Good afternoon. My name is Latonya, and I will be your conference operator today. At this time, I would like to welcome everyone to CohBar’s Third Quarter 2019 Financial Results Conference Call. [Operator Instructions] Now I’d like to turn the conference over to your host today, Glen Garmont of LifeSci Advisors. Please go ahead, sir..

Thank you, Latonya, and thank you, everyone, for joining CohBar’s third quarter 2019 financial results conference call. Joining me on today’s call is Steve Engle, Chief Executive Officer; Ken Cundy, Chief Scientific Officer; and Jeff Biunno, Chief Financial Officer.

CohBar’s financial results press release was issued earlier today and may be downloaded from the website, www.cobar.com. If you’re having issues joining the Webex, you can access the slide presentation from CohBar’s homepage.

Jeff will begin with an overview of the third quarter financial 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 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 CB4211 and other mitochondria-based therapeutics.

Statements regarding ongoing and planned research and development activities; potential partnerships and capital resources and ability to fund 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 the website, cobar.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.

Cohort 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. With that, I’d like to turn the call over to Jeff Biunno, CohBar’s Chief Financial Officer.

Jeff?.

Thank you, Glenn, and thank you, everyone, for joining us this afternoon. I will now provide you with a summary of our financial results for the third quarter ended September 30, 2019, compared to the third quarter ended September 30, 2018.

Total operating expenses in Q3 2019 were $3,228 million as compared to $4,498 million in Q3 2018, a decrease of approximately $1,270 million. Operating expenses included noncash expenses of $621,000 for the quarter ended September 30, 2019 and $1,633 million for the quarter ended September 30, 2018.

Noncash operating expenses include stock-based compensation and depreciation and amortization costs. Research and development expenses were $1,944 million in Q3 2019 compared to $3,436 million in the prior year period, a decrease of approximately $1,492 million.

The decrease in research and development expenses was primarily due to lower stock-based compensation costs as the timing of preclinical and initial clinical costs incurred in the prior year period. These decreases were partially offset by an increase in expenses related to our continuing development of peptides.

General and administrative expenses were $1,284 million in Q3 2019 compared to $1,062 million in the prior year period, an increase of approximately $222,000.

The increase in general and administrative expenses was due to higher premium costs in the current year period for D&O insurance, higher investor relations costs and an increase in directors’ fees.

For the quarter ended September 30, 2019, CohBar reported a net loss of $3,349 million or $0.08 per basic and diluted share compared to a net loss for the quarter ended September 30, 2018 of $4,613 million or $0.11 per basic and diluted share.

Net loss included noncash expenses of $726,000 for the quarter ended September 30, 2019, and $1,738 million for the prior year period. Moving to the balance sheet. As of September 30, 2019, CohBar had $14.4 million in cash and investments compared to $22.2 million as of December 31, 2018.

The cash burn for the quarter ended September 30, 2019 was approximately $2.5 million. We estimate that based on our cash and investments balance as of September 30, 2019, we have sufficient capital to finance our operations into the fourth quarter of 2020. I will now turn the call over to Steve..

Thanks, Jeff. This is our agenda for the rest of our third quarter discussion, we will follow this with a Q&A session. As you can tell from our press release yesterday and today, we have made significant progress in the last quarter, and we want to share that with you.

Most importantly, we are very pleased to complete the Ia stage of the CB4211 study and moved into the Ib stage. Of course, it is the first mitochondria based therapeutic in humans, but it’s also a major milestone for clinical progress of CB4211 and a proof point for our peptide platform technology.

And just as a quick note, as you noticed, the increased activity in the Mitochondria medicine area. We will be speaking about that as well. Next slide. This is a cornerstone slide for CohBar, summarizing the company. It may be a review for some of you who know the story well.

Beginning with Item one, the discovery behind CohBar’s technology is finding that mitochondria are more than powerhouses of the cell, that we learned in biology class, and have generated signals in regulation that affects cells and systems across the body, a real stunner.

Based on the last decade of research, dysfunction of the mitochondria underlies multiple chronic and age-related diseases, like NASH, obesity, diabetes, cardiovascular and maybe cancer. CohBar has discovered over 100 peptides encoded in the mitochondria genome.

As a result, we believe we have a platform technology, which will provide multiple shots on goal. We are very pleased to complete the Ia stage of the 4211 study and move into the next stage, Ib. We believe that CB4211 is the first of a number of candidates that our platform technology will identify for advancements into the clinic.

We did this while continuing to progress on our evaluation of additional novel peptides targeting fibrotic diseases, cancer and type 2 diabetes, which Ken will speak more about in a moment.

Obviously, there are a number of potential indications with high unmet medical need, both in large populations like NASH, and orphan populations like certain cancers and other diseases.

Our intellectual property portfolio continues to expand, and we have an experienced management team that is well leveraged by clinical and research organizations, outside experts and world-class expert founders. This provides strong talent and breadth on a timely basis and with financial efficiency.

Now our Chief Science Officer, Ken Cundy, will share our R&D progress.

Ken?.

Thanks, Steve. I’ll now give a brief update of our R&D programs, beginning with our CB4211 clinical program. Next slide, please. So CohBar’s lead candidate is CB4211, a mitochondria based therapeutic, currently in Phase Ia/Ib clinical testing as a potential treatment of NASH and obesity.

The Phase Ia stage of the study has now been completed, and no significant safety or tolerability issues have been observed since resuming the study in June of this year.

The Phase Ia part of this study was a conventional double-blind placebo-controlled single ascending dose, multiple ascending dose assessment of the safety, tolerability and pharmacokinetics in healthy adults designed to identify the most appropriate dose for use in the follow-on Phase Ib stage.

Now the Phase Ib part of the study will be a double-blind placebo-controlled evaluation of the chosen dose of CB4211 in obese subjects with NAFLD and 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.

The Phase Ib stage is currently recruiting subjects. At this time, we anticipate availability of top-line activity data somewhere in mid-2020. The exact timing of the study will be a function of the recruitment rates, and we will have more clarity on that as the study progresses.

The study is still blinded, an analysis of data from both stages of the study will only occur when the database is finally locked, and the study is un-blinded after completion of the Phase Ib stage. Now as we stated on the last quarterly call, we expect to provide updates on the progress of the study at significant milestones.

If the study goes as planned, the next such milestone would likely be the end of dosing in the last obese NAFLD subjects, and we will update you on our progress on the next investor call. We have previously shared the preclinical data for 4211, which demonstrated efficacy in animal models of both NASH and obesity.

CB4211 has a novel mechanism of action involving the regulation of fatty acid release from fat cells, and that novel mechanism presents an opportunity for a combination of CB4211 with other drugs that have different mechanisms.

We also previously shared data showing synergy of CB4211 with GLP-1 and PPAR gamma agonist, 2 classes of drugs commonly used to treat type 2 diabetes. And it’s good to note that about 50% of patients with NASH are also diabetic. We’ll cover some of the historical data on this briefly in the next few slides. Next slide, please.

So this is a high-level review of some of the published preclinical efficacy data on CB4211. Showing on the left, the significant reduction in the NAFLD Activity Score, the NAF, after 21 days of CB4211 treatment in the STAM mouse model of NASH.

In the middle, you can see the significant reduction in body weight observed after 21 days of dosing in diet induced obese, or DIO mice, maintained on a high-fat diet.

And on the right, you can see selective reduction in fat versus lean less in these DIO mice resulting in a clear decrease in the number of white deposits of fat seen in the liver under the microscope. Next slide, please. Here, we review some of the previously disclosed data on the synergy of CB4211 with a different mechanism of action.

In a study of 4211 in DIO mice, the peptide showed synergistic effects with liraglutide, a GLP-1 agonist approved for the treatment of type 2 diabetes and obesity.

After 21 days of treatment, the combination of 4211 and liraglutide produced a greater reduction in body weight and in the proportion of body fat mass loss compared to the liraglutide alone. On the right, you can see images of the livers of these animals at 21 days.

And in animals given liraglutide alone, there are still many white fat deposits present, while the combination with 4211 greatly reduced the liver fat content. This synergy results from using 2 drugs with completely different and complementary mechanisms.

This result also suggests there could be potential for use of 4211 in a setting where patients are already on other medications like GLP-1 agonist. Next slide, please. Now this slide shows a high level schematic of the proposed mechanism of action of CB4211 in the setting of NASH, which involves regulation of free fatty acid release from fat cells.

In healthy people, insulin is a key regulator of metabolism in liver, muscle and fat cells and in abdominal fat cells, insulin regulates the process of lipolysis that generates free fatty acids from stored fats, which then flow into the bloodstream.

However, in subjects with NAFLD, the fat cells become less sensitive to insulin, resulting in dysregulated metabolism and uncontrolled lipolysis. This leads to a release of excess free fatty acids from abdominal fat cells into the blood and accumulation of the fat in the liver, a condition known as hepatic steatosis.

Excess fat in the liver can then cause lipotoxicity, which starts a cascade of events leading to inflammation, tissue damage and fibrosis. Now CB4211 acts on the foundational event in NASH.

It enhances the effect of insulin on fat cells, decreasing the lipolysis and blocking the excess flow of free fatty acids into the blood, thereby reducing the accumulation of fat in the liver that can lead to NASH.

This specific mechanism of action appears to be unique among the drugs currently under investigation for NASH and appears to explain some of our previous observations of synergy with other drug mechanisms in animal models.

While this mechanism of action may not be the only one exerted by CB4211 in animals and in the body, it does provide a basis for the potential efficacy of CB4211 in the setting of NASH. Next slide, please.

Now I’ll talk about the rest of CohBar’s pipeline and our research efforts towards identifying additional mitochondria based therapeutic candidates, and broadening our assessment of their therapeutic potential. It’s important to note that not – that all of these new peptides are not structurally related to MOTS-c or CB4211.

Each peptide family has its own distinct structural properties, and that determines their activity. We recently made significant progress in 3 main areas, and we’ve shared some of that progress on our last call.

The first area I’ll cover is in the setting of fibrotic diseases where we’ve shown promising anti-fibrotic effects for a novel peptide analog, which decreased biomarkers of fibrosis in culture human cells and decreased fibrosis in a model – in an animal model of idiopathic pulmonary fibrosis.

The second area of progress is in cancer, where we’ve identified a number of novel peptide analogs that enhance the ability of human immune cells to kill cancer cells in vitro, what is referred to as an immuno-oncology model.

The third area of progress is in the setting of type 2 diabetes research, where we recently identified a novel family of peptides with beneficial effects on glucose regulation in animal models of diabetes. We shared details of this new family of peptides at the American Diabetes Association meeting in June.

And that included our discovery of an important interaction between these peptides and a key cell surface receptor, called the apelin receptor. Now we’re in the process of optimizing peptides in all 3 of these discovery areas.

The optimization process is iterative, and it requires a cycle of synthesizing improved analogs and assessing them for numerous factors including physical chemical properties, chemical stability, ease of synthesis in vitro and in vivo potency metabolic stability, the potential for off-target activity and the potential for IP protection.

The cycle repeats until we reach an appropriate profile for our intended indication and the final selection of an optimized peptide as a clinical drug candidate for a specific clinical indication also involves numerous factors such as the unmet need, the market opportunity, the competitive landscape, the clinical and regulatory pathways, timing to prove a concept, reimbursement risks and a number of other factors.

Now although we cannot guarantee when our next clinical drug candidate will be identified. This is a high priority for CohBar, and our goal is to identify our next clinical drug candidate in 2020. Next slide, please. So in the area of fibrotic diseases, we previously shared data from the identification of new peptides with antifibrotic potential.

Fibrosis is a normal tissue response to injury but fibrosis also underlies the age and disease-related process of scarring in tissues like liver, lung, kidney and heart, including the progression of NASH and other age-related diseases.

We initially showed the CohBar’s peptide MBT number 2, produced a significant decrease in key biomarkers of fibrosis and inflammation in a cell-based model of pulmonary fibrosis. On this slide, you see, again, some of the in vivo data for MBT number 2 in a well-established mouse model of lung fibrosis.

In this study, mice were dosed with bleoMycin to induce a response very similar to the human disease, idiopathic pulmonary fibrosis. Animals were then treated for 3 weeks with vehicle control or with CohBar peptide and compared to normal animals that did not receive bleomycin.

After 21 days, lungs were examined by microscopy, and lung tissue changes was scored using an objective scale called the Ashcroft scale, which grades the fibrosis based on lung damage and the extent of fibrotic changes. In the top left – on the top figure on the left, you can see that it’s 21 days.

Animals treated with controlled vehicle had significant fibrosis, reaching about 3 on the Ashcroft scale. While those treated with CohBar peptide once-daily had a significantly lower Ashcroft fibrosis score. You can also see that visually in the photo micrographs of the lungs on the bottom of the slide.

On the far left, there are lungs of a normal animal,that did not receive bleomycin. In the middle, you see effects of the Bleomycin induction, followed by 21 days of treatment with a vehicle control.

There is significant lung damage with the appearance of fibrous thickening of tissue and the formation of many fibrotic knots, some of which are marked here with red arrows. However, in animals exposed to bleomycin and then treated for 21 days with CohBar’s peptide, there is clear protection, indicating anti-fibrotic activity.

These preliminary data show a direct translation of an in vitro efficacy signal into efficacy in a disease model. And now we’re conducting additional confirmatory studies in lung fibrosis, and we’ve expanded our evaluation to animal models of other fibrotic diseases. Next slide, please.

This slide shows some of the previous data from the same bleomycin induced mouse lung fibrosis study. In this case, we see that MBT number 2 produced a significant reduction in lung inflammation based on the decrease in the number of inflammatory cells that were present in the lung fluid after 21 days of treatment. Next slide, please.

And in this slide, we put these animal study data into perspective. On the left, you can see the results of a very slow mouse lung fibrosis study of MediciNova’s clinical drug MN-001, which is currently in Phase II studies for IPS and NASH. The study was conducted by the same site in Japan using the same study design.

After 21 days of treatment, the MediciNova drug produced a reduction in fibrosis score that is similar to the reduction we see with MBT number 2 on the right. Now MBT number 2 is still in the process of optimization.

But these preliminary data suggest additional opportunities for CohBar’s MBTs as potential treatments for a range of fibrotic and inflammatory diseases. Ongoing studies include the confirmatory studies in lung tissue and also evaluation in animal models of other fibrotic diseases. Next slide, please. So turning to our efforts in the area of cancer.

This slide reviews an example of a CohBar novel peptide that enhances the ability of our own immune cells to kill cancer cells. A treatment approach known as cancer immunotherapy or immuno-oncology.

Recently, there have been enormous advances in this field using approaches that boost the ability of our own immune cells to recognize and kill invading cancer cells. In this slide, we see the preliminary data from an in vitro immuno-oncology model run by our external CRO partner, PhenoVista Biosciences.

In this study, human blood cells, called PBMCs, are peripheral blood mononuclear cells, which include, for example, immune cells like T cells, B cells, Natural Killer cells, these are grown together with a standard human tumor cell lines called SK-Mel-28, a human melanoma cell line. The immune cells have been stimulated to induce an immune response.

Activated PBMCs attack the cancer cells. Now when we incubate the same cells in the presence of our peptide, we can measure their effect on the number of live cancer cells by microscopy, using specific stains and imaging techniques. We look for any potential enhancement of the stimulated immune response as reflected in more cancer cell death.

In this specific case, we saw a highly significant increase in the killing of cancer cells in the presence of this particular CohBar peptide MBT number 3.

On the left, you see representative images of the cells at 48 hours, using stains designed to specifically show all cells, labeling the nuclei of PBMCs and cancer cells in blue or just the cytoplasm of the Cancer cells labeled in green. You can see, there was a substantial decrease in providing cancer cells when the peptide was present.

Now these are, of course, early data, and now we’re moving forward with additional studies and evaluating these peptides in animal models of cancer. Next slide, please. So the third area we’ll review briefly is our ongoing evaluation of the potential of CohBar novel peptides as treatments for type 2 diabetes.

This slide is a summary of some of the published data that was presented at the 79th annual scientific sessions of the American Diabetes Association meeting in San Francisco in June. We reported the discovery of a family of novel peptide analogs of a Mitochondrial-Encoded Peptide CB5064, that was discovered by CohBar.

This new family of peptides had beneficial effects in diet induced obese, or DIO mice, a human – a model of human type 2 diabetes. Now analogs of CB5064 produced significant body weight loss and fat mass loss compared to placebo in the DIO mice. In addition, these peptides also improved glucose tolerance.

The ADA poster presented our discovery of a very selective interaction of these peptides with one specific receptor, the apelin receptor. Now apelin is a natural peptide that’s expressed in many different tissues, including adipose tissue, heart, lung, kidney, liver and brain.

And the function of apelin and the apelin receptor has been explored by others and appears to play a key role in regulating energy metabolism, cardiovascular function, fluid homeostasis and a number of other cellular processes.

This interaction opens the door to potential utility of these novel peptides in type 2 diabetes but also in other metabolic disease settings. Next slide, please. This final slide is a high-level overview of our current R&D programs for MBTs.

CB4211, our first clinical candidate, is now entering the Phase Ib stage of clinical testing for its activity relevant to both NASH and obesity. Behind that is an expanding list of potential indications where new MBT analogs are showing promising effects and are now in the optimization process, with a number of ongoing animal studies.

These include fibrotic diseases, cancer and type 2 diabetes. And with that, I’ll turn the call back to Steve..

Thank you, Ken. I think everybody can see why we’re so excited. So you may remember that we mentioned the increasing awareness and activity in the area we call mitochondria medicine on our last call. We wanted to share with you some of the news in that area for the other companies.

And regarding the other companies targeting mitochondria’s defects, Reata recently announced positive results in its Phase II study in a mitochondrial disease called Friedrich’s Ataxia, a neuromuscular degenerative disorder.

This kind of event raises pharmaceutical company awareness and increases confidence in the mitochondria area of drug development. We believe this helps CohBar as well in reaching pharmaceutical companies and institutional investors.

We have seen this in drug delivery and other areas where, for example, no one initially was interested in the pharmaceutical companies. And then as deals were done in the first skin patches, many companies began to come and see the company. So we think all of this is for the positive.

It’s also somewhat of a surprise because I think some people were betting against this outcome and the fact that it came out this way really did raise the confidence of some people on the institutional side.

In the partnering area, Alexion, one of the big biotech companies at a market cap of $23 billion, just completed a co-development commercialization deal with Stealth pharmaceutical company for its mitochondria candidate. And recently, Reata exercised its right to repurchase rights from AbbVie on its own candidates.

We believe that these activities have also attracted investor attention, which we believe helps CohBar. Next slide. So at a high level or strategic perspective, major diseases with metabolic impairment like obesity are driving medical and financial costs. We hear about it every day in the news.

Mitochondria are critical to metabolic health and Mitochondria dysfunction is a likely cause of these diseases, may not be the only cause, but certainly a likely cause. The academic research and pharmaceutical interest in mitochondrial medicine is increasing. And with that, the investor awareness is also growing.

So breakthrough discoveries by CohBar’s founders and scientists have revealed Mitochondrial-Encoded Peptide regulating major systems in the body as Ken has shown with both a clinical and preclinical kinds of results.

We believe CohBar’s translation of these discoveries into mitochondria-based therapeutics will provide novel treatment for chronic and age-related diseases. Next slide. I’d like to talk for a moment about where we are against the goals we have for this year.

We’ve actually achieved most of those goals for 2019, and I remain excited about the progress we’ve made year-to-date, and I think you can see why. As I look at the challenges we face, they’re very common to a biotech company at our stage, and I feel confident based on our progress that we can fully realize the potential of the company.

So as you can see, the clinical and preclinical programs continue to advance, and I can talk through those things. Also that we’ve been able to gain additional scientific recognition for our approach at the diabetes meeting. And we continue to expand the number of biotechnology veterans on our management team and the Board.

And finally, growing investor interest continues at conferences and meetings. Here, I wanted to emphasize that we did speak at the Cancer Fitzgerald conference in New York and the Bio Investor Forum in San Francisco in October. We’d like to continue to have those kinds of conferences that we are speaking at.

We also met with investors at major biotech investing centers like New York and Boston, and we are targeting biotech-focused institutional investors and generalists looking for innovative solutions to chronic diseases and aging.

And in addition, on the analyst side, we have ongoing discussions with several analysts, of course, we can’t predict the timing of anticipated coverage. And there’s certainly growing interest in the mitochondria space among those research analysts, which we believe, will accrue to our advantage. Regarding evaluating the funding alternatives.

I’d just like to talk for a moment about how we think about this. As stated, we believe we have sufficient cash and investments to finance our operations into the fourth quarter of 2020.

As in the past, we will fully evaluate the funding alternatives, so as to balance between spending to fully exploit the potential for our platform of peptides and maintaining capital to guard against potential going concerns. As a public company, we are obviously limited in what we can say about our plans for funding.

But I thought it would be helpful if I spoke generally about our strategy, which balances several factors, such as the market conditions, both globally and in biotech, the timing of the clinical and preclinical results, the maintaining of adequate funds to move our clinical and preclinical programs forward, the risk factors, the amount and timing and the relative cost of money and, of course, dilution.

We are looking at the – all of these and using this framework to regularly evaluate our financing needs. As we go forward, we’ll give you more visibility on those thoughts. But the company fundamentals, though, are strong, and the management team is quite enthusiastic.

As a result, we believe the stock is, of course, substantially undervalued, especially as you look at some of the other companies in this space. All these factors are being conveyed in our meetings with potential new investors, and they have been well received. And I would add also that we did advance through our preclinical programs. Next slide.

So our plan for this year, as you can see here – as you look at this goals for 2020. We’re looking at completing the Phase Ib stage of the Ia/Ib study and providing results mid-2020. We’re also identifying our next clinical candidate, continuing research into our 3 preclinical programs into fibrotic diseases, cancer and type 2 diabetes.

And while we’re doing this, of course, we want to maintain our financial runway and our ability to invest in our clinical program and preclinical programs. And on the investor side, we continue to broaden our institutional investor base and to secure research coverage.

On the partnering side, I would say that we will expand the activities as we go forward. But I would also note that when it comes to the NASH area, although there’s a great deal of interest. I think most people will be looking for the results out of our study, our Phase Ib study, before they make any decisions.

So we will be active, but the timing of a deal would be after that, based on what we know right now. And on the intellectual property, we continue to expand our IP portfolio to maintain our leadership in mitochondrial-based therapeutics. Next slide. So we continue to realize the CohBar vision.

In the last year, we’ve made substantial progress with the initiation and conduct of the study and more recently, with the additional movement into the Ib as well as the exciting new peptide data. We believe the company fundamentals are strong, and the management team is moving forward as quickly as possible.

Again, we convey these factors as we go through these meetings and we think that as more and more people understand what we’re doing. We will take a higher and higher visible position in the market, and that will be reflected in many ways in the company. Thank you very much. We can go to the questions now..

Thank you. [Operator Instructions] Our first question comes from Robert LeBoyer with Ladenberg Thalmann. Please proceed with your question..

Good afternoon and thank you for all the data presentation. My question has to do with the clinical candidate and the identification.

Is there any particular area that you’re looking at? Or is everything fair game? And also in the area of partnership? Are you thinking of licensing in existing peptide that you have some data for? Or would this be something you haven’t worked in before? Or any additional details you can give on that strategy?.

Great. Thank you, Robert, for the question. Let me just ask on the first part, when you said area, I was not quite sure what you’re looking for.

Can you be a little more specific?.

Well, there were – there are two areas listed on the chart as being in clinical. And then there are other four, and one is Other diseases. So any elaboration or additional details would be welcome..

Yes. So let me try and address that for you, Rob. The obvious ones that are on the list right now and high priority are fibrotic diseases. So that range is, as you know, from those that might be considered orphan indications like idiopathic pulmonary fibrosis to more common fibrotic diseases.

And so we are currently exploring across a number of potential fibrotic disease indications. In the setting of cancer, again, it’s open to identification of particular cancers that fall into a narrow orphan setting. And that going forward, we still have to fully explore what the activity of our peptides across those possibilities.

So there are – there’s many possibilities. You said it’s pretty open at that point. Type 2 diabetes is a pretty clear target for the third category.

When it comes to Other, that encompasses the other age-related disease areas that we have previously seen activity in, including activity for some of the MBTs in the setting, neuroprotection and cardiovascular, they’re obviously less progressed than the ones that we have presented here on fibrosis and cancer and type 2 diabetes, but there are many possible directions those peptides can go..

Thank you, Ken. And Robert, also on the partnership question, whether we would do earlier stage deals in the preclinical stage of things or even entertain deals that were aimed at using the platform with someone else’s specific area, not related to the ones that we’ve already identified. I think the answer is, yes, on both of those.

Obviously, in the oncology area, there have been a number of deals done at a preclinical level. So it, kind of, depends on what the results are as we go through and get these additional studies done. In addition to which, on the use of the technology in a more general way.

Obviously, there’s some of the big pharma companies as well as big biotech that are experts in areas that we probably wouldn’t pick up and start focusing on in the short term, but they’ve already got all the assays and experts to do that. So we have indeed brought that up with one or two of them.

And we’ll continue to do that as we go through the process of introducing the technology and talking to them about what we have.

Does that help?.

Yes. That is helpful. That’s pretty much what I was getting to, and it is the kind of answer I was looking for. Thank you..

Great. Thank you..

[Operator Instructions] There are no further questions in queue. I’d like to turn the call back over to management for closing comments..

Great. Well, thank you, everyone, for joining us, and please check in. We’re really getting a lot done right here, and we’ll enjoy talking to you as we get additional results. Thank you very much..

This does conclude today’s teleconference. You may disconnect your lines at this time, and have a great day..