Good afternoon. My name is Lisa, and I will be your conference operator today. At this time, I would like to welcome everyone to CohBar's First Quarter 2019 Financial Results Conference Call. [Operator Instructions]. At this time, I would like to turn the call over to Glenn Garmont of LifeSci Advisors. Please go ahead, sir..

Thank you, Lisa, and thank you, everyone, for joining CohBar's First Quarter 2019 Financial Results Conference Call. Joining me on today's call is Phillippe Calais, CohBar's Interim 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 our website at www.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 first quarter financial results, followed by a business and R&D update from Philippe 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 can 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 mitochondrial-based therapeutics, statements regarding ongoing and planned R&D activities, potential and effects of newly discovered mitochondrial-derived peptides, potential partnerships, capital resources, future financing plans and ability to fund our operations and protect and expand our intellectual property.

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?.

Thank you, Glenn, and thank you, everyone, for joining us this afternoon. I'll now provide you with a summary of our financial results for the first quarter ended March 31, 2019, compared to the first quarter ended March 31, 2018.

Total operating expenses in Q1 2019 were $2.828 million as compared to $3.594 million in Q1 2018, a decrease of approximately $766,000. Operating expenses for the quarter ended March 31, 2019, included non-cash expenses of $798,000. Non-cash expenses include stock-based compensation and depreciation and amortization costs.

Research and development expenses were $1.372 million in Q1 2019 compared to $2.681 million in the prior year period, a decrease of approximately $1.309 million.

The decrease in research and development expenses was primarily due to the timing of preclinical and initial clinical cost incurred in the prior year period, a decrease in stock-based compensation cost for partially invested new grant made in the prior year period and the revaluation of consultant's options also in the prior year period.

These decreases were partially offset by the increased cost of our research program focused on the continuing development of our peptides. General and administrative expenses were $1.456 million in Q1 2019 compared to $913,000 in the prior year period. It's an increase of approximately $543,000.

The increase in general and administrative expenses was due to a net increase in stock-based compensation primarily related to the current period cost of grants made in prior year periods, an increase in the recruiting costs related to our CEO search, and an increase in Directors' fees.

For the quarter ended March 31, 2019, the company reported a net loss of $2.921 million or $0.07 per basic and diluted share compared to a net loss of $3.587 million or $0.09 per basic and diluted share for the quarter ended March 31, 2018. Moving to the balance sheet.

As of March 31, 2019, CohBar had $19.5 million in cash and investments compared to $22.2 million as of December 31, 2018. We estimate that based on our cash and investments balance as of March 31, 2019, we have sufficient capital to finance our operations into the middle of 2020. I'll now turn the call over to Philippe.

Philippe?.

"Mitochondria, a Source for Novel Therapeutics," supported by world-leading experts in aging and mitochondrial science, Doctors David Sinclair and Hassy Cohen, and gathering a lot of new people and potential new investors exposed to the company for the first time.

Finally, this morning, we announced the late-breaking news of the announcement of Steve Engle as CohBar's new CEO. Next slide. Some of you will be familiar with this slide, describing our core areas of expertise. What is new and very exciting is that we are adding new potential disease targets to our armamentarium.

As our research efforts are bearing fruit, we have identified new peptides allowing us to explore new therapeutic targets that are being evaluated in type 2 diabetes, oncology and several other aging diseases sharing fibrosis as the common theme, such as cardiovascular, pulmonary or kidney diseases.

With this mouthwatering introduction, I will now turn to Ken Cundy, our Chief Scientific Officer, who will describe those major advances.

Ken?.

Thanks, Philippe. I will now give an update on our R&D programs beginning with CB4211. Next slide. So as a reminder, CohBar's lead program is CB4211, a mitochondrial-based therapeutic currently being developed for the treatment of NASH and obesity. CB4211 is a novel improved analog of MOTS-c, one of the MDPs discovered by our Founder, Dr. Hassy Cohen.

CB4211 has a novel mechanism of action involving regulation of fatty acid release from fat cells.

Preclinical data for 4211 demonstrated efficacy in animal models of both NASH and obesity, including a reduction of the NAFLD activity score, or NAS, in the well-established STAM mouse model of NASH, improvement of liver fat levels and circulating markers of liver damage, and a selective normalization of body weight in obese animals.

A Phase Ia/Ib study of CB4211 was initiated last year designed to provide an activity readout that is potentially relevant to both NASH and obesity. We filed a comprehensive intellectual property protection around CB4211 and its related analogs, and CB4211 represents the first in a new class of drugs.

It's the first-ever analog of an MDP to advance to clinical testing. Next slide, please. This slide shows the design of our clinical study of CB4211. This is a Phase Ia/Ib study. Phase Ia is a conventional single-ascending dose, multiple-ascending dose evaluation of safety, tolerability and exposure in healthy subjects.

Phase Ib is a placebo-controlled evaluation in a single cohort of obese subjects with NAFLD, nonalcoholic fatty liver disease. This last segment of the overall study is a 4-week exploratory evaluation of the activity of CB4211 relevant to both NASH and obesity.

It's not a pivotal study, but it should provide a shorter-term readout on multiple endpoints such as changes in liver fat, which is a foundational event in NASH, using a noninvasive imaging technique called MRI-PDFF. In addition, it will assess changes in body weight, the primary outcome in obesity, and changes in other disease biomarkers.

Next slide, please. Now we announced back in November the dosing in the study was temporarily suspended to address mild but persistent injection site lumps. And just last week, we announced that we will be moving forward again with the study. So let's talk about that process in more detail.

Following the suspension of dosing, we developed a plan for mitigating the injection site issue and submitted that plan together with all available data on the injection site reactions to FDA for comment and advice at the end of November.

Our first opportunity to discuss this with FDA was done in March, and over the last several weeks, we've been discussing with FDA the amended study plan, and we will now be incorporating FDA's feedback into our study protocol.

We're working with our clinical partner Covance to implement that revised protocol, and we expect to be able to resume dosing in June.

Obviously, Covance has to schedule all of the many activities involved in executing the remainder of the clinical study, and we expect to be able to provide a clearer picture on the projected timing of the rest of the study on our next investor call which is scheduled for June 18. Next slide, please.

Now on this slide, we see a recent study of CB4211 in diet-induced obese mice, or DIO mice, that were maintained on a high-fat diet, demonstrating synergistic effects with liraglutide. These data has been presented in the past. Liraglutide is a GLP-1 agonist approved for the treatment of type 2 diabetes and obesity.

Now after 21 days of treatment, the combination of CB4211 and liraglutide produced a greater reduction in body weight and in the proportion of body fat mass loss compared to liraglutide alone. On the right, you can see the livers of these animals at 21 days.

In animals given liraglutide alone, there are many small white fat deposits, while the combination with CB4211 greatly reduced the liver fat content. This synergy arises because the two drugs have complementary and different mechanisms.

This result suggests there could be potential to use CB4211 in a setting where patients are already on other medications like GLP-1 agonists. Next slide, please.

And here, we see more recent evidence of synergistic effects of CB4211, this time in combination with pioglitazone, a member of another class of antidiabetic drugs called PPAR gamma agonists, which regulate glucose and lipid metabolism.

After 10 days of treatment of obese mice with a low dose of pioglitazone alone, there were minimal effects on glucose tolerance measured here by blood glucose levels after a standard glucose injection. However, the combination of CB4211 and pioglitazone produced a significant reduction in the blood glucose excursion after a glucose challenge.

This effect points to the potential for combination of CB4211 with other drugs in the setting of NASH or potentially diabetes. Combination therapy is expected to play a major role in treating NASH since the underlying pathology and the different stages of the disease require multiple mechanisms to address. Next slide, please.

Now let's move on to the rest of CohBar's R&D efforts aimed at identifying additional novel, improved analogs of mitochondrially encoded peptides for development as mitochondrial-based therapeutics. Next slide.

Among the many new peptides that CohBar has discovered are some that have shown effects on regulating glucose tolerance, suggesting potential for management of diseases like type 2 diabetes. Here, you see some earlier data from a glucose tolerance test in diet-induced obese, or DIO, mice after 10 days of treatment.

Now a glucose tolerance test involves administering a large glucose dose and looking at the resulting changes in blood glucose levels. In obese mice, blood glucose levels are elevated and insulin is much less effective in controlling glucose, a condition we call insulin resistance.

So when challenged with a large glucose dose, the blood glucose levels in these obese mice rise at very high levels and slowly decline. Approved diabetes drugs like the GLP-1 agonist liraglutide are able to blunt the blood glucose rise by improving insulin release.

In this study, you can see that one of our new MDP analogs had a similar effect to liraglutide on improving glucose tolerance.

Now we've since further optimized this family of peptides, and we've recently uncovered an important component of their mechanism of action involving interaction with another key cell surface receptor that plays a role in many age-related diseases.

That work has now been accepted for presentation at the American Diabetes Association meeting next month, and unfortunately, we will not be able to share more details of the new data prior to that presentation. Next slide, please. Beyond diabetes, we've been exploring the activity of our peptides in a number of phenotypic screens.

Here, we see an example of a new CohBar peptide that has shown preliminary evidence of anti-fibrotic activity. Anti-fibrotic agents are used to slow the age and disease-related process of scarring in tissues like liver, lungs, kidneys and heart, including the treatment of NASH and other age-related diseases.

Now here we see a CohBar peptide tested in an in vitro fibrosis model using a coculture of human lung airway cells and lung fibroblasts. This is intended to model the complex biology of a fibrotic lung disease such as idiopathic pulmonary fibrosis. That's a chronic progressive lung disease with limited treatment options.

And now, here you see that after two days of treatment of the cells, increasing concentrations of CohBar's peptide produced a significant decrease in the expression of the biomarkers Collagen Type I, Collagen Type III and alpha-smooth muscle actin, or alpha SMA, all of which are extracellular matrix components involved in fibrosis and inflammation.

The big question here, of course, is do these effects translate to efficacy in animal models of disease. Next slide, please. So the same CohBar peptide was tested in vivo in a mouse model of lung fibrosis, and the preliminary data are shown here.

In this widely used model, mice were dosed with bleomycin to induce a response that's very similar to the human disease idiopathic pulmonary fibrosis. Animals were then treated for three weeks with vehicle control or CohBar peptide, and then compared to normal animals who did not receive the bleomycin. After 21 days, lungs were examined by microscopy.

Lung tissue changes were scored using an objective scale called the Ashcroft score, which grades the fibrosis based on lung damage and the extent of fibrotic changes. At 21 days, animals treated with control vehicle had significant fibrosis.

However, animals treated with CohBar's peptide once daily had significant reduction in the Ashcroft fibrosis score. Next slide, please. Now here, we take a closer look at the lungs of the same mice after 21 days. On the left, you can see a representative slide from the lungs of normal animals that did not receive bleomycin.

The lungs show the characteristic structure of alveoli. In the middle, you see the effects of bleomycin induction followed by 21 days treatment with the vehicle control. There is significant lung damage with the appearance of fibrous thickening of tissue and the formation of many fibrotic knots, some of them 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 an anti-fibrotic effect.

This preliminary result shows a direct translation of the in vitro efficacy signal into an in vivo effect, and it opens the door for further exploration of this peptide and its related analogs in other fibrotic diseases. Next slide, please. Now on this next slide, we put these data into context.

MN-001 or tipelukast, is an anti-fibrotic drug under development by MediciNova that is currently in Phase II clinical testing for idiopathic pulmonary fibrosis and is expected to end the Phase II for NASH. Here, we see the data for that drug tested in exactly the same mouse lung fibrosis model run by the same test site, SMC in Japan.

Now you can see the Ashcroft fibrosis levels in the two studies were very similar for vehicle-treated animals. This is in the presence of bleomycin. And the effect size we saw for our new peptide MBT 2 here is the same range as that seen for MN-001.

So again, this new peptide is still in the process of optimization, but this result opens a new area of exploration for CohBar's MBTs as potential treatments for fibrotic diseases. And Philippe will say more on the importance of fibrosis in a wide variety of age-related diseases, and all of these present additional opportunities for CohBar.

Next slide, please. So finally, we want to turn now to our efforts in the area of cancer. In the past, we've presented data showing that certain select CohBar MBTs appear to have the ability to slow the growth of a broad range of human tumor cell types in vitro.

However, in this slide, we're looking at a different approach to treating cancer, using CohBar's novel peptides to enhance the ability of our own blood cells to kill cancer, a treatment approach known as cancer immunotherapy or immuno-oncology.

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

In this study, human blood cells called PBMCs, or peripheral blood mononuclear cells, are grown together with a standard human tumor cell line called SK-Mel-28. This is a human melanoma cell line. The blood cells are then stimulated with LPS, lipopolysaccharide, which is a component of bacterial cell walls that stimulates an immune response.

The activated PBMCs then attack the cancer cells to some extent. We incubate the same cells in the presence of our peptide to measure their effects on this by counting the number of live cancer cells by microscopy using specific stains and imaging techniques.

Here, we're looking 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 killing of the cancer cells in the presence of this particular MBT #3.

On the left, you see representative images of the cells at 48 hours, using stains designed to specifically show all the cells, labeling the nuclei of both PBMCs and cancer cells in blue, or just the cytoplasm of the cancer cells in green.

And you can clearly see there was a substantial decrease in the surviving cancer cells when the peptide was present. Quantitative techniques like this can be used to measure the relative activity of our peptide and help guide the optimization process before we move into in vivo models.

These are, of course, early data but we have more to do to turn this into a novel immuno-oncology treatment. But this finding has now opened new areas of promise for CohBar's portfolio of peptides. Okay. On this final slide, I'm just showing a high-level overview of our current R&D programs for MBTs.

CB4211, our first clinical candidate, will be resuming Phase I clinical testing for NASH and obesity. Behind CB4211, is an expanding list of indications where new MDP analogs are in the discovery and optimization process.

Some of these peptides are more advanced than others, and there are recently discovered peptides with promising activity in models of type 2 diabetes, cancer and other age-related diseases. And these include the most recent advances in the area of fibrotic diseases, and potentially, cancer immunotherapy.

So with that, I will hand the presentation back to Philippe..

Thank you very much, Ken, for this very exciting update. So not only we are now moving forward with our clinical study with CB4211 in NASH and obesity but we are also making significant progress on several fronts with our research efforts.

I will now provide a brief overview of fibrosis and immuno-oncology as we will be evaluating further the addressable age-related indications and markets over the next few months. In this slide, you can see that fibrosis is an underlying process in many age-related diseases.

Fibrosis progresses over time and is a core component of cardiac, pulmonary, renal or liver diseases as well as many other such as diabetic retinopathy or pancreatitis, to list a few. On the next slide, please. On the following slide, you can see how fibrosis affects all organs in the body. The biology of fibrosis is a complex but also dynamic process.

Fibrosis is defined by the formation of fibrous scar diseases – scar tissues in response to injury and is part of the normal healing process. In young people, the scars resolve over time and are replaced by new tissue. In the elderly, the scars do not resolve or fade and scar tissue can build up.

In organs such as heart, the lungs, kidneys or liver, the buildup of scar tissue can interfere with the normal function with potentially devastating results over time, leading to major organ failure, and ultimately, death. It is now well understood that fibrosis is a silent killer that accounts for up to 1/3 of deaths worldwide.

Some people even believe that the death rate can reach up 40%. Multiple biological pathways are involved in the pathogenesis of fibrosis, which explains the large unmet medical need and the few drugs approved. For example, in idiopathic pulmonary fibrosis, the only two drugs that are approved show limited efficacy.

Fibrotic diseases are also a source of orphan diseases or diseases only found in small population. The industry recognizes early-stage transaction from pre-clinical stage to Phase I, therefore, the rewards can come early in the drug development process. Next slide please.

Age is a well-known risk factor for cancer, as the normal aging process affects many important biological processes within our bodies that result in the deterioration of proteins and DNA itself. In fact, the longer we live, the more errors our genes accumulate. Over time, this mutation can lead to cancer.

The number of older people aged 65 and older living with cancer is set to triple between 2010 and 2040. And by 2040, people over 65 would account for 77% of all people living with a cancer diagnosis.

The global economic cost of cancer is staggering, with the average annual cost of treatment in the $150,000 range and is increasing as cost associated with oncology care are higher than the treatment cost for any other disease.

Beyond the cellular changes, other body system become less effective with age, such as the immune system becoming less protective and efficient in detecting and fighting infection, diseases and cancer. Immunotherapy, empowering the immune system to fight the disease, has become the new oncology therapeutic paradigm.

The success in immuno-oncology reside in the development of treatment combination protocols that result in long-term remission as the immune system recognizes and selectively attacks the cancer cells.

This is a major advance, when compared with more conventional treatments that are toxic to the body, have a short efficacy span and do not prevent relapse. Next slide please. This slide illustrates the huge potential of the industry effort and the associated partnership rewards.

Oncology research and development benefit from well-defined and readily available disease models with streamlined clinical development path including in several orphan diseases. Oncology today is the most active research area for pharmaceuticals, with the most recent advances focusing on checkpoint inhibitors and CAR T therapies.

The graph on the right-hand side illustrates the magnitude of the pharma licensing effort in the $30 billion range and focusing mostly on immuno-oncology. Next slide please. Now we switch gears and look at the financing, investor relation and strategic partnering. So for the financing, we continue to evaluate alternatives for additional funding.

On the investor relationship side, we had a busy quarter in terms of investor relation, meeting with investors, analysts and bankers at the JPMorgan Healthcare Conference in January. I also presented and participated to a panel on aging at the BIO CEO conference in February.

I also participated in most part of the NASH panel at the Roth Conference in March. And we had our key opinion conference call on May 2. We will also participate to BIO in June. We have plans for non-deal roadshows as we target institutional investors.

We are pursuing our coverage discussion with research analysts and continue to build our investment banking relations. As we continue to work with partnering advisers, we are also planning on resuming partnership discussion for CB4211, either as a stand-alone program or in combination with other agents.

We are also evaluating the potential for research collaboration for our new peptides. On a final note, I wish to point out that I fully enjoyed my last 5 months at the helm of our company. I will continue to serve on the company's Board and support our efforts to advance all of our projects.

I want to thank all of you for your support, and wish Steve all of the success he deserves. With this, I will now turn to you and take your questions.

Operator?.

[Operator Instructions] We'll take our first question from Robert Giordano, Network 1..

Gentlemen, first and foremost, I wish to congratulate you on being the new leader in educating both the lay public and indeed the scientific community to the importance of the mitochondria.

Following on that movement, if you will, could you help relay people in explaining what is actually the advantage of approaching these various disease categories, oncology, diabetes, et cetera, et cetera, where you are utilizing the mitochondria as a vehicle? What is it about the mitochondria that presents an advantage either in efficacy and perhaps even more so in safety?.

Great. This is Ken. Thanks for that question. So the way we look at it is these peptides that we're developing are obviously analogs of naturally occurring peptides, peptides encoded within the mitochondria that have had an opportunity to evolve over 1 billion years.

So we believe that there's built into their design very important structural features towards efficacy and safety. So by making analogs of a naturally occurring peptides, it's not just a random sequence that we're working with. It has already, if you like, been naturally selected to some extent.

And that's why we think its safety is likely to be something more manageable than a completely random synthetic molecule. And on the efficacy side, we believe that mitochondria have a role in communicating with other organs within the body without the cell types, and it is via these secreted peptides that they can communicate.

So we are taking advantage of that communication pathway..

So does it bring into play both the ability – the enhancing ability of the mitochondria to create more ATP under all circumstances and be more robust? And/or is it possibly having any of these abilities governance over a proptosis or both?.

So we are not directly attacking mitochondria with these peptides. We are taking mitochondrial secreted peptides that signal to other locations. So we're not, with these molecules we are developing expecting to just to be affecting the function of the mitochondria.

We're looking at how they affect other cell types and regulate other pathways in things like liver, lung, cardiovascular tissue as well. So there's a broad list of opportunities here outside of the mitochondria where these peptides can regulate through other pathways..

[Operator Instructions] The next up, we'll go to [Tom Sander], an investor..

I just want to really shout out for Philippe and thank him for his really, I think, phenomenal interim CEO and really getting everybody engaged. I've seen a lot. I've seen more new changes and improvements in the last 6 months than I have in the last 3 years.

I am speaking for all of us shareholders who have been in the game for more than 3 years with CohBar. And I also want to welcome Steve. And Ken, I wanted to ask you. You were discussing orphan drugs and you were discussing with the GLP-1 agonist. And I forget which drug you were referring to. But Exenatide is also a GLP-1 agonist.

So do you think that the CB4211 would also work well with Exenatide?.

Yes. Yes, sure. I think it's a good question, but it's reasonable to assume that because our mechanism is complementary to the signaling pathway of GLP-1 that this would be synergistic with other drugs from that class. And the same is true with the PPAR gamma agonist.

If that mechanism is complementary to our mechanism, it's really not so much a question of which drug you're using for GLP-1 or for PPAR gamma. There's a reasonable expectation that we'll have useful properties by combining with any member of that class..

And I think that's just phenomenal because I guess everybody knows that there's a plethora of companies out there that might be a little – they have products further advanced along the lines of NASH and type 2 diabetes, but I always thought of these mitochondrial drug peptides as a great combination drug..

Right. I think that....

No question, I just....

The opportunity for us, yes, absolutely, is the ability to use these in the setting of drugs that are already being used, already effective but maybe could be more effective in combination with ours..

Absolutely. And so just in conclusion, I want to thank everybody. I want to tell everyone that between Ken and Dave Sinclair and Nir Barzilai, Hassy Cohen, Philippe Calais that brings 30 years of biotechnology to the company, we're really in a good boat. Thanks, guys..

Thank you..

[Operator Instructions] And we do have a question from [Graham Bonkowski]..

First, I just wanted to say how fortunate we are as shareholders to have you as our – CohBar's Chief Scientific Officer. You've done just an outstanding job, and very much appreciated..

Well thank you very much for that comment..

Yes. I was reading abstract that stated about 7% of the approved drugs are purported to have no known primary target and up to 18% lack a well-defined MOA.

So is CohBar's current understanding of CB4211 MOA and with our abstract presentation for type 2 diabetes at the ADA conference on June 7, can you speak to the importance of the MOA and how big pharma might view this new development as CohBar continues to increase the value of their assets and their proprietary technological platform?.

Sure. Absolutely. That's a great question. And it really breaks down to a number of advantages of knowing the mechanism of action. To begin with, if you know a target for your drug that is already associated with a disease, then it helps to validate why your drug should work in that setting.

And if that particular receptor involved in that mechanism is involved in a number of other diseases, it actually opens other doors you may not have considered for your molecule as potential disease targets.

And when you get into a discussion of that with a partner like a big pharma that wants to pursue a particular disease, their interest in mechanism is to both understand why your drug should work, but also why your drug should be safe. So the more you know about it, the more comfort they have in both of those areas.

So it really produces a lot of opportunity for a company when they understand the mechanism, even though there, as you said, many drugs out there that are not that well understood..

Yes. Well that's fantastic. I appreciate that. I just have a follow-up question, not on this subject, but I know you mentioned on last week's webcast about the possibility of pursuing orphan drugs.

Is there any area in particular you're targeting right now?.

I'd say, the opportunities are there in a number of settings. Obviously, in fibrosis there are settings where fibrotic disease occurs in – on a smaller number of people but very impactfully.

So idiopathic pulmonary fibrosis would be an example where the number of people may be smaller, but it's extremely impactful if you could treat pulmonary fibrosis in that age-related chronic and essentially terminal disease..

Because most of those gets fast-tracked if I'm not mistaken, right?.

Yes. There are advantages to being in a position of pursuing an orphan drug indication. It's a slower hurdle for approval. It's also a shorter path to the clinic. And at the end of the day, you also get exclusivity in terms of being able to market your drug. So there are some advantages to that, to be weighed in that calculation..

Yes. Okay, well, I appreciate you answering the questions. And once again, I'm very excited. I am just grateful for all the management team and all their efforts over the last, well, many years, but particularly the last six, seven weeks. So once again, thank you kindly. I appreciate that..

And everyone, at this time, there are no further questions in the queue..

Right. So then it will be time to conclude. And as we'll be having our next investor call around our General Annual Meeting that is scheduled to take place on June 18, this will give you the opportunity to welcome more formally and know our new leader, Steve, at the time.

So with this, I would like to thank you very much for joining our call today, and have a nice afternoon or rest of the day. Thank you..

And once again, that does conclude today's conference. We would like to thank you all for your participation today. You may now disconnect..