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Edited Transcript of CWBR.OQ earnings conference call or presentation 16-Nov-20 10:00pm GMT

·37 min read

Q3 2020 CohBar Inc Earnings Call MENLO PARK Nov 17, 2020 (Thomson StreetEvents) -- Edited Transcript of CohBar Inc earnings conference call or presentation Monday, November 16, 2020 at 10:00:00pm GMT TEXT version of Transcript ================================================================================ Corporate Participants ================================================================================ * Jeffrey F. Biunno CohBar, Inc. - CFO, Treasurer & Secretary * Jordyn Tarazi CohBar, Inc. - Director of IR * Kenneth C. Cundy CohBar, Inc. - Chief Scientific Officer * Steven B. Engle CohBar, Inc. - CEO & Director ================================================================================ Conference Call Participants ================================================================================ * Elemer Piros Roth Capital Partners, LLC - MD & Senior Research Analyst * Kumaraguru Raja Brookline Capital Markets, LLC, Research Division - Director & Senior Biotechnology Analyst * Stephen Gilbertpaul Brozak WBB Securities, LLC, Research Division - Senior Equity Analyst ================================================================================ Presentation -------------------------------------------------------------------------------- Operator [1] -------------------------------------------------------------------------------- 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. (Operator Instructions) 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, CohBar, Inc. - Director of IR [2] -------------------------------------------------------------------------------- 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 (inaudible) results, followed by a business and R&D update from Steve and Ken. Before we begin, I'd like to take a moment to remind listeners that the remarks on today's conference call may include forward-looking statements within the meaning of the securities laws. These forward-looking statements include, but are not limited to, statements regarding the company's plans and expectations for its lead CB4211 drug candidate program, the therapeutic and commercial potential of the company's lead drug candidate CB4211 and other mitochondria-based therapeutics; statements regarding ongoing and planned research and development activities, potential partnerships and our capital resources and ability to fund our operations. Forward-looking statements are based on current expectations, projections and interpretations that involve a number of risks and uncertainties that could cause actual results to differ materially from those anticipated by CohBar. These risks and uncertainties are described in our registration statements, reports and other filings with the Securities and Exchange Commission and applicable Canadian securities regulators, which are available on our website at cohbar.com, sec.gov and sedar.com as well as in the safe harbor statement included with today's press release. You are cautioned that [such statements] are not guarantees of future performance and that our actual results may differ materially from those set forth in the forward-looking statements. CohBar does not undertake any obligation to update publicly or revise any forward-looking statements or information, whether as a result of new information, future events or otherwise. Now I'd like to turn the call over to Jeff Biunno, CohBar's Chief Financial Officer. Jeff? -------------------------------------------------------------------------------- Jeffrey F. Biunno, CohBar, Inc. - CFO, Treasurer & Secretary [3] -------------------------------------------------------------------------------- Thank you, Jordyn, and thank you, everyone, for joining us this afternoon. As Jordyn mentioned, if (inaudible) listed 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 (inaudible) 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. Net of noncash costs, total operating expenses in Q3 2020 were $2.211 million as compared to $2.607 million in Q3 2019, a decrease of approximately $396,000. Noncash operating expenses include stock-based compensation and depreciation and amortization costs. Research and development expenses were $1.246 million in Q3 2020 compared to $1.944 million in the prior year period, a decrease of approximately $698,000. The decrease in research and development expenses was primarily due to lower clinical trial costs, resulting from the timing of those expenses and lower stock-based compensation costs, which are partially offset by an increase in consulting expenses. General and administrative expenses were $1.372 million in Q3 2020, compared to $1.284 million in the prior year period, an increase of approximately $88,000. The increase in general and administrative expenses was primarily due to professional fees related to protecting our intellectual property. For the quarter ended September 30, 2020, CohBar reported a net loss of $3.237 million or $0.06 per basic and diluted share compared to a net loss for the quarter ended September 30, 2019, of $3.349 million or $0.08 per basic and diluted share. Net loss included noncash expenses of $947,000 for the quarter ended September 30, 2020, and $726,000 for the quarter ended September 30, 2019. Excluding the noncash expenses, CohBar's net loss was $2.290 million for the quarter ended September 30, 2020, as compared to $2.623 million for the prior year period. Total noncash expenses include stock-based compensation, depreciation and amortization and equity modification costs. Moving to the balance sheet. As of September 30, 2020, CohBar had $23.4 million in cash, cash equivalents and investments compared to $12.6 million in cash and cash equivalents as of December 31, 2019. During the quarter, we completed a public offering in order to finance our clinical and preclinical programs and raised approximately $15 million before commissions and expenses. CohBar issued 12.3 million units at a price of $1.22 per unit with each unit consisting of 1 share of the company's common stock and 1 warrant to purchase 0.75 of a share of common stock at a per-share exercise price of $1.44. The cash burn for the quarter ended September 30, 2020, was approximately $2.9 million. We estimate that based on our cash and investments balance as of September 30, 2020, we have sufficient capital to finance our operations into the first quarter of 2022. During the quarter ended September 30, 2020, the company entered into amendments with certain holders of its unsecured promissory notes, which extended the due date of these notes from June 30, 2021, to June 30, 2022. The amendments also included the issuance of warrants to those holders that extended the due date of their notes. I will now turn the call over to Steve. Steve? -------------------------------------------------------------------------------- Steven B. Engle, CohBar, Inc. - CEO & Director [4] -------------------------------------------------------------------------------- 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. Next slide. Based on the last 2 decades of research, mitochondrial dysfunction is a primary problem underlying many chronic and age-related diseases. We believe CohBar's peptides may hold the answers for a number of the major diseases shown on the right. Spending on these diseases represents as much as $0.5 trillion at the inpatient level annually. Importantly, 5 of the 8 leading causes of death are associated with the impact of mitochondrial dysfunction. And as we are targeting the cellular process, we believe this approach may be disease-modifying rather than just ameliorating the symptoms. In addition, some mitochondrial peptide keys can actually open multiple locks. Next slide. We have achieved 2 key milestones in the development of our portfolio. One is the initiation of first clinical study evaluating a mitochondria-based therapeutic, that is, CB4211. The second is a significant expansion of the number of programs, supporting the portfolio-like nature of our platform, which we accomplished this year. Note that each one of these compounds represents a different family of peptide structures. They are not the same. And each program is targeting multiple indications. So this is a true portfolio. It has the potential to provide multiple shots on goal. And if one program is delayed, the others can move forward. Next slide. Before we discuss progress in the last quarter, let's take a step back and look at the body of data that CohBar has generated over the last few years. We have come a long way. We've identified over 100 peptide sequences and developed over 1,000 analogs. We have successfully tested a number of those peptides in multiple indications in preclinical studies. We've shown that a number of the peptides can generate a consistent therapeutic impact on the targeted organs in preclinical models of key human diseases. And based on their natural origin, MBTs may have the potential for improved safety compared to synthetic small molecules. Today, we are pleased to announce that half of the planned subjects have reached the end of their treatment in the Phase Ib stage of clinical study evaluating CB4211. We are moving our guidance to expect top line results in the second quarter of 2021 due to the impacts of COVID on the enrollment in the study, which Ken will speak more about in his section. Of course, many companies are experiencing delays associated with the COVID-19 pandemic. In our antifibrotic program, recent preclinical data demonstrates the combination of one of our analogs with nintedanib produced enhanced effects compared to either treatment alone, suggesting potential utility for combination therapy in IPF. In our apelin agonist program, we generated initial positive results in a preclinical model of ARDS and are moving the program forward to a candidate identification. We did this in only a few months after announcing the program. In order to finance our pipeline, we significantly strengthened our finances, which I will speak more about in the next slide, and we continued educating both pharmaceutical companies and investors about our mitochondria-based peptide platform and portfolio. Next slide. As Jeff noted, we expect our current cash to take us into first quarter 2022. We raised $15 million to advance our expanded pipeline, added biotech-focused institutional investors and gained additional research analyst coverage, bringing the total to 3 analysts. We look forward to continuing to develop our biotech institutional investors base and provide additional visibility for the company. Next slide. The company presented at 8 industry and health care bank conferences. The Metabesity Conference focused on metabolic dysfunction, which reflects the growing interest in developing therapies to target this area. Thomas Seow and the team at Kytalys Institute put on one of the best all-round conferences of the year. Two conferences focused on new therapies for COVID-19, one hosted by ROTH Capital Partners and one by Sachs. No surprise with the interest in this area. A key part of our strategy is to collaborate on R&D with pharmaceutical companies and leading academic and medical centers around the world. A few weeks ago, we attended the BIO-Europe Conference, where we continued to build on our partnering efforts. Next slide. Now I will turn the call over to Ken. -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [5] -------------------------------------------------------------------------------- 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. Next slide, please. So as we discussed on the last call, the clinical trial process for this study involves a rolling enrollment as shown in this simplified diagram. This is a continuous process, starting for each individual subject as soon as they're able to enter the study. Each subject has to be enrolled, dosed and followed up for safety. This process continues until the last subject has completed the final study follow-up. So the process of recruiting and screening is also continuous. We identified potential subjects from the database at our clinical sites or through advertising. They must consent to be tested and then they are carefully screened to ensure that they qualify for the study by meeting the extensive list of criteria for participation, including the initial MRI scan to show that they have sufficient liver fat. When a subject passes all the tests and qualifies for the study, they can be enrolled or entered into the study and then dosed without waiting for the rest of the subjects to enroll. When each subject receives their last dose, there's still a follow-up period for safety observation to ensure there are no issues. So subjects enter the study at different times, and we effectively create a pipeline or rolling process with subjects moving through the various steps in the process in a staggered manner all the way to the final follow-up. Data are collected throughout this entire process and entered into a database. At this stage, all the data are blinded, meaning we do not know yet who received CB4211 and who received placebo. When all subjects have completed the final follow-up and after all required data for safety, pharmacokinetics, liver fat, body weight and biomarker levels have all been collected, the data are then checked for errors, the errors are systematically resolved and then the database is locked. And then the data are finally unblinded and the analysis of the data begins. So as we stated, half of the target subjects have now completed the dosing, and we will update when the last subject completes their last final follow-up. Next slide, please. Now moving to our preclinical programs. I'll focus today on 2 programs where we've made significant progress during the last quarter, starting with our antifibrotic peptides or CB5138 analogs. This is a family of novel molecules related to a mitochondrially encoded peptides that have 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 cells, these peptides 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 have built on those initial discoveries by demonstrating clear antifibrotic and anti-inflammatory effects in animal models of IPF. In the first prophylactic IPF model in which bleomycin is used to induce fibrosis, we showed that immediate treatment of animals without peptides reduce the extent of fibrosis and inflammation in the lungs 21 days later. Then in the therapeutic model, we showed the treatment of animals beginning 1 week after induction of fibrosis with bleomycin had positive effects on all study outcomes, reducing the lung fibrosis, reducing the levels of collagen, cytokine secretion and inflammation. We further demonstrated the efficacy of multiple CB5138 analogs in the same therapeutic model. Now most recently, using this therapeutic model, we have shown that a combination of a CB5138 analog with nintedanib, one of the 2 approved IPF drugs and the current standard of care, produced greater effects than dosing with nintedanib alone. This points to a potential for use of CB5138 analogs on top of current therapy in IPF. We currently expect to complete the necessary activities required to support identification of a clinical candidate early in the first quarter of 2021, subject to the successful outcome of those remaining activities and then to initiate IND-enabling activities with the goal of potentially filing an IND around the end of 2021. At the same time, the broad antifibrotic and anti-inflammatory effects of CB5138 analogs suggests there's potential for their use in treating other fibrotic diseases, and we're exploring that potential in preclinical models, such as scleroderma, kidney fibrosis and NASH. Next slide, please. So on this slide, we see some of the data that were released this summer at the American Thoracic Society Virtual Annual Meeting. Looking here at potential for monotherapy using the mouse therapeutic model of IPF. In addition to the first CB5138 analog previously called MBT2, animals were treated with 2 newer analogs alone and then compared to placebo vehicle treatment in the red bars, on nintedanib in the green bars. Now nintedanib is one of the 2 approved IPF drugs. It's a tyrosine kinase inhibitor that blocks several different targets, leading to a slowing of the progression of IPF. But nintedanib also has significant off-target effects, including nausea, vomiting and diarrhea. Here, you see we have consistent antifibrotic and anti-inflammatory effects across the board, including reductions in fibrosis, reduced lung weight, reduced inflammation in terms of lymphocytes in the lung fluid, reduced levels of collagen, both in the lung tissue and secreted into the lung fluid. Next slide, please. So moving now to the most recent data released just 3 weeks ago. This was a study designed to look at the potential for combination of our CB5138 analog with the standard of care, in this case, nintedanib. Our study was again conducted in the therapeutic mouse model of IPF, where treatment was initiated 7 days after the bleomycin induction of fibrosis. The treatments included CB5138-2 alone, nintedanib alone and the combination of both drugs together. And here, you can see the effects of these treatments. The dark blue bars are the combination of CB5138-2 with nintedanib compared to the green bars for nintedanib alone. You can see there was a greater reduction in lung fibrosis, lung weight and levels of collagen for the combination. And that positive combination effect also carried over to the other slides -- other study endpoints on the next slides. Next slide, please. Okay. So in the same experiment, we see here the levels of pro-inflammatory cytokines secreted into the lung fluid. This includes key cytokines such as IL-1-beta, TNF-alpha and IL-6 as well as other key chemokines involved in the inflammatory response, such as the monocyte chemoattractant protein, MCP-1 and the macrophage inflammatory protein, MIP-1-alpha. In all cases, the combination of the CB5138 analog with nintedanib was much more effective at reducing these pro-inflammatory cytokines than nintedanib alone. Next slide, please. So on this last data slide here, we're looking at the infiltration of inflammatory cells into the long fluid. You can see that the combination of the CB5138 analog with nintedanib in the dark blue bar was again more effective at reducing the infiltration of macrophages, lymphocytes and neutrophils when compared with treatment with nintedanib alone in the green bars. Next slide, please. Now our key adviser on this fibrosis program is Dr. Toby Maher. He is the Professor of Clinical Medicine at the Keck School of Medicine at the University of Southern California and also Professor of Interstitial Lung Disease at the National Heart and Lung Institute of the Imperial College of London. Now Dr. Maher has been involved in more than 50 trials in fibrotic lung diseases from Phase Ib to Phase IV, including IPF studies. In our recent key opinion leader call, Dr. Maher gave a compelling clinical perspective on the devastating impact of IPF and the continuing unmet need for new treatments. According to Dr. Maher, future treatment of IPF will likely move towards combinations of new mechanisms with the current standard of care, and he believes that CohBar's preclinical data for CB5138 analogs in combination with nintedanib are a step towards that goal. Next slide, please. Moving now to our CB5064 analogs. This is a different family of peptide analogs that have the potential to reduce mortality in acute respiratory distress syndrome, or ARDS, and in COVID-19-related ARDS by simultaneously blocking many of the processes that lead to global damage. Now on the right, you can see that COVID-19 is more than a lung disease. In severe cases, it can cause fluid accumulation, vascular leakage, sepsis, inflammation and thrombosis and even a cytokine storm that can lead to multi-organ failure. So together, these damaging effects of the virus can lead to respiratory failure, cardiac failure, stroke and even multi-organ failure. There are no approved drugs to treat ARDS. And even without COVID-19, ARDS affects 3 million people. Our CB5064 analogs work by selectively activating the apelin receptor, a key adipokine signaling pathway that has broad protective rebalancing effects on numerous systems, including the control of fluid levels, vascular tone, blood clotting, inflammation and cytokine production. Apelin signaling has been shown to protect animals in models of ARDS, sepsis, thrombosis and stroke. So engaging the apelin receptor has the potential to block many of these damaging effects of COVID-19. We have previously shared in vivo data showing efficacy of our CB5064 analogs in an animal model of ARDS, leading to reduced fluid accumulation in the lungs, decreased secretion of pro-inflammatory cytokines. And now we're currently conducting confirmatory studies in the ARDS model and moving forward towards potential candidate selection, scale up and the initiation of IND-enabling studies. And with that, I'll return the call to Steve. -------------------------------------------------------------------------------- Steven B. Engle, CohBar, Inc. - CEO & Director [6] -------------------------------------------------------------------------------- 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. ================================================================================ Questions and Answers -------------------------------------------------------------------------------- Operator [1] -------------------------------------------------------------------------------- (Operator Instructions) Our first question is coming from the line of Elemer Piros with ROTH Capital Partners. -------------------------------------------------------------------------------- Elemer Piros, Roth Capital Partners, LLC - MD & Senior Research Analyst [2] -------------------------------------------------------------------------------- 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 4211 have been -- completed their treatment phase, and you described the continuum of the pipeline in this trial. Are there any other patients at the beginning of the screening phase or elsewhere in this continuum that are being contemplated now? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [3] -------------------------------------------------------------------------------- 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, Roth Capital Partners, LLC - MD & Senior Research Analyst [4] -------------------------------------------------------------------------------- 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? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [5] -------------------------------------------------------------------------------- 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, Roth Capital Partners, LLC - MD & Senior Research Analyst [6] -------------------------------------------------------------------------------- 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? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [7] -------------------------------------------------------------------------------- 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 [8] -------------------------------------------------------------------------------- Next question comes from the line of Kumar Raja with Brookline Capital. -------------------------------------------------------------------------------- Kumaraguru Raja, Brookline Capital Markets, LLC, Research Division - Director & Senior Biotechnology Analyst [9] -------------------------------------------------------------------------------- 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? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [10] -------------------------------------------------------------------------------- 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. -------------------------------------------------------------------------------- Kumaraguru Raja, Brookline Capital Markets, LLC, Research Division - Director & Senior Biotechnology Analyst [11] -------------------------------------------------------------------------------- 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? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [12] -------------------------------------------------------------------------------- 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. -------------------------------------------------------------------------------- Kumaraguru Raja, Brookline Capital Markets, LLC, Research Division - Director & Senior Biotechnology Analyst [13] -------------------------------------------------------------------------------- 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? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [14] -------------------------------------------------------------------------------- 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. -------------------------------------------------------------------------------- Kumaraguru Raja, Brookline Capital Markets, LLC, Research Division - Director & Senior Biotechnology Analyst [15] -------------------------------------------------------------------------------- And finally, with regard to the CXCR4 inhibitors, when can we expect the next update on that? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [16] -------------------------------------------------------------------------------- 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. -------------------------------------------------------------------------------- Steven B. Engle, CohBar, Inc. - CEO & Director [17] -------------------------------------------------------------------------------- Kumar, thank you very much. -------------------------------------------------------------------------------- Operator [18] -------------------------------------------------------------------------------- The next question comes from the line of Steve Brozak with WBB. -------------------------------------------------------------------------------- Stephen Gilbertpaul Brozak, WBB Securities, LLC, Research Division - Senior Equity Analyst [19] -------------------------------------------------------------------------------- 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? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [20] -------------------------------------------------------------------------------- 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. -------------------------------------------------------------------------------- Stephen Gilbertpaul Brozak, WBB Securities, LLC, Research Division - Senior Equity Analyst [21] -------------------------------------------------------------------------------- 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? -------------------------------------------------------------------------------- Kenneth C. Cundy, CohBar, Inc. - Chief Scientific Officer [22] -------------------------------------------------------------------------------- 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 [23] -------------------------------------------------------------------------------- (Operator Instructions) Our next question will come from the line of [Bandra Sebra], private investor. -------------------------------------------------------------------------------- Unidentified Participant, [24] -------------------------------------------------------------------------------- Oh, sorry, it's an accident. I didn't mean to press. I didn't mean to ask a question. -------------------------------------------------------------------------------- Operator [25] -------------------------------------------------------------------------------- At this time, I will turn the floor back to Steve Engle for closing comments. -------------------------------------------------------------------------------- Steven B. Engle, CohBar, Inc. - CEO & Director [26] -------------------------------------------------------------------------------- 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 [27] -------------------------------------------------------------------------------- Thank you, everyone. This will conclude today's conference. You may disconnect your lines at this time. Thank you for your participation.