CohBar, Inc.
Q4 2020 Earnings Call Transcript

Published: 30 Mar 2021

[Operator:]

Good afternoon. My name is Paul and I will be your conference operator today. At this time, I would like to welcome everyone to CohBar's Fourth Quarter 2020 Financial results conference call. All lines have been place on mute to eliminate background noise. A brief question-and-answer session will follow the formal presentation. As a reminder, this conference is being recorded. Now I would like to turn the call over to Jordyn Tarazi, Director of Investor Relations at CohBar to begin.

[Jordyn Tarazi:]

Thank you, Paul, and thank you everyone for joining CohBar's fourth 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.

[Jeff Biunno:]

Thanks so much, Jordyn, and thank you, everyone, for joining us this afternoon. As Jordyn mentioned, if you're 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 we'll conclude with Q&A.

[Steve Engle:]

Thanks, Jeff. Welcome everyone to our fourth quarter 2020 call. We believe that mitochondria-based therapeutics will provide a treasure trove of potential therapeutic agents for treating multiple diseases. CohBar is elucidating the function of multiple peptides, defined by sequences found 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 healing therapies in multiple chronic and age-related diseases. This represents a rare opportunity in biotech. So let's start our review of the quarter with four key points. Number one, yesterday we announced completion the enrollment in the Phase 1b study. Next, we plan to announce when the last subject has completed their last visit. Ken will speak more about the importance of this step in his section. Currently, we are expecting top line results at the end of the second quarter of 2021 based on a number of factors, including the timing of the last clinical study subjects visit. We made significant progress with our preclinical projects, and expect 2021 to be a transformative year for CohBar as we advance our clinical programs towards the clinical stage. For example, we announced CB5138-3 as our next clinical candidate for the potential treatment of IPF and other fibrotic diseases. We have chosen IPF as our initial indication due to a combination of factors, both commercial and technical. Number three we announced the initiation of the collaboration with the US government's National Institute of Allergy and Infectious Diseases, signing an agreement called an NCEA to evaluate our CB5064 Analogs in models of COVID-19 ARDS. As a reminder, we will be providing our Apelin agonist peptides to NIAID for them to administer the preclinical COVID-19 studies at their expense. CohBar will continue to develop and evaluate compounds in this program in parallel with the activity being conducted at NIAID. And four, Wall Street analysts covering CohBar have increased from four to five.

[Ken Cundy:]

Thanks, Steve. I'll now give a brief update on recent progress in our key research and development programs. Next slide please. So let's start with the clinical program. CB4211 is currently in Phase Ia/Ib clinical testing as a potential treatment for NASH and obesity. The Phase Ia stage of the study is completed and we recently announced that we have also completed the enrollment of the Phase Ib stage of the study. Now as a reminder, this Phase Ib stage of the study is a double-blind placebo-controlled study with a target enrollment of 20 obese subjects with NAFLD in order to provide 10 on placebo and 10 on one active dose level of CB4211 given once-daily by injection. The Phase Ib stage 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 are measured by MRI-PDFF and all subjects were required to 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. We were able to complete enrollment in this study despite the earlier issues, which have included COVID-19 related impacts on the study pause, on slower enrolment, dropouts due to positive COVID-19 tests at one of our sites. And even more recently, we've had to deal with ice storms in Texas that impacted even routine lab testing across many regions of the state. We currently expect to have the top line results at the end of the second quarter of 2021 subject to any further unpredictable factors and we expect to update the status of the study again when the last subject has completed their final follow-up safety visit. Next slide please. So as we discussed on the last call, the clinical trial process for this study has been a rolling enrollment. As shown in this simplified diagram, each new subject was enrolled dosed and followed up for safety. When each subject receives their last dose, there's still a follow-up period for safety observation to ensure there are no issues. This process continues until the last subject has completed the final study follow-up as shown by diamond. Now data are collected throughout this entire process and entered into a database. And at this stage, all data are still blinded meaning we do not yet know who received CB4211 and who received placebo. When all subjects have completed, the final follow-up visit and after all required data for safety pharmacokinetics, liver fat, body weight and biomarker levels have all been collected, the data are then cleaned, checked for errors, the errors are systematically resolved and then the database is locked. Only then will the data finally be unblinded and the analysis of the data will begin. Next slide please. So what can we expect out of this Phase Ib study? Well, there are multiple possible outcomes. The primary endpoints of the study are the safety and the tolerability. The secondary endpoint will be the pharmacokinetics. The exploratory endpoints include the changes in liver fat, body weight and biomarkers after four weeks of dosing that we will be analyzing for trends. And what about historical precedent for four-week studies with other NASH compounds? What have they shown? While there have been several other published studies that have looked at trends in these same types of activity outcomes in either NAFLD or NASH subjects after a similar four-week treatment period. A number of companies including Merck, NGM, Metacrine, Hepion and DURECT have released data from four-week studies in either NAFLD or NASH subjects. In some cases, they looked at liver fat changes. In others, they looked at biomarkers and sometimes both. There was a wide range of outcomes in these studies from statistically significant changes to smaller trends and in at least one study the positive effects were only detected using a subgroup of the study subjects. So this range of outcomes may be the result of testing drugs with completely different mechanisms of action and some of which have already been validated in other indications, meaning there was already a sense of their clinical potency and some knowledge about the best way to give the drug. There are also some important differences between these prior studies and CohBar's Phase 1b. Our study is a double-blind placebo controlled study, while some of the published studies were open-label designs, meaning there was no attempt to conceal the identity of the treatment from the subjects or the investigators and there was no control group to demonstrate the underlying placebo effect. CB4211 has a unique mechanism of action compared to the agents assessed in those prior studies. And also unlike those earlier studies, our subjects were confined for the duration of their treatment. As this is the first-in-human study of CB4211, we will obviously need to wait for the top line data. Next slide, please. Now let's talk about what's next with CB4211. We plan to complete the ongoing Phase 1a/1b study with readouts for NASH and obesity and prepare for the next clinical study in NASH, including seeking a corporate partner. Now based on positive clinical results and additional funding from potential partnerships and general fundraising, we then plan to initiate preparations for Phase 2 in 2021 and then initiate a Phase 2 study in 2022. Our plans for another clinical study for NASH will depend on what we see from the Phase 1b data in terms of trends in liver fat reduction by MRI-PDFF and trends in the biomarkers. This is a small study involving four weeks treatment, so we will not be looking for the same outcomes, such as biopsy driven outcomes of larger Phase 2 studies that have a longer duration of 12 or 16 weeks. In planning for another clinical study, there are a number of factors that normally must be considered. Based on the Phase 1b outcome, we need to select the optimum dose regimen or regimens to take forward, the study design and duration and we need to understand how the regulatory landscape is evolving around the most appropriate primary and secondary endpoints. We will need to select the most appropriate patient population for our drug, the right stage of fibrosis to study and carefully consider the potential contribution of diabetes and other comorbidities in the NASH study population. It may be advantageous to use a diabetic population on a GLP-1 agonist to take full advantage of potential synergy with CB4211 mechanism and help differentiate our product. Now we also need to conclude all necessary Phase 2 preparations, including any remaining manufacturing toxicology, et cetera. And as we progress in development, we will continue to refine our formulation towards a final commercial form. And then independent of the NASH outcome, we will continue to look at the potential for CB4211 in obesity and possibly other alternative indications. Now ultimately NASH is a complex disease involving a progression from fat accumulation in the liver to inflammation to fibrosis, cirrhosis and eventually liver failure or cancer. There will continue to be a need for multiple treatment options that can be used in combination to address the different stages of the disease. And as we previously described the mechanism of CB4211 is synergistic with some of these other mechanisms like GLP-1 agonists and that suggests potential utility in that combination treatment setting. Next slide please. Now let's move on to our preclinical program, with the antifibrotic peptides or CB5138 analogs, these are a family of novel molecules related to mitochondria coated peptide that showed strong antifibrotic and anti-inflammatory properties in multiple in vitro and in vivo models of idiopathic pulmonary fibrosis or IPF. Now based on studies conducted in cultured human lung cells, these peptides appear to work by reducing the production of key proteins involved in fibrosis and by inhibiting the pathological fibrotic process of cell transformation from healthy lung cells to fibrotic cells. We've built on those initial discoveries with improved analogs, demonstrating clear antifibrotic, and anti-inflammatory effects in vivo, in prophylactic and therapeutic animal models of IPF. In the therapeutic model, we showed the treatment of animals beginning one week after induction of fibrosis with bleomycin had positive effects on all study outcomes, reducing the long fibrosis, the levels of collagen, cytokine secretion and inflammation. We further demonstrated the efficacy of multiple CB5138 analogs in this therapeutic model. And then using the same therapeutic model, we showed that a combination of CB5138 analog with nintedanib one of the two approved IPF drugs and the current standard of care produced greater effects than dosing nintedanib alone. Additional combination studies are ongoing. However, we will likely use monotherapy for the initial clinical proof-of-concept. Most importantly, we recently announced the nomination of a new clinical candidate CB5138-3 as a potential treatment for idiopathic pulmonary fibrosis. We have initiated IND-enabling activities, and we plan to potentially file an IND and start clinical studies in 2022. At the same time, the broad anti-fibrotic and anti-inflammatory effects of CB5138 analog suggests, there is a potential for using them to treat other fibrotic diseases. We're exploring that potential now in the preclinical setting in models such as NASH, systemic sclerosis, and kidney fibrosis. Next slide please. On this slide, we see some of the data for that final CB5138-3 candidate that were released last year at the American Thoracic Society Virtual Annual Meeting. This is looking at efficacy of the peptide as monotherapy, using the mouse therapeutic model of IPF. So one week after bleomycin induction of fibrosis, animals were treated with placebo vehicle in the red bars, nintedanib in the green bars, our CB5138-3 shown in the orange bars. Now nintedanib, as I said is one of the two approved IPF drugs. It's a tyrosine kinase inhibitor that blocks several different targets leading to slowing of the progression of IPF. But nintedanib also has significant off-target effects, including nausea vomiting and diarrhea. And here you see CB5138 has consistent anti-fibrotic and anti-inflammatory effects across the board, including reductions in fibrosis, lung weight, inflammation in terms of lymphocytes in the lung and levels of collagen both in the lung tissue and secreted into lung fluid. Next slide please. And here, we see some photomicrographs of the lung tissue from these mice. Top left, you see an example of healthy lung tissue from an animal that did not receive bleomycin. Top right, is the lung tissue of an animal given the bleomycin to induce fibrosis and then treat it for two weeks with vehicle control, it shows significant fibrosis and infiltration of inflammatory cells. On the bottom left, is the lung of an animal given bleomycin followed by nintedanib the standard of care. There is less fibrosis and inflammation. But on the bottom right, we see the lung of an animal given bleomycin followed by CB5138-3 even more significant reduction in the fibrosis and the inflammation. Next slide please. Here we see another study in the therapeutic mouse model of IPF. In this case, we're looking at levels of pro-inflammatory cytokines, secreted into the lung lavage fluid, after induction of fibrosis, again, waiting a week before treating for 14 days with either vehicle nintedanib or CB5138-3. Treatment with nintedanib had no effect on the levels of these pro-inflammatory cytokines. In contrast, treatment with CB5138 reduced the levels of all of these cytokines. Next slide please. And from the same study, here we're looking at infiltration of inflammatory cells into the lung by the end of the treatment. And treatment with nintedanib for 14 days reduced the levels of cell infiltration, but treatment with CB5138-3 produced a greater reduction in the levels of macrophages lymphocytes and neutrophils in the lungs. Next slide please. So now let's talk a little bit about the candidate selection process. Obviously, we can't go into this specific way in which we design new analogs or how we go about changing their structures to improve their properties. That's part of our proprietary optimization approach. But we generate analogs in an iterative process that incorporates improvements into their design. There are many factors that need to be considered in selecting the final clinical candidate. We evaluate the analogs in various in vitro and in vivo models. We look at efficacy in animal models of the target indication. We look at drug-like properties which include things like physical properties, chemical and metabolic stability, pharmacokinetics, and suitability for the intended route of administration. We also need to consider how easy they are to synthesize and scale up for eventual clinical or commercial use. We need to look at preliminary safety data. And beyond that there are several other factors involved. Out of this process, we have identified CB5138-3 as the lead candidate. But there are other peptides that are still useful as potential backups. The next step for CB5138-3 is to complete the necessary IND-enabling activities and the IND submission to FDA that will potentially support a first-in-human clinical study. Next slide please. Well, lastly, I'll briefly give an update on the CB5064 analog program. This is our family of Apelin agonist peptides under development as a potential treatment for acute respiratory distress syndrome, ARDS and COVID-19 related ARDS. We previously announced that we've signed a non-clinical evaluation agreement with the National Institute for Allergy and Infectious Diseases, NIAID. And under this agreement, NIAID will evaluate the efficacy of our CB5064 analog in their model of COVID-19 at their expense and the model could be something such as the hamster model of SARS-CoV-2 infection. That model has been reported to reproduce some of the acute lung changes that are seen in the lungs of COVID-19 patients with ARDS. The conduct and the timing of that study is now in the hands of NIH, so we cannot provide guidance on when the data may be available. However, we do look forward to that opportunity to assess the protective effects of CB5064 analogs in the model of COVID-19 related ARDS. And in the meantime, we'll continue to move this program forward for ARDS in general subject to available resources. Next slide please. Now, in this slide, we present some recent data from a follow-on efficacy study of the CB5064 analogs in a mouse model of ARDS. This involves using lipopolysaccharide or LPS-induced acute lung injury. The animals received a single dose of these peptide analogs one hour before the LPS administration and then bronchoalveolar lavage fluid was collected from the lungs at four hours after the LPS induction. And here we're looking at the levels of key inflammatory cytokines that are found in the bronchoalveolar lavage fluid. We see that CB5064 analogs reduced the levels of pro-inflammatory cytokines and these are the same cytokines that are part of the cytokine storm that is characteristic of severe COVID-19 ARDS. So, we're continuing to move this program forward as I mentioned and further development after candidate selection will depend on availability of resources. So, with that, I'll turn the call back to Steve.

[Steve Engle:]

Excellent Ken. Next slide. In closing, I would like to speak about our priorities and why we see this as a transformational year for CohBar. Our priorities are to generate topline results from the Phase Ia/Ib study. And number two to conduct the IND-enabling studies to bring CB5138-3 into first-in-human trials next year. And number three, continue to execute on the rest of our preclinical pipeline programs. From this plan, you can see why we believe 2021 represents a year of progress from conducting preclinical studies in multiple indications to potentially enable multiple clinical studies in 2022. I am pleased with our advancements across the board and look forward to the continued change in our pipeline. Given the potential impact of last year's pandemic, I'm also pleased with the pace of execution. 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. Finally, I would like to end my remarks by thanking the many people who participate in our clinical studies, including the healthy volunteers, patients and physicians. We also would like to thank the great team at CohBar for working hard every day to make this vision a reality. Lastly, I'd like to thank our loyal shareholders for believing in our vision. Next slide. Now we'll turn the line over to the operator to open the line for questions and answers.

[Operator:]

Thank you. We will now be conducting a question-and-answer session. Thank you. Our first question comes from Michael Morabito with Chardan Capital Markets. Please proceed with your question.

[Michael Morabito:]

Hi, Steve. Thanks for taking the questions. So I just wanted to try to touch on a little bit of your expectations for 4211, specifically regarding the liver fat. We've seen a lot of NASH compounds come out and report liver fat data, especially from early trials. And the numbers can be all over the place as far as how much liver fat is impacted. So based on the mechanism of action, roughly I'm not looking to get a number for me or anything, but roughly what kind of impact would you expect on liver fat reduction from 4211 that we should be looking for? And I also wanted to find out if the delays in the trial are due to more COVID impacts and the ice storms in Texas. I know that they involve -- they affected enrollment, but did they also affect patient visits for patients that had already been enrolled. And finally, you mentioned that you'd like nominate a new third candidate by the end of the year. Do you think that would be likely to be ARDS or CXCR4 something that you've talked about before, or is this something that maybe is something new that maybe we haven't heard about before?

[Steve Engle:]

Ken?

[Ken Cundy:]

Yeah. Let me take those one at a time Michael. Thanks for the question. So the first one about 4211 and the liver fat expectations. What I said and as you're aware several four week studies have been conducted. Some are in NAFLD some are in NASH or presume NASH and the liver fact changes as you said have been quite varied. I think it's very difficult for us to predict a number that we would expect to see, but we would hope to be able to see a trend in liver fat out of the four week setting based on prior observations over that period. It is possible to impact liver fat significantly in that duration of treatment. But again, we're not necessarily looking for a powered significant change so much as a trend in liver fat. As for a number, your guess is as good as mine. We can't directly predict from the animal studies what the number will be at the end of a four week study in humans and that's pretty clear from what's been published from those other studies, but that's as far as we can go I think. On your second question which was about the COVID-19 ice storms and the other impacts of COVID-19. Yeah, as we mentioned, we did have dropouts related to COVID-19 positive clinical testing. We've had subjects that came back later for safety visits and unrelated to their time on the study became infected after the fact that hasn't impacted their ability to generate data as far as them having completed their dosing. So that's a minor component as opposed to subjects that have to drop out of the study because they are positively tested. But as we said, we've now completed enrolment, achieved our target and awaiting this less couple of subjects to get through the process and complete their last follow up visit. And then your third question was about our third candidate. So yes, I think the likelihood is that would come from the ARDS program, based on the progress we have there and the fact that we are now moving towards a candidate selection. We've demonstrated in multiple models the activity that we expect to see for something that is stimulating the Apelin agonist pathway, that's clear from these acute lung injury models. The next step there of course is select a candidate and move through the same process that we've just started with CB5138-3, but of course in the case of ARDS will also be dependent on available resources. So let me know, have I hit on the three things you brought out there Michael?

[Michael Morabito:]

Yes, you have. Thank you very much for the thought.

[Ken Cundy:]

Thanks Michael.

[Operator:]

Thank you. Our next question comes from Elemer Piros with ROTH Capital Partners. Please proceed with your question.

[Elemer Piros:]

Yes, thank you so much. Maybe if I could pre-empt a housekeeping question with Jeff. Jeff, I think you mentioned that the fourth quarter R&D expense was confluence of events that made it a onetime higher than previous quarters. Looking forward if you were to look at 2021 estimated expenses, would the $6.5 million to $7 million would be the right range, based on previous trends, or do you expect that to increase higher than that range?

[Jeff Biunno:]

Hi Elemer, thanks for the call. It will probably be that as a base and slightly higher than that as we get through. As we get through the programs and the clinical trial, we're going to start incurring the cost now that sort of pushed through to this year. So, we'll probably be around that to a bit higher than that as we invest more in the R&D, as well in the other programs.

[Elemer Piros:]

So north of $7 million and some...

[Jeff Biunno:]

I didn't hear what you said I'm sorry?

[Elemer Piros:]

North of $7 million that's what you're referring to?

[Jeff Biunno:]

Right. Yes.

[Elemer Piros:]

Okay. Okay. Thank you. And Ken if you could just come back to the 4211 study. You listed a number of safety and efficacy biomarkers and biomarker information that you're collecting in the top line release. Which of those would you focus on or concentrate on?

[Ken Cundy:]

We would definitely have -- by the time we have our top line data information on all the ones listed. So we will certainly have an initial sense of trends across those -- that entire list. But as you know when you get data of that magnitude as far as that many outcomes there's a lot of follow-on analysis you need to do. So we would expect to be able to tell when we first put out top line data towards the end of the second quarter what was our impact specifically on each of those biomarkers.

[Elemer Piros:]

Right. And as far as collection of these biomarkers at multiple time points in the 20 patients or 20 subjects you have a fairly good sense that there is good completion rate or that you have the number of data points that you need for the analysis?

[Ken Cundy:]

Yes. And part of that Elemer is because we are -- these subjects are confined for the duration of treatment. So by definition, we are pretty much assured of having access to biomarker readouts. And many of these are taken on a weekly basis. So we'll have quite a lot of data out of this readout.

[Elemer Piros:]

And if you could just lastly remind us that how many doses in the active arm are you testing?

[Ken Cundy:]

There's one dose level of active versus placebo head-to-head in the Ib. So it's a dose that was selected out of the Ia Stage of the study and that's the same dose being used. Yes. But just to clarify it is once-a-day dosing for the 4-week duration by subcutaneous injection.

[Elemer Piros:]

Got it. Thank you so much for your help.

[Ken Cundy:]

Sure, thanks Elemer.

[Operator:]

Thank you. Our next question comes from Steve Brozak with WBB Securities. Please proceed with your question.

[Steve Brozak:]

Hey, good afternoon gentlemen. And thanks for taking questions. Just one, can you give as much detail as possible on your programs, specifically around COVID? And the focus I guess, because a lot of people are just simply looking at COVID as a single issue. But the area that I'm interested in asking about specifically is, what I guess is now turned long haulers. And where the critical importance of CohBar and its programs would be for them? And I'll hop back in the queue. Thank you.

[Jeff Biunno:]

Ken?

[Ken Cundy:]

Yeah. Thanks, Steve. Yeah, I'll take that one. Thanks, Steve. Thanks for the question. Yeah, you're absolutely right. COVID is an evolving situation as far as the squally the downstream effects of the infection. It's not just what happens when you're hospitalized and you recover and you think you're returning to a healthy life. There are many people that have long-term consequences or infection. Some of these are manifesting in different ways in terms of things like, persistent thrombotic issues. There's evidence of lung fibrosis, as a result of the initial injury caused locally in the lungs by COVID as well. So, there will be continuing need for ways to treat COVID subjects even after we have vaccinated as many people as we can. And not just because of these long-haul issues, but because of the emergence of new strains, as I'm sure you're very familiar with the possibility of new strains emerging. When you are unable to vaccinate everyone obviously there are then pockets where continuous infection and re-infection occurs and mutation will occur. So we see the possibilities for treatment with Apelin agonists are not just in the setting of the acute current vision of what COVID is, but the longer-term issues related to COVID which go in many directions related to the downstream damage that the COVID infection has caused. And actually overlaps somewhat with our other indications. So if you think about it fibrosis now we have an antifibrotic peptide. That is not our current Apelin agonist program targeted to COVID, but may very well be an asset that could be used in the setting of the long haulers for COVID, as fibrosis becomes more apparent.

[Steve Brozak:]

Great. Thank you for detailing, that because it was one of those things that obviously a lot of people just don't grasp the totality of it. Thank you again.

[Ken Cundy:]

Yeah. Thanks a lot Steve…

[Jeff Biunno:]

Thanks.

[Ken Cundy:]

Thanks for the question.

[Operator:]

Our next question comes from with Brookline. Please proceed with your question.

[Unidentified Analyst:]

Hi. Thank you. Thanks for the business update. I'm on behalf of Kumar from Brookline. And I had a quick question related to what Steve asked, regarding the studies with CB5064, your COVID-related ARDS program. I was just wondering if you could throw some light on how you plan to move with it. In terms of the clinical studies do you expect to have partnership with possibly big Pharma, maybe in the ARDS or diabetes space?

[Ken Cundy:]

Yeah, that's a good question. As far as the near-term setting, so we would progress towards healthy subject initial clinical entry. Then for the ARDS, non-COVID-related population that would be obviously a longer-term design probably looking at the same readouts that we're demonstrating or affected by the Apelin and signaling pathways. So, what effects are we having on those circulating cytokines in the setting of ARDS? So driven more by the mechanistic readout in a proof-of-concept kind of study is how I think we would take that forward initially into ARDS. And now that may of course change, if the results we see in the SARS-CoV-2 ARDS setting are convincing there may be added momentum if we get interest from the U.S. government in that program based on those outcomes.

[Unidentified Analyst:]

Okay. Yeah. Thank you.

[Ken Cundy:]

Steve wants to add to that, but...

[Unidentified Analyst:]

Okay.

[Steve Engle:]

No, no, that was great, Ken. I think the only other thing I'd add is that, there's two sides of this right? There's the acute disease situation and there's the chronic. So that's another piece in thinking about partnering and so forth.

[Unidentified Analyst:]

Correct. Thank you so much.

[Steve Engle:]

Thank you.

[Jeff Biunno:]

Thank you.

[Operator:]

Thank you. Our next question comes from Nathan Weinstein with Aegis Capital. Please proceed with your question.

[Nathan Weinstein:]

Hey, good afternoon. Thanks for the update and for taking my question. So I suppose we could just start perhaps you wouldn't mind talking a little bit about the mitochondria derived peptide the platform itself, the potential you see I know you've discovered over 100 of the peptide and 1,000 analogs. So perhaps you could speak about the variance you've seen in those peptides and maybe the range of indications they could address perhaps even beyond what's the clinical stage?

[Steve Engle:]

Ken?

[Ken Cundy:]

Yeah. Let me take that one. So it's a great question and it points to what is it that you think mitochondria are, right? Obviously they're not just organ ALS that are there generating ATP. We know that now from not just the work of our founders when they first uncovered the original MDP list so things like humanin and the SHLPs and MOTS-c, but there is definitely a broad range of possible interactions here from these mitochondrial derived signaling peptides that we are just scratching the surface of. We have as we said uncovered over hundred sequences and moving from those outwards in terms of improved analogs what are they doing, what are they capable of doing. Again we're scratching the surface there. We're using things like target screening and phenotypic screening to guess and go and try and find their targets. Sometimes that's very clear as in the case of the CXCR4 antagonist, which have nanomolar potency. So by definition highly evolved to a purpose. And in other cases the effects are more clear than the target. That would be the case in some of the other settings that we're looking at. But the effects are still very strong and protective and useful. So we think there's going to be many opportunities here where we'll find indications. We weren't even aware we're involved with mitochondria as we test these across a larger range of things. Initially we focused on metabolic indications because of the paradigm that mitochondria are metabolically related, but the answer is no they're more than that. They control the immune system. They control cell proliferation. They control things like apoptosis in different settings. So there is a broad possibility that these regulatory peptides that we've uncovered could be used in many different indications, some of which we don't yet appreciate.

[Nathan Weinstein:]

Thank you. I really appreciate that -- the answer. It's very interesting. And I suppose I just have one follow-up. It's, sort of, a thematic question around longevity. Yes go ahead.

[Steve Engle:]

No, it was exactly that. You're headed in that direction. So the work by Cohen and Barzilai as well as other collaborators in the field, besides metabolic and oncology there's also indications of an increase around longevity as well as other areas. And so in the work that's been published out there, you can go through it. And you can see there's a broad range of indicators of what might be possible. And so -- and I do think that as you help people with their health span that is avoiding some of these diseases, you will probably have a big impact on their total time period in terms of longevity. And so we think that will be a possible outcome at some point as well. Obviously with the situation with the way drugs get approved in the United States there's a target here on specific diseases, but I think most people recognize that some of these diseases are the key reasons whether it's cardiovascular or otherwise that people aren't living longer and certainly aren't living well longer. And so I think that there is that opportunity as well.

[Nathan Weinstein:]

Yeah, thank you. You pretty much saw my question coming, so I'm always more transparent than I think I am and you've anticipated that very nicely. So I appreciate the color.

[Steve Engle:]

Well, thank you. And I just want to say the other day, I was there with someone if you suddenly discovered five new hormones in the body, people would be scientifically be jumping up and down. And if you knew there were another 95 of those, it would be pretty mind-boggling. And so far, we've got five programs moving forward. And do I think there are more? Yes, absolutely. And we don't know what they all do by any means yet. It's really part of the discovery process that Ken and his team are executing on. But it is a matter of executing on it. As we've shown this last year, it's a matter of time and money to figure out what these different compounds do. And we've made big progress, both in our clinical program, as we approach the results, as well as in staging the preclinical programs and beginning to move those towards the clinic. So, I think the machine is working in the right direction. So, we're very excited about that.

[Operator:]

Thank you. Our next question comes from Greg Wan Cowski with Private Investor. Please proceed with your question.

[Unidentified Analyst:]

Yes. Hello gentlemen. Thank you for taking my call. I see here on your accomplishments in 2020, one of them is your financing, raising $19.5 million and you were added to the Russell 2000. My question is, how it being removed from the Russell 2000 affect your abilities to finance your operations going forward in the second half?

[Steve Engle:]

I appreciate the question. And yes, we're not going to really be able to say anything about that on this call. So sorry, we can't speak more about it. I mean directly. Because it directly involves stock price and so forth. So -- but we are well aware of all the possibilities.

[Unidentified Analyst:]

Okay. Well, that was my question. Thank you.

[Steve Engle:]

Thank you.

[Operator:]

Thank you. There are no further questions at this time. I would like to turn the floor back over to Steve Engle for any closing comments.

[Steve Engle:]

Well, as investors, I hope you have a feel that, we have been moving forward consistently over the last 12 months. We've been doing it within the kinds of resources and funds. And in fact, we've probably delivered on many promises more than usual for a biotech company. And we are looking forward to continuing that record and in particular to the Phase Ib results soon. So stay tuned. Thank you very much.

[Operator:]

This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation and have a wonderful evening.