CohBar, Inc.
Q3 2020 Earnings Call Transcript

Published: 17 Nov 2020

[Operator:]

Good afternoon. My name is Rob, and I’ll be your conference operator today. At this time, I would like to welcome everyone to CohBar’s Third Quarter 2020 Financial Results Conference Call. Please note, this conference is being recorded. Now, I would like to turn the call over to Jordyn Tarazi, Director of Investor Relations at CohBar.

[Jordyn Tarazi:]

Thank you, Rob, and thank you, everyone, for joining CohBar’s third quarter 2020 financial results conference call. Joining me on today’s call is Steve Engle, CohBar’s Chief Executive Officer; Ken Cundy, CohBar’s Chief Scientific Officer; and Jeff Biunno, CohBar’s Chief Financial Officer. CohBar’s 10-Q filing and financial results press release were issued earlier today and may be downloaded from our website at cohbar.com. If you’re having issues joining the Webex, you can access the slide presentation from the homepage of CohBar’s website to follow along. Jeff will begin with an overview of the second quarter financial results, followed by a business and R&D update from Steve and Ken.

[Jeff Biunno:]

Thank you, Jordyn. And thank you, everyone, for joining us this afternoon. As Jordyn mentioned, if you are having issues with Webex, the slide presentation is posted on the home page of the CohBar website. Next slide, please? As Jordyn noted, I’ll begin with a review of the financials, followed by a business overview by Steve. Ken will then review the recent developments in our clinical and preclinical programs and will conclude with Q&A. Next slide, please? I will now provide you with a summary of our financial results for the third quarter ended September 30, 2020, compared to the third quarter ended September 30, 2019. Total operating expenses in Q3 2020 were $2.618 million as compared to $3.228 million in Q3 2019, a decrease of approximately $610,000. Operating expenses included noncash costs of $407,000 for the quarter ended September 30, 2020, as compared to $621,000 for the quarter ended September 30, 2019.

[Steve Engle:]

Thanks, Jeff. Welcome, everyone, to our call. We believe CohBar represents a rare opportunity in biotech and that mitochondria-based therapeutics represent a treasure trove of potential therapeutic agents for multiple diseases. We are elucidating the function of the peptides defined by sequences in the human mitochondrial genome. We are reading the language of the mitochondria, speaking to the rest of the body. Based on our progress to date, we expect this will enable us to develop key therapies in multiple chronic and age-related diseases. Let’s start our review of the quarter with 3 key points. In the Phase Ib study, half of the planned subjects have reached the end of their treatment. We made significant progress with our preclinical projects. For example, we announced new preclinical data showing enhanced effects when our antifibrotic peptide is combined with a commonly prescribed IPF drug. And third, based on continued progress in the antifibrotic program, we plan to nominate a second clinical candidate in the first quarter of 2021 based on completing several research tasks. Next slide? What is the CohBar opportunity? We believe that we are the leaders in developing a new class of therapeutics based on our founder’s discovery that mitochondrial peptides regulate multiple systems in the body. Think about that. Prior to 2001 Drs. Cohen and Barzilai’s discovery, people thought mitochondria were just the powerhouses of the cell and not a key player in regulating some of the body’s key functions. Because it is a new class of drugs, we believe mitochondria-based therapeutics represent a large, untapped and exciting group of potential therapeutics. Amazingly, our Chief Science Officer, Ken Cundy and his scientists have discovered over 100 peptides in the mitochondrial genome and developed over 1,000 analogs. It is like we have 100 keys on the wall and we’re taking them down one-by-one to discover which biological clock or lock they open. Based on our research results, we believe that some keys may actually open multiple locks, such as NASH and obesity. We are targeting a wide range of diseases that are associated with mitochondrial dysfunction. And because we’re targeting the problem at the cellular level, we believe mitochondrial peptides will work on the cause rather than just the symptoms. Mitochondria-based therapeutics benefit from over 1 billion years of evolution and may generate entirely new approaches to treating diseases. We need new and different approaches. In doing so, we are taking advantage of the mitochondrial-driven system of peptides that the body has evolved in developing our compounds, we are surfing on the wave of the evolutionary biology behind mitochondrial peptides. We believe that they represent a better starting point for developing therapeutic agents. As a result, our peptide medicines may have a higher probability of technical success compared to the traditional discovery approach. In the last year, the company’s portfolio has grown from 2 to 5 programs. We are no longer just a NASH-focused company and now have programs targeting ARDS, fibrosis and oncology. It is an exciting time. We continue to learn new things about this class of potential therapeutics, new indications, new targeted organs, new mechanisms of action and new approaches to helping patients. We expect to have a number of near-term milestones. And finally, as the leader in the development of mitochondria-based therapeutics, we are committed to strengthening our comprehensive intellectual property position. We have benefited greatly from a first-mover advantage.

[Ken Cundy:]

All right. Thank you, Steve. I’ll now give a brief update on recent progress in our research and development programs. Next slide, please? Let’s start with the clinical program. CB4211 is currently in Phase Ia/Ib clinical testing as a potential treatment for NASH and obesity. As a reminder, the Phase Ib stage of this study is a double-blind, placebo-controlled evaluation of one dose level of CB4211 given once a day in obese subjects with NAFLD. This phase is designed to assess the potential effects of CB4211 on liver fat, body weight and various biomarkers that are relevant to NASH, obesity and metabolic disease. Changes in liver fat will be assessed by MRI-PDFF, and all subjects must have a minimum of 10% liver fat at baseline during screening. This is a short study, not a pivotal Phase II study, so we will be looking for trends in the data. And we’ve been actively enrolling and dosing subjects and, currently, half of the target number of 20 subjects have already reached the end of their treatment. We’ve made this significant progress despite COVID-19-related issues, which have included the initial pause, slower enrollment and more recently, dropouts due to positive COVID-19 tests at one of our sites. With appropriate safety precautions, that site continues to dose already enrolled subjects on site while enrolling new subjects. These types of issues are not unique to us. Many other companies are experiencing similar COVID-19-related issues with their ongoing clinical studies. We currently expect to have the top line results in the second quarter of 2021, if the study continues to progress at the current rate, which may change due to the unpredictable nature of the COVID-19 pandemic and other factors such as the availability of subjects over the holidays. We expect to update the status of the study once the last subject has completed their follow-up.

[Steve Engle:]

Thanks, Ken. Next slide? So briefly, we wanted to make sure the opportunity was clear. As you know, with the NASH situation, it’s a large unmet medical need. There is no approved treatment for NASH, and over 30 million patients are at risk for NASH in the United States. In terms of landscape then, it’s a large and growing population, and it has been a bumpy ride for certain later-stage companies. However, this has very little to do with us because we have a unique mechanism of action. We do learn a lot, and we believe watching some of the companies that are in a later stage helps us design better future studies and regulatory strategy. Regarding the competitive landscape, it’s a very large opportunity at $30 billion as estimated. So there’s plenty of room for multiple therapies, and physicians believe there is a need for combination therapy. Again, there is no direct competitor for our mechanism of action. And previously, we’ve explained that there are synergies with the existing compounds like GLP-1s. Partnering is an important part of our strategy, and we think that our unique MOA is potentially applicable to all stages of NASH and, again, synergistic with the GLP-1s. As we note, the later-stage companies have valuations over $1 billion. We believe clinical results and partnering will be future drivers on our value and then we also believe that CohBar’s other programs will add to the overall value. Next page. Now I’d like to focus in a little bit on idiopathic pulmonary fibrosis, one of the targets in our preclinical antifibrosis program. In 2019, there were about 187,000 cases worldwide. It’s expected to grow to 220,000 by 2028. And the disease onset often occurs after 65. There’s a high unmet medical need. 1% of the deaths in the U.S. are caused by IPF. Unfortunately, only 50% of the patients live to 3 years and only 10% survive for 5 years. The current approved drugs slow the progression of disease, but do not reverse fibrosis. There is a clear need for combination therapies. You can see the global market numbers, but the real issue is that the current therapies have gastrointestinal and other problems like skin problems. They’re not well tolerated and, as a result, many patients either cannot stay on them or find themselves living in a very difficult situation, particularly when the drugs are combined. In our case, as Ken’s indicated, we have shown this ability to combine with nintedanib and show an enhanced effect. Next slide? And then as far as the opportunity in our other programs, clearly, there’s a high unmet need in the ARDS area. As Ken has talked about, there is no safe and effective treatment, and the survival rate is only 25% amongst COVID-19 patients with ARDS. And of course, our program targets potentially the other 3 million ARDS patients worldwide as well as patients with COVID-generated ARDS. And we have shown, as Ken said, some pretty interesting results. The one other preclinical program is our CXCR4 inhibitors for cancer and orphan diseases. The CXCR4 receptor is over-expressed in more than 75% of cancers. Therefore, we and others believe that the indications for a compound in this category include multiple cancer types, stem cell mobilization and genetic defects. And there, we have already shown that our inhibitors reduce mean tumor volume in a melanoma model by 61% in combination with temozolomide, a chemotherapy drug, versus 38% when temozolomide is used by itself. Next slide? These are the near-term milestones for us over the next 6 to 9 months. We expect to have additional results in ARDS in this quarter. We also plan to nominate a clinical candidate for one of these programs in Q1 2021. We are also expecting top line results from the Phase Ib in the second quarter of 2021, subject to the impact of COVID-19. And our overall goal for the pipeline is continuing generating programs, which could lead to multiple clinical studies over the next few years. Next slide? To close then I’d like to speak about why we are so excited about our development products and what they can do for patients. Let’s start with our innovative insulin-enhancing CB4211 compound. Again, there are no approved products, and the morbidity and mortality caused by NASH can be devastating. With the unique mechanism and the need for combination drug treatment in NASH, our novel molecule has potential to be an important compound in the future treatment of NASH. We also believe that the problems at different stages of NASH can be treated with therapeutics like ours. We have shown CohBar’s MBTs have unique mechanisms. And we originally had shown this with the NASH compound. And now we see the same combined effect with our antifibrotic peptides with nintedanib in IPF. Our priorities now are to generate top line results of the Phase Ib trial, to execute on our preclinical pipeline. And I am pleased with the progress across the board so far in 2020, especially with preclinical data from our IPF and ARDS programs and, finally, to nominate a new clinical candidate in the first quarter. In summary, we are pleased with the pace of progress. The key highlights from this quarter are the exciting preclinical results, which further demonstrate the depth and breadth of the program. We know that we have a special opportunity with mitochondria-based therapeutics. We remain committed to delivering on the promise of our science to bring forward a new class of medicines for patients. Next slide? Now I will turn the line over to Rob to open up for the Q&A.

[Operator:]

Our first question is coming from the line of Elemer Piros with ROTH Capital Partners.

[Elemer Piros:]

Gentlemen, thank you very much for the comprehensive update. I only have a handful of questions. Ken, you alluded to that half of the patients in the 4211 have been -- completed their treatment phase, and you described the continuum of the pipeline in this trials. Are there any other patients at the beginning of the screening phase or elsewhere in this continuum that are being contemplated now?

[Ken Cundy:]

Yes, without getting into patient-by-patient details, we’re still in the recruiting, screening, enrolling phase. So we’re bringing in patients continually, and they’re exiting continually. That’s the way I describe it.

[Elemer Piros:]

Okay. And with regards to 5138, the antifibrotic peptide, the follow-on that you will announce, it’s not going to be a replacement, did I understand correctly, to 5138, but for potentially an additional antifibrotic indication?

[Ken Cundy:]

That’s right. It would be potentially adding to the breadth of possible uses of the lead that we choose as a clinical candidate for IPF, in other words, have the opportunity to also pursue it for other fibrotic indications, and on the list, as you heard, just as a start, exploring scleroderma preclinically, kidney fibrosis and potentially NASH.

[Elemer Piros:]

Okay. And the last question I had. We all, obviously, heard the good news on the vaccine front from 2 different companies. What would a highly effective, let’s assume that it remains as effective as it was announced today and a week ago, a vaccine mean for the ARDS market, especially the COVID-related ARDS?

[Ken Cundy:]

Right. Well, to the first question, which is to the ARDS market, in general, even a very effective COVID-19 vaccine is not going to diminish the unmet need of those existing 3 million that didn’t get their ARDS as a result of the COVID inflection. That’s a huge continuing unmet need. But for COVID itself, I think it’s too early to really conclude that the vaccines currently in development are good enough or will last long enough or will have effects in the severely affected subjects, which is the key here. The ones that are suffering from ARDS and have a high risk of mortality are a subset of the population, and it’s really important to understand how they are protected. Regardless of that, people who recover already from COVID infection are going to have longer-term consequences. And we think there are other molecules within our portfolio as well that could be applicable to those longer-term downstream consequences of severe COVID infection.

[Operator:]

Next question comes from the line of Kumar Raja with Brookline Capital.

[Kumar Raja:]

Yes, I would like to continue with regard to the recruiting and screening. Can you give us a sense like what proportion of patients kind of end up being dosed, starting with the recruiting and screening? And also, with regard to the Phase I, what kind of trends in terms of liver fat as well as body weight and other biomarkers do you guys think will be optimal?

[Ken Cundy:]

Okay. Two good questions there, Kumar. Thanks for the questions. The first, as far as recruiting and screening, as I said, it’s an ongoing continuous process. If you were asking more about what’s the screen failure rate here, so how many people do we have to screen to find successfully qualified subjects, that’s a common thing across studies that there will be a screen failure number because you have a long list of criteria. So we’re looking at finding a lot more subjects than actually enter the study, but that’s just part of this process. And we’ve been successful in getting halfway through it so far despite the COVID issues that arise, as they have arisen with many clinical studies right now. So that’s about as much detail as I can give you on the screening side. To your second question, what trends are we expecting to see out of this study? Well, I’ll give you kind of a perspective on this. There were some recent results released in the space for NASH studies in a 4-week setting, one example being direct that put out their data recently. And then we’re happy to report in their case something that amounted to when you look at the data around a 7% reduction in liver fat, and that translated, obviously, to the suspicion that there is good efficacy in that period. So I’m not saying that’s what we’re targeting, but I’m saying we’re going to need to look at the data carefully to judge what a predictive trend is as to how that translates to a 12-week study or a Phase II study. And that’s just the liver fat. So then we’ll also be looking at body weight, and it’s a long list of biomarkers. And that’s less clear going into it as to what constitutes, as you said, optimal outcome. It will probably be looking across multiple biomarkers for an indication of a continuum, if you like, of effects that are related to NASH or obesity or even to metabolic disease.

[Kumar Raja:]

Okay. And in preclinical studies, we have seen synergistic effects with GLP-1. So how do you think that will kind of fit into how you guys think in terms of future studies?

[Ken Cundy:]

That’s a good question because it is a consideration in designing a follow-on study. If a follow-on study is a Phase II 12-week or a 16-week study in the NASH population, it may be better to do that study in the setting of diabetic NASH subjects because 50% of NASH subjects are diabetic, in particular, those that may already be on a stable regimen of a GLP-1 agonist. Because we do have this evidence that the mechanism of our drug is synergistic complementary to a GLP-1 mechanism. And that may be true of other mechanisms, too. So, I’d say that factors very significantly into our thinking around what the next study might be in this program.

[Kumar Raja:]

Okay. And you touched about expanding into scleroderma, kidney fibrosis and NASH. What preclinical data do you have in that front that gives you confidence? Or this is something that studies need to be done in the future?

[Ken Cundy:]

Yes, the studies are initiated and ongoing in some cases and about to be ongoing. So, we’ll have these data probably in the next few months on those parallel indications. So this will be new preclinical data we’ll be generating with our lead analogs in the CD5138 setting so that by the time we are in a position to select the candidate for IPF, we will be -- have a good understanding of its utility for those other indications as well.

[Kumar Raja:]

And finally, with regard to the CXCR4 inhibitors, when can we expect the next update on that?

[Ken Cundy:]

Yes. Sure. That program is continuing in our preclinical studies right now and progressing kind of on the schedule with plan. So we’re expecting to update on that program at the next call, hopefully, with some new data to demonstrate their utility there. As we said, we’re exploring utility in the setting of things like stem cell mobilization, and we’ll give an update on the next call.

[Steve Engle:]

Kumar, thank you very much.

[Operator:]

The next question comes from the line of Steve Brozak with WBB.

[Steve Brozak:]

I only have one, given most of the things have been asked and answered. And it goes back to one of your earlier questions. And it’s specific to the COVID sequelae that is now becoming very well documented and, unfortunately, untreatable. Can you go back and cover what you were saying originally about the potential for your platform to treat these issues that exist long after the patients have left the hospital and rehabilitation, please?

[Ken Cundy:]

Sure. Yes, Thanks, Steve. Let’s talk about that. So, the immediate use of our CB5064 analogs, the apelin agonist in the setting of COVID or ARDS, whether it’s related to COVID or not, is addressing the acute injury. So, it’s an acute injury phase when there’s a lot of damage going on in the lungs and the other tissues. And that’s where we think that program will have immediate utility. Obviously, if you’re reducing those -- that damage, you’re also going to reduce the downstream sequelae of that, the downstream consequences of the damage that could translate in the longer term into things like more lung fibrosis, more kidney failures, more chronic morbidity related to the damage you caused in other tissues. But having said that, we’ve also got a portfolio of peptides here. So we have other peptides and an example being the antifibrotic peptide that you could potentially directly use to treat the type of fibrosis that might be developing now in these subjects that had a severe COVID infection and had damaged lungs and are now looking at dealing with this chronic situation that is just emerging now, as you said, becoming very clear.

[Steve Brozak:]

And in terms of the mechanism, which you’d be looking at, it wouldn’t be a leap of faith at all to be able to go out there and utilize that mechanism to deal with these issues that, as you put it, were once acute and now are chronic. Is that a good way of looking at?

[Ken Cundy:]

Yes. I think that’s true. It’s not really a stretch of the imagination to say that’s something that you’ve already shown directly can improve lung fibrosis when it’s induced by an injury. There are some who would argue that the bleomycin model is actually a model of COVID-related injury as well because the downstream effects are similar. So, I would say, yes, there’s a good likelihood that antifibrotic peptides might have utility in a setting like the downstream consequences of COVID.

[Operator:]

Our next question will come from the line of Bandra Sebra, private investor.

[Unidentified Analyst:]

Sorry. It’s an accident. I didn’t mean to press. I didn’t mean to ask a question.

[Operator:]

At this time, I will turn the floor back to Steve Engle for closing comments.

[Steve Engle:]

Thanks, Rob. Hey everybody out, you get a sense of how excited we are at making now past the halfway mark with the study for CB4211 and also that we just continue to make progress that adds to not only the knowledge about specific programs, but about the peptides in general. So, we look forward to sharing more with you in the next call, and we’ll look forward to that at that time. Thanks very much for joining us today.

[Operator:]

Thank you, everyone. This will conclude today’s conference. You may disconnect your lines at this time. Thank you for your participation.