential to regulate the ability of the adenoviruses to be taken up into cells. So that's certainly something that is a possibility.

But even if that is not the case, certainly combination therapy with gene therapy is definitely something that is very likely to be very effective..

Great, some helpful points there. I guess one more question based on what's been going on in gene therapy for DMD recently. It seems like there's been some data on CK levels in patients that have been treated and that's been seen as an important biomarker to follow there.

I'm curious on edasalonexent what is the importance of CK levels in understanding the effect of your drug and what have you seen with regards to your drug and the effect on CK levels so far?.

Let me start. As - so we've seen - what's been I think particularly exciting about the edasalonexent data set from MoveDMD is that we've seen durable statistically significant reductions in not only CK over 72 weeks of treatment but also three other muscle enzymes that are typically followed in Duchenne.

And so, all four of the muscle enzymes have been significantly reduced at every time point - 12 weeks, 6 months, 9 months, 12 months, 15 months, 18 months now - which is exciting to see that durable effect.

And those reductions are consistent with what we are seeing in terms of the stabilization of the disease state in these boys across the functional assessments. And so, I think that's a good sign.

Did I answer all your questions or was there another part?.

You did, that's very helpful. Thank you very much..

Thank you. And I'm not showing any further questions. I'll now turn the call back over to Jill Milne..

Thank you, Bridget and thank you all for joining our call today and for your continued support of Catabasis. We look forward to speaking with you again soon and keeping you updated on our Phase 3 PolarisDMD trial for edasalonexent and our other areas of progress. Have a good day.

Andrea?.

That concludes today's call. A webcast replay will be available for 90 days via the Investor Relations page on our website at www.Catabasis.com. Thank you..

Ladies and gentlemen, this does conclude the program. You may now disconnect. Everyone have a great day..