Good afternoon. My name is Chuck, and I will be your conference operator today. At this time, I would like to welcome everyone to CohBar’s Second Quarter 2021 Financial Results and Clinical Trial Update Conference Call. All participants will be in a listen-only mode.

[Operator Instructions] After today’s presentation, there will be an opportunity to ask questions. [Operator Instructions] Please note this event is being recorded. Now, I would like to turn the conference over to Jordyn Tarazi, Director of Investor Relations at CohBar. Please go ahead, ma’am..

Thank you, Chuck, and thank you, everyone, for joining CohBar’s second quarter 2021 financial results and CB4211 topline data conference call. Joining me on today’s call is Joe Sarret, CohBar’s Chief Executive Officer; Ken Cundy, CohBar’s Chief Scientific Officer; and Jeff Biunno, CohBar’s Chief Financial Officer.

CohBar’s CB4211 topline data and financial results press releases were issued earlier today and may be downloaded from our website at cohbar.com. Joe will begin with an introduction followed by the CB4211 topline data from Ken. Jeff will then provide an overview of the second quarter financial results.

Before we begin, I’d like 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 business and financial strategies, plans and expectations for its pipeline product candidates including its lead CB4211 drug candidate program, partnership discussions and opportunities, the therapeutic and commercial potential of the company’s pipeline product candidates including a lead candidate CB4211, and other mitochondria-based therapeutics, statements regarding ongoing and planned research and development activities including ongoing and planned clinical trials and regulatory status and strategies, and the timing of announcements and updates relating to our clinical trials and related data, potential partnerships and our capital resources, financial and operating performance 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 a 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’ll cover a few housekeeping items prior to turning the call over to Joe.

If you are having issues with Zoom, the slide presentation is available on the homepage of the CohBar website. As I noted earlier, Joe will begin with an introduction. Ken will then review the recent CB4211 topline data followed by a financial overview from Jeff. We’ll then conclude with Q&A.

Now, I’d like to turn the call over to Joe Sarret, CohBar’s Chief Executive Officer.

Joe?.

Thank you, Jordyn, and thank you, everyone, for joining us this afternoon. I’d like to start by discussing the positive topline data from our Phase 1a/1b trial for CB4211 our lead program being developed for nonalcoholic steatohepatitis or NASH and obesity.

The announcement earlier today was a major milestone for CohBar and represents the results of years of effort that began with our founders groundbreaking insights into the potential role of certain natural mitochondrially encoded peptides, such as MOTS-c as regulators of key systems in the body.

Through the innovative efforts of CohBar scientists, we designed and tested numerous novel analogs of MOTS-c selected our clinical candidate and then design and executed a complex clinical study, while contending with an unprecedented global pandemic.

Ken will provide more details in a few moments, but the key takeaways are first that the study met its primary end points of safety and tolerability. And second that we saw robust and significant improvements in both ALT and AST, which are markers of liver damage in subjects treated with CB4211 compared to placebo.

We also demonstrated a significant decrease in glucose in the CB4211 group compared to placebo, as well as the trend towards weight production with CB4211 treatment. Taken as a whole, we think these results constitute compelling evidence that CB4211 has the potential to play a meaningful role in the treatment of patients with NASH. Next slide please.

Before Ken provides a more detailed review of the topline data, I wanted to take a few minutes to review the CohBar story for those of you who may not be familiar with the company. We are a leader in developing therapeutic peptides that are analogs of natural sequences encoded within the genome of the mitochondria, as opposed to the nucleus.

One of the key early insights was the recognition that the effects of some of these mitochondrially encoded peptides were not limited to local regulation within the mitochondria, but could and did have important roles to play in critical biological pathways, quite distinct from what has traditionally been thought of as mitochondrial function.

In fact, we are now developing analogs of these peptides to treat a variety of serious systemic conditions with the focus on diseases involving inflammation and fibrosis.

As I mentioned earlier today, we reached a key milestone with the announcement of the positive topline data for our first human trial of CB4211 under development for the treatment of NASH and obesity. And we have a second clinical candidate CB5138-3, which has broad anti-fibrotic properties.

And it’s currently an IND enabling studies targeting an initial indication of Idiopathic Pulmonary Fibrosis or IPF. The power of our platform has resulted in the discovery of over 100 different mitochondrially encoded peptides. And we have generated more than a 1,000 analogs.

These discoveries have led to the creation of a broad, robust and valuable patented state. Next slide please. Well, many companies are developing products for the treatment of NASH, CB4211, which is an analog of a naturally occurring peptide named MOTS-c discovered by one of our founders and his academic collaborators has a unique mechanism of action.

Part of the underlying pathophysiology in NASH involves dysregulation of the process called lipolysis resulting in the release of excess free fatty acids from adipocytes or fat cells. High levels of free fatty acids can accumulate as fat deposits in the liver leading to lipotoxicity and liver inflammation.

This process can ultimately progress to fibrosis, cirrhosis and liver cancer. And in vitro studies CB4211 enhances the effects of insulin resulting in a reduction in free fatty acid release by decreasing lipolysis in fat cells. CB4211 also has the potential to impact insulin effects and other tissues resulting in a reduction in glucose levels.

In addition to these effects in animal models of NASH, we have demonstrated that CB4211 results in reduced liver inflammation by histopathology, which correlated with significant reductions in ALT and AST. With that background, I’ll hand it over to Ken to review the topline CB4211 clinical data in more detail.

Ken?.

Thanks, Joe. I’ll now give a brief update on the topline data from a Phase 1a/1b study of the safety, tolerability and pharmacokinetics of CB4211 in healthy non-obese subjects and subjects with non-alcoholic fatty liver disease or NAFLD. Next slide please.

The first stage of the study was a randomized double blind placebo controlled study in healthy adult volunteers, randomized in dose cohorts of up to eight subjects per cohort at a ratio of three to one for CB4211 versus placebo.

In total, there were six cohorts of single ascending dose treatment and three cohorts of multiple ascending dose treatment treated for seven days in the Phase 1a portion of the study.

A total of 65 subjects were enrolled in the Phase 1a stage, and we initially conducted four single ascending dose cohorts and one multiple dose cohort with our original clinical formulation.

In that initial dose escalation, we observed persistent local deposition of the drug at the injection site manifesting as local palpable bumps that in some cases lasted for several weeks. To address this, we interrupted this study, examined the injection site reactions and modified the formulation.

With input from FDA, we then resumed a study and conducted an additional two single ascending dose cohorts and two multiple ascending dose cohorts using the modified formulation. All of the subjects in the Phase 1a stage of this study completed their treatments as assigned and none discontinued. Next slide please.

The Phase 1b stage of the study was a multicenter randomized double blind placebo controlled study of CB4211 versus placebo in obese subjects with NAFLD. The target enrollment was 20 in order to have 10 on placebo and 10 on one fixed dose level of 25 milligrams CB4211 given once per day by subcutaneous injection using the modified formulation.

Subjects enrolled in the study had to meet a very strict set of entry criteria, including a BMI of greater than 30 kilograms per meter square and the minimum of 10% liver fat content by MRI-PDFF at baseline. We kept the body weight at 115 kilos, and there were numerous other criteria that is detailed in our ClinicalTrials.gov record.

Notably only one diabetic subject was enrolled in this study and they were required by protocol to maintain their existing stable regimen of metformin throughout the study.

This Phase 1b stage was designed to assess the safety, tolerability and pharmacokinetics of CB4211 and its potential effects on exploratory outcomes, such as liver fat, body weight, and various biomarkers that are relevant to NASH obesity and metabolic disease. This was a short study, not a pivotal Phase 2 study.

So our goal from the outset was to look for trends in the data. There were four clinical sites and the subjects were confined for the duration of the study to ensure a close monitoring of injections and potential injection site reactions. Next slide please.

In total, 23 subjects were enrolled in the Phase 1b stage of the study to replace three dropouts and ensure 20 would have complete data for the end of treatment assessments. Of the three subjects that dropped out before completing their end of study assessments, two were for positive COVID-19 tests, and one withdrew consent.

The final distribution for subjects with complete data was 11 on CB4211 and nine on placebo. Next slide. In this table, we showed the clear effects of CB4211 treatment on key biomarkers of liver disease determined at the end of treatment on day 28.

Treatment with CB4211 led to a robust and significant reduction in circulating liver enzymes that are markers of liver damage and a widely used as indicators of efficacy in NASH studies. The levels of ALT alanine aminotransferase drops by a mean of 21% from baseline in the CB4211 treated group compared to an increase of 4% in the placebo group.

The net difference from placebo was 25%. Notably a reduction in circulating ALT levels by at least 17 units per liter has been shown to correlate with an improved histologic outcome in NASH patients.

Using that threshold, the percentage of responders achieving that clinically meaningful level of ALT decrease what’s substantially higher in the CB4211 group compared to the placebo group.

In addition, there was a corresponding robust and significant decrease in circulating levels of AST, aspartate aminotransferase another liver enzyme that is a major indicator of liver damage.

These data also agree with that previously reported preclinical data in animal models of NASH and obesity showing decreases in ALT and AST after treatment with CB4211 or related analogs.

Beyond the liver enzymes, there was also a significant decrease from baseline in fasting glucose levels in the Phase 1b study in the CB4211 treatment group compared to placebo. This suggests potential improvement in metabolic homeostasis.

In addition to these significant changes, there was a trend towards reduction in body weight for the CB4211 treated group that appears to corroborate our preclinical data in models of obesity. Next slide please.

In these plots, you can see the time course of the reductions in ALT and AST in the two treatment groups, levels in placebo subjects remained close to baseline while levels in subjects treated with CB4211 separate rapidly from placebo within two weeks and continue to decline.

These curves also suggest that further reductions in ALT and AST could be possible with longer CB4211 treatment. Next slide.

This slide further illustrates the responder analysis, showing that a greater proportion of subjects in the CB4211 treatment arm achieved a meaningful reduction in ALT of at least 17 units per liter, which again is predictive of potential clinical benefit in NASH. Next slide.

To put the ALT data in perspective, this table compares our Phase 1b ALT results with data that have been published or released on the ALT reductions produced by other drugs currently under development for NASH based on outcomes in a similar four-week timeframe.

As you can see the percent reduction from baseline and the difference from placebo in ALT levels after four weeks of CB4211 treatment compare favorably with the four-week data from Metacrine, Durect and Hepion, but also with data from NASH candidates that are now in late stage Phase 3 development, such as Obeticholic acid, Resmetirom, and Semaglutide.

We think this position CB4211 well as a potentially differentiated therapy with a completely different mechanism of action from agonists targeting FXR, THR-β or GLP1. Next slide, please.

In this slide, we see the time course of the reduction in glucose with CB4211 treatment that separates from placebo early in the study and reaches significance at week four, with a difference from placebo of 6%.

These data also suggest that CB4211 may be particularly effective in subjects with fatty liver disease and elevated glucose levels such as diabetic NASH subjects. Notably, about 50% of patients diagnosed with NASH are also diabetic.

The unique mechanism of action CB4211 also positions it well for use in potential combination therapy in that population. On the right, we see the time course for changing body weight, showing a trend to reduce body weight in the CB4211 treatment group, beginning at week one.

This corroborates previous data showing a reduction in body weight for obese animals treated with CB4211. Next slide, please.

Turning now to the liver fat data in the Phase 1b study, measurement of liver fat content by MRI-PDFF showed a main absolute reduction from baseline of 5.03% for CB4211, which is comparable to absolute fat reductions achieved in other four-week NASH studies.

However, the placebo treated subjects in our study also had a similar substantial reduction from baseline in liver fat by week-four.

We believe this may have been the result of confining the subjects in their clinical study sites during the treatment, while confined all subjects were provided standardize meals based on their calculated daily energy expenditures at baseline that was necessary for the inpatient setting, but it may differ from what their normal practice of ad lib food consumption is.

The proportion of subjects achieving a clinically meaningful 30% reduction in relative fat content was 36% in the CB4211 arm, which again was comparable to other studies. A relative reduction of 30% in liver fat is associated with a histological response in a NASH based outcome on published – based on published reports.

It appears the placebo changes may have matched the true drug effects on liver fat. Despite that similar drop in liver fat CB4211 was clearly more effective in reducing markers of liver damage and the other outcomes then placebo. That suggests that the beneficial effects of CB4211 are not driven just by reducing liver fat levels. Next slide, please.

In terms of safety, the study also achieved a positive primary outcome. CB4211 was well tolerated and appeared safe with no serious adverse events. Adverse events in the study were generally mild to moderate and transient.

No persistent injection site reactions were seen in the Phase 1b, the only adverse events occurring in more than 10% of subjects treated with CB4211 were transient injection site reactions, which were saying in 79% of the CB4211 treated subjects compared to 33% of the placebo treated subjects. Next slide please.

So to summarize the exploratory outcomes, the top line data for the Phase 1a/1b study showed clearly positive effects supporting the potential of CB4211 for treating NASH. CB4211 treatment produce robust and significant reductions versus placebo in key enzyme markers of liver damage ALT and AST.

The ALT reduction seen at week four with CB4211 was as good or better than any other NASH candidate that has been tested in a similar four week studies in patients with NASH or presumed NASH.

Furthermore, the higher percentage of ALT responders with a reduction in ALT of at least 17 units per liter is predicted of a potential benefit in histologic resolution of NASH based on 2019 report published by Dr. Rohit Loomba.

Beyond the markers of liver damage, we also saw a significant reduction in fasting glucose levels compared to placebo treated subjects, suggesting potential improvement in metabolic homeostasis.

In addition, there was a trend towards lower body weight in the CB4211 treated group, consistent with the bodyweight decline observed in obese animals in preclinical studies. With regards to the liver fat content by MRI-PDFF, there was a substantial reduction in liver fat in both active and placebo arms.

That suggests the effects of confining subjects during the study and providing them with a diet that was standardized to their basal metabolic rate may have led to a large reduction in liver fat that masked the contribution from the drug.

Despite that, the improvements in ALT, AST, glucose and body weight only occurred in the CB4211 treated subjects, showing that CB4211 exerts its positive effects by more than just reducing liver fat. Additional analysis of the data from this study is planned and the pharmacokinetic data from the study are still pending.

In conclusion, the positive topline data from this Phase 1a/1b study support the further development of CB4211 for NASH and we plan to work with disease area experts to define the most appropriate clinical path forward. We look forward to sharing more of the data from this Phase 1a/1b study at an upcoming scientific meeting.

And with that, I will return the call to Joe..

Thanks, Ken. With that additional detail, you can see why we’re so excited about today’s announcement. Next slide. To put these results in context, it is helpful to take a step back and remember the rationale for treating NASH patients in the first place. NASH is a progressive disease.

The goal is to reduce the serious consequences of NASH that result from the damaging effects of inflammation and fibrosis in the liver, thereby improving liver function and preventing or delaying the insidious progression to cirrhosis, liver failure or cancer.

Reductions in key markers of liver injury, like, the circulating levels of the liver enzymes ALT and AST have the most predictive value for the ultimate objective of decreasing liver inflammation and injury.

The improvement in ALT seen with CB4211 treatment at four weeks is not only greater than that seen another four week studies, but it’s favorable compared to many 16 week and longer studies among competitive products under development for the treatment of NASH.

The significant reduction in AST provides further evidence of the improvement in liver health after treatment with CB4211. Notably, we saw these impressive changes in ALT and AST compared to placebo, despite the fact that the robust reduction in absolute liver fat in the treatment arm was comparable to that seen in the placebo group.

This strongly suggests that the mechanism of improvement in liver function after treatment with CB4211 is distinct from the liver fat changes. We believe that the reduction in glucose levels is also notable, particularly in light of the fact that approximately 50% of NASH patients have diabetes as a co-morbidity.

While only one subject in this trial was diabetic. This result raises intriguing possibilities for future study, especially since our preclinical work demonstrated synergies between CB4211 and common diabetic treatment such as GLP1 agonists. Next slide, please.

These results are not only encouraging for our CB4211 program, but as the first human data from an analog of a mitochondrially encoded peptide, they also provide important validation of CohBar’s overall approach.

We now have clear evidence that analogs and peptides encoded within the mitochondrial genome can have significant beneficial impacts on relevant disease processes in human subjects. The results also provide confirmation of our hypothesis that analogs that these naturally occurring peptides are likely to have superior safety and tolerability profiles.

In terms of next steps for our CB4211 program, keep in mind that we only recently received the top line data and need times to determine how these results can best be incorporated into the next clinical trial. We are also still waiting for the pharmacokinetic or PK results, which may provide additional helpful context for the PD and safety data.

We plan to reach out potential partners to discuss the study results over the coming weeks. As discussed previously, we also plan to continue to refine the formulation for CB4211 and complete the necessary steps to be able move forward with a new formulation into clinical studies and initiate a Phase 2a study.

Timing for these activities will depend on the availability of funding and the progress in our partnering discussions.

In addition to the tremendous potential from our CB4211 program, we also have a pipeline of novel peptides that show promise as potential treatments for a variety of indications, including IPF, acute respiratory distress syndrome, cancer and other diseases.

I’d now like to ask our CFO, Jeff Biunno to walk you through our second quarter financial performance. Jeff..

Thank you, Joe, and thank you everyone for joining us this afternoon. I will now provide you with a summary of our financial results for the second quarter ended June 30, 2021, compared to the second quarter ended June 30, 2020. Next slide please.

Total operating expenses in Q2 2021 were $ 5,202,000 as compared to $2,936,000 in Q2 2020, an increase of approximately $2,266,000. Operating expenses included non-cash expenses of $994,000 for the quarter ended June 30, 2021 and $693,000 for the quarter ended June 30, 2020.

Net of the non-cash expenses, total operating expenses in Q2 2021 were $4,208,000 as compared to $2,243,000 in Q2, 2020, an increase of approximately $1,965,000. Non-cash operating expenses includes stock-based compensation and depreciation and amortization costs.

Research and development expenses were $2,618,000 in Q2, 2021 compared to $1,545,000 in the prior year period, an increase of approximately $1,073,000. The increase in research and development expenses was primarily due to the continuing development of our peptides and our clinical trial costs.

Those increases were partially offset by a decrease in stock based compensation costs. General and administrative expenses were $2,584,000 in Q2, 2021 compared to $1,391,000 in the prior year period, an increase of approximately $1,193,000.

The increase in general and administrative expenses primarily due to higher compensation and stock based compensation costs and D&O insurance premiums.

For the quarter ended June 30, 2021, CohBar reported a net loss of $5,223,000 or $0.08 per basic and diluted share compared to a net loss for the quarter ended June 30, 2020 of $4,103,000 or $0.09 per basic and diluted share.

Net loss included non-cash expenses of $1,004,000 for the quarter ended June 30, 2021 and $1,779,000 for the quarter ended June 30, 2020. Excluding the non-cash expenses, CohBar’s net loss was $4,219,000 for the quarter ended June 30, 2021 as compared to $2,324,000 for the prior year period.

Moving to the balance sheet, as of June 30, 2021, CohBar had $13.8 million in cash and investments that compares to $21 million as of December 31, 2020. The cash burn for the quarter ended June 30, 2021 was approximately $4.6 million.

During the quarter ended June 30, 2021, CohBar realized net funding of $882,000 from the sale of its common stock under its ATM program. Due to the timing of the sales made during the quarter ended June 30, 2021, $239,000 was received subsequent to the quarter end.

Additionally, subsequent to the quarter ended June 30, 2021, proceeds of $123,000 related to stock option sales were received. We estimate that based on our cash and investments balance as of June 30, we have sufficient capital to finance our operations into the second quarter of 2022. I’ll now turn things back over to Joe.

Joe?.

Thanks, Jeff. Next slide please. I’d now like to highlight some key upcoming milestones and events to watch out for during the remainder of this year and the beginning of 2022.

First, we plan to continue our analysis of the results of the CB4211 clinical data and plan to identify an appropriate scientific conference to formally present these results and any additional insights.

With additional funding, we expect to move forward with the necessary work to enable a Phase 2 study, while in parallel accelerating our partnering discussions. Next, we will continue our ongoing work to conduct the IND-enabling studies for CB5138-3 for IPF. Our goal is to file an IND and began a first in human trial in 2022.

And finally, with additional funding, we plan to select the next clinical candidate to progress towards IND-enabling studies, which would provide us with the potential to have three clinical stage programs. Based on the positive top-line data from the CB4211 trial we announced today.

We are more convinced than ever in the power of our approach and the ability of our pipeline to deliver peptide therapeutics that can make a real difference in the lives of patients.

As a result, we are focused on ensuring that we have sufficient capital to continue to advance our pipeline and our evaluating the range of financing options available to us, including non-dilutive funding opportunities.

Before opening up to questions, I would like to thank everyone involved with the CB4211 trial, particularly the volunteers for the study without whom drug development would not be possible.

Operator, can you please open the line for questions?.

Yes. We will now begin the question-and-answer session. [Operator Instructions] And the first question will come from Jason McCarthy with Maxim Group. Please go ahead..

Hi, everyone. It’s [indiscernible] on the line for a Jason. Thanks for taking my question. I was just wondering if you could maybe shed some color on what potential next steps would be for CB4211.

Could we – can we expect to trial with a longer treatment duration or could we even expect a NASH study with histologic endpoints potentially?.

Hi, [indiscernible] this is Joe. Thanks for your question. As I mentioned earlier, I think that the – currently we’re still figuring out how best to incorporate the findings that we saw here into the next clinical trial. And there is some additional work that we need to do in terms of optimizing formulation, et cetera, to set us up for the Phase 2.

So we’re working through that. So we don’t have specific details yet on the trial that we can share or on specific timing, but we’ll look forward to updating you on that when we have a little bit more clarity..

Great. Thanks for that color.

And then just one more question, regarding the AST data you had, I was just wondering if you aware of any trends that could correlates or reductions in AST to potential – potentially positive histologic responses in NASH, similar to what you mentioned for of ALT, like, is there a range, possibly with AST?.

So Ken, you want to take that one?.

Yes. So there’s obviously a correlation as far as multiple different assessments of liver enzymes that are circulating in general, but AST per se, we’re not aware of a specific threshold for responder analysis related to AST, that may well be one.

And that’s one of the things we’ll be discussing with our disease area experts as we prepare the data for a potential presentation at an upcoming scientific event..

Okay. Thanks for the additional color. Appreciate it..

The next question will come from Nathan Weinstein with Aegis Capital. Please go ahead..

Hi, Joe and CohBar team. Thanks so much for taking my questions. Congrats on the data. It’s nice to see that. I guess just the first one regarding the biomarker improvements in the study, did you see any correlation there based on stratification by BMI or liver fat..

Ken, do you want to….

This is Ken. Yes, I’ll answer that one. So we have not gone deep enough yet into looking at additional subgroups and stratification. That is part of the ongoing analysis that will happen as a follow-up to these. What we consider to be the obvious first major changes that we pick up from the line data.

So we will hopefully be able to tell you more about that in the presentation that we see coming up soon at a upcoming scientific meeting..

Awesome. Thank you. Looking forward to that. And on the second asset on CB5138 for IPF, just any learnings from the CB4211 trial that might help you inform the design of that study..

Well, so I can take maybe the first and then Ken, if you want to add any more color. I think that – so one thing to keep in mind is that, all of our programs are involving different peptides with different structures and different mechanisms of action.

So the – having said that, however, we do think the fact that these mitochondrial peptides now that we’ve shown results in humans, I think that validates the approach as I was mentioning earlier, and we do think that the safety profile there should carry forward to other peptides given that they’re all analogs of naturally occurring peptides.

But in terms of specifics, the programs are actually unique in that sense, but Ken, I don’t know if there’s more you want to say about that?.

Yes. I mean, if your question was about, what we learned from clinical study design in this setting, I think it is different in the setting of IPF. One of the possibilities for IPF is that you start in healthy subjects and move quickly to IPF subjects with a biomarker readout.

So that’s a possibility that we’re looking into, clearly, the longer-term readouts in IPF take more time. But obviously, those are the things we’re discussing with our disease area experts in the IPF area..

Okay, thanks. That’s helpful. I guess moving just down the line now to the sort of abundant library of the thousand characterized analogs, just maybe you could speak in general to how much ongoing activity you have in the preclinical work with those assets and just kind of want to get a sense for the ongoing investigations there..

Sure. So I think that our – we’re a small company, obviously with a limited resource. And so we’ve really been focusing our efforts more recently on the most advanced programs, which include obviously CB4211 and the CB5138 program for IPF and fibrosis more broadly. So currently those are where the bulk of the activities are.

I think with additional time and resource, we do think there’s a lot of additional value to be mind out of those, a hundred or so initial peptides and the analogs thereof. But that’s not a huge push at the moment, again, pending additional resources in the future..

Okay. Fair enough. Thanks so much for taking my questions..

Sure. Thank you..

The next question will come from Kumar Raja with Brookline. Please go ahead..

Hi. I’m Shubhendu calling in for Kumar from Brookline. Congratulations on the promising CB4211 results. I just had a question with regards to, do you think a combinatorial therapy of CB4211 and the other drugs that are there in Phase 3, say for example, semaglutide, that could be more effective for NASH than CB4211 monotherapy alone..

Yes. So thanks for the question. So as we indicated in the presentation, we did see the reduction – significant reduction in glucose in this patient population.

And again, keeping in mind that these were – with one exception patients that didn’t have or subject that did not have diabetes, we do think that there is an intriguing opportunity to study this further possibly in a diabetic population.

In our preclinical work, we did see an animal models, we did see synergies with other diabetic drugs, including GLP1 agonist. So we think there’s certainly potential there. And I think that given the complexities of NASH the disease, I would not be surprised in the future if there combination therapy becomes more common.

The other thing to keep in mind as our mechanism of action is unique compared to the other products that are – product candidates that are further along in development. So again, there may be scientific rationale for combining those. So yes, I think it’s something that’s definitely worth looking into further.

Ken, I don’t know if you have more you’d want to say..

I think that’s exactly right. It’s a case of a completely unique mechanism that there’s no reason to expect. It wouldn’t be complimentary to many of these other mechanisms and is worth the exploration..

Yes. Thank you so much. My other question is with regards to IPF, where some studies have indicated the SARS-CoV-2 may regulated the beta signaling that would be done in terms of IPF.

So with regard to patient enrollment for IPF studies, is there a protocol in place for patients that may test positive for COVID-19 during the trial and also do you plan to enroll patients who have recovered from COVID-19?.

So you want me to answer that one?.

Go ahead, Ken. Yes, yes. Go ahead..

Yes. Let’s say it’s a little too early to be specific about inclusion exclusion criteria in that first clinical study. Obviously COVID is an evolving landscape as far as the consequences of subjects exposed to COVID-19 and recovering.

I mean, one of the things we learned from area experts in IPF is that many subjects who are IPF patients are doing better during this period because they’re wearing masks and protecting themselves from things that exacerbate their disease in general. So having previously been exposed to coronavirus may not be a reason to not include someone.

I think that’s just one of those things we’ll be taking into consideration when we design that first clinical study..

Sounds great. Thank you so much for taking my questions..

Thank you..

The next question will come from Elemer Piros with ROTH Capital Partners. Please go ahead..

Yes. Good afternoon, gentlemen. Thank you for the presentation.

And I just would like to confirm that the 25 milligram dose was it the highest that you tested in the 1b portion from the 1a?.

Ken, do you want to answer that?.

Yes. So with respect to the – yes, I’ll answer that one. With respect to the doses in the dose escalation, we’ll go into more detail in the presentation when we give this information in full at the scientific meeting. This was the dose we selected as being the highest practical dose we could administer going into the Phase 1b.

So there were no limitations based on safety for selecting that dose..

Thank you.

And if you could talk about the injection volume a little bit, Ken, and the rationale for further optimization, is it the injection site reactions that you can continue to see or in what way would you further optimize the formulation?.

Yes. I mean, as you can imagine, a Phase 1 study generally starts with a prototype formulation, which is clearly what we have and we’re gradually optimizing that towards the commercial form. So issues around how much drug we can administer and things like that are all taken into consideration in that process.

With respect to volumes or details on the formulations can’t really get into that at this stage, but we’ll – because part of that’s proprietary information, but we’ll provide more details on exactly what was dosing and how when we get to the scientific presentation..

Thank you. And if Jeff could potentially confirm that your G&A expense line at $2.5 million at least for near-term would be the new norm.

Is that your projection, Jeff?.

Yes. It may go up slightly, but you could probably leave it around there, that that steady state of that 2.5 to 3 years probably where we’ll be at going forward..

Yes. Thank you so much for the answers..

Hey Elemer, absolutely..

The next question will come from Steve Brozak with WBB Securities. Please go ahead..

Hey, thanks for taking the questions and congratulations obviously on the results. And Ken on the ALT, on the trial, I know the end is small, but it’s actually fascinating to see how the plus – the control group actually had an increase from baseline and yours had a significant decrease, which meant more than statistical significance.

What do you think that, and again the end is small, what do you think that increase was in the control? It’s a small increase, but it shows the wrong trend and you would expect it given the how the trial was set up that these people would have had a reduction. What are your thoughts there? And I’ve got a couple follow-ups after that, please..

Sure. Yes. I think to say you expect a reduction in a small four-week study based on the other parameters would be a stretch. They clearly did not drop in their ALT. They had a small increase above baseline, but it’s really the difference as you mentioned, that that shows the effects of 4211.

So compared to placebo a 25% difference is a very substantial difference in ALT..

A lot of other studies don’t even bother to have controls and they use some historical parameters. How does this that compare to what you’ve seen on the historical side? Just a quick question there..

Yes. Well, with respect to placebo outcomes, in four-week studies, there are very limited examples as you mentioned, I mean, many companies don’t have a parallel arm, which makes it hard for you to understand exactly what was drug related and what was placebo related. So we definitely address that with our design.

Now with respect to what are the placebo changes in other settings, it varies by study, and obviously the conditions of the study, you will see some longer-term Phase 2 or Phase 3 studies with placebo arms, but they’re not really an apples-to-apples comparison to a four-week setting like ours..

Well, for instance, with Madrigal, you can have a control that is as tight as or even a trial that’s as tight as yours has taken place.

So looking at that, I’m kind of curious to see what was the clinicians that were looking at this, what were their reactions? Because this is more than just in my opinion anyway, this is more than just a Phase 1b, this is a proof of concept in terms of what you’re looking at for the 4 – at least for 4211 possibly for your platform.

So what are your clinicians telling you coming back on?.

Yes. So we did mention the discussion with Rohit Loomba who’s one of our key opinion leader consultants on this area. And he was as mentioned in the press release, quite impressed by the level of the ALT reduction, the AST reductions, corroborating that change and sees that as promise for this being potentially a differentiated therapy for NASH.

So yes, I would agree in other settings, you might look at this study and say, this was actually more like a Phase 2a in that these patients had significant baseline liver fat and ALT levels that were diagnostic in many respects of them being subjects who would be otherwise at risk of NASH..

All right. Last question, you obviously mentioned one patient in terms of on in diabetes.

What other comorbidities should we be made aware of, because obviously these are patients that have other issues? What are the other items there? And did you have any kind of color, even if it’s anecdotal around that, because I’m kind of curious and I’ll hop back in the queue. Thank you..

Yes. Too early to say, although we did not include patients who had significant comorbidities, they were excluded from the study. The only really allowed comorbidity was diabetes, if it was controlled with metformin, and that’s all detailed in the criteria, which are quite long, but they’re in the ClinicalTrials.gov record.

So we will be looking at the data in more details, but not expecting to pull out comorbidities as an indicator..

Got it. Great. Again, congrats and thanks for taking the call..

Sure. Thanks a lot..

Thank you..

This concludes our question-and-answer session. I would like to turn the conference back over to Joe Sarret for any closing remarks. Please go ahead, sir..

Thank you, and thank you, everyone, for joining us this afternoon. We’d also like to particularly thank our shareholders for your continued support, and we look forward to updating you on our continued progress on our next call.

Chuck, would you please conclude the conference call?.

The conference has now concluded. Thank you for attending today’s presentation. You may now disconnect..