Lantern Pharma Inc. (LTRN) Earnings Call Transcript & Summary

Okay. Good afternoon, everybody. I'm Nicole Leber with Investor Relations at Lantern Pharma and welcome to our Brain Tumor Awareness Month, GPM key opinion leader Webinar. May is bringing tumor awareness month, among dedicated to supporting empowering and amplifying the voice of the brain tumor community. According to braintumor.org, an estimated 700,000 Americans are living with a primary brain tumor and an additional 88,970 people will be diagnosed with the primary brain tumor in 2022. Additionally, the 5-year relative survival rate for all malignant brain tumors is only 35.6%. For today's KOL webinar will be focusing heavily on the primary brain tumor glioblastoma, which is the most common malignant brain tumor among adults with an estimated 13,000 patients diagnosed per year in the United States. In addition to being one of the most common primary cancers, it is one of the most deadly with an average median survival of 15, 16 months. Several of our panels today are experts in the treatment and research of cures for glioblastoma. And with that, I would like to introduce our esteemed panelists. We have Dr. John Laterra, who is the Professor of Neurology, Oncology and Neuroscience and Director of the Department of Neurology Division of Neuro-Oncology at the Johns Hopkins School of Medicine and Kennedy Krieger Institute. We also have Dr. Matthias Holdhoff, Associate Professor of Oncology, Neurology and Neurosurgery at the Johns Hopkins University School of Medicine. And we also have with us Dr. Kishor Bhatia, who is the Chief Scientific Officer at Lantern Pharma. And now I'll turn the call over to our panelists for some more personal introductions starting with Dr. Laterra.

Hello, and it's a pleasure to join you all and be here during a Brain Tumor Awareness Month for this session. So as I was introduced, I'm a professor and research scientist clinician at Johns Hopkins with my research laboratory at the Kennedy Krieger Institute. I've been exploring mechanisms of brain cancer malignancy and therapeutic target identification for the past 30 years, primarily on the preclinical side with the goal to translate our findings to clinical trials. And I'm excited to be here, particularly with regard to what we'll be discussing today, this novel chemotherapeutic agent LP-184. I'm Matthias Holdhoff. I'm an Associate Professor of Oncology and Neuro-surgery here at Johns Hopkins and at the Sidney Kimmel Comprehensive Cancer Center. I'm a Co-Director of our brain cancer program. And as such, I am contributing to the work we're all doing jointly here in our group and in fact, at many centers around the world with the one goal of improving lives of our patients with primary brain cancers. And of course, glioblastomas are the most common primary brain cancer in adults, and I really welcome this opportunity and appreciate the invitation to this webinar. I think we are going to talk about a very interesting drug, and this is sort of right up my alley because I'm a clinical investigator on clinical trials with the main focus on new drugs in an ideal setting of bench-to-bedside translation for the treatment of malignant gliomas and also CMS lymphomas.

I'm the Chief Science Officer for Lantern Pharma. My name is Dr. Kishor Bhatia and I spent 2 decades doing research in oncology, most specifically in epidemiology and transformational oncology, glad to be here to discuss GBF.

Great. So Dr. Bhatia, could you provide background on Lantern in our pipeline and discuss how LP-184, one of Lantern's drug candidates is being targeted for the potential treatment of glioblastoma.

Yes. Lantern is a unique biopharmaceutical company. It is one of the few companies that actually leverages the growing amount of data using our proprietary RADR artificial intelligence platform and machine learning, the intent of using data is to transform the cost base and timeline of oncology drug development and make newer, more potent drugs available faster to patients making the life of cancer patients better. Lantern at this time is currently developing 4 drug candidates, and these are across 8 disclosed tumor targets, including 2 Phase II programs. By targeting drugs to patients whose genomic profile identifies them as having the highest probability of benefiting from the drug, Lantern's approach represents the potential to deliver best-in-class outcomes. Lantern Pharma is advancing LP-184 for the treatment of solid tumor indications. That also includes glioblastomas. LP-184 is an acylfulvene-derived prodrug. When I say product, it requires to be activated in the tumor cells, providing some kind of tumor preferential necessity by an oxidoreductase enzyme called PTGR1 which is often expressed much higher in tumor cells than in normal cells. The prodrug LP-184 once activated, acts as a synthetic lethal agent in tumors that harbor some specific mutations, particularly low in the DNA damage repair parts base and appears to be more sensitive based upon in silico RADR assessment to tumors that have some activated passes, such as the EGFR...

Can you both tell us a bit about GBM, what challenges are currently associated with glioblastoma treatment? And how might they be overcome?

Glioblastomas has been very challenging to treat. And as you mentioned before, this is the most common primary brain cancer in adults. We have made less progress than we had hoped for over the last 20 years. Specific challenges for this tumor in the presence of the blood-brain barrier and difficulties with drug delivery. We know that about 98% of the drugs that we give to treat cancer, including many chemotherapy drugs do not reach therapeutic constructions in the brain. So the armamentarium, the [Indiscernible] drugs we have, we can use is quite limited. We have so far only one class of drugs, alkylamine agents and namely temozolomide [ in those areas ] that have used as chemotherapy drugs and truly only temozolomide that provided a survival benefit in patients with glioblastoma. We know that only a subset of these tumors tends to truly benefit from the addition of chemotherapy. And it's not only the drug delivery, that's the challenge, it's also the tumor itself. So these tumors are somewhat heterogeneous. It's often several pathways that play a role activating these tumors. We've had -- it's not for lack of trying. There have been numerous clinical trials, including targeted drugs, including immunotherapies that have not provided additional meaningful benefit to our patients. So we have a lot to do. So other challenges include that other than cancers for which immunotherapy has been a promising new tool, and we -- so we hear about it all over the literature, all the media the response to these treatments has been so far disappointing. And this is in part, we believe, due to a different microenvironment that these tumors are embedded in an immunosuppressive microenvironment, also the fact that these tumors have considerably few abnormal mutations so that the immune system is not as attractive to these cancers as, for example, to some lung cancers or certain melanoma, bladder cancer, et cetera. And there is also the issue that we're dealing with rare cancers. Glioblastomas are the most common cancer in adults in terms of primary [ vehicles ]. However, compared to other diseases, we are dealing with a small number of patients. And so there is always a challenge for us to advocate for these cancers to be more represented in clinical trials -- in earlier phase clinical trials. And there is some, I would call it, annihilism on the side of investigators and industry and the cancer community saying that, well, these cancers are so stubborn, things haven't worked that well. And also, it's too much as difficult to treat. So that has limited the number of clinical trials we have. Limited eligibility for trials that otherwise might be really interesting to study new drugs. So -- so it's -- [Indiscernible] to clinical trials for cancers other than cancer of the central nervous system.

I thought that was excellent Matthias because you sort of covered the landscape both clinically some aspects of the cell biological physiologic challenges and then also the sort of social medical environment challenges of glioblastoma and other common primary brain malignancies. And I would just expand on a couple of points you raised, and that is with regard to the temozolomide. And so that really has been the most major advance in our treatment of glioblastoma. And then I have to qualify that because that advance really entered the mainstream in 2005. So we're talking about 17 years ago. And as also as Dr. Holdhoff pointed out, only about 35%, 40% or so of patients with glioblastoma are actually found to be sensitive to temozolomide due to a particular molecular feature of glioblastoma. And regardless of whether you're initially sensitive to temozolomide or not. These tumors invariably recur after receiving temozolomide. And those tumors are invariably no longer sensitive to temozolomide or other known chemotherapy agents. And at this point in time, we really have no proven therapy that is known to effectively treat recurrent glioblastoma.

Thank you, I'll move on to the next question, which is what knowledge from Genomics have we gained about GBM -- are any pathways amenable to being considered as druggable in GBM?

It's interesting that glioblastoma is one of the most well-characterized malignancies when it comes to the identification of driver mutations and that being mutated oncogenes and mutated tumor suppressor genes. And in light of that, one would think that there are targetable mutations and we've discovered them and they have been successful clinically. But that unfortunately has not been the case. In part because of blood-brain barrier issues that Dr. Holdhoff mentioned, the drugs that we know can effectively target mutations and systemic cancers don't adequately enter the brain and the brain tumor. And the other aspect is the heterogeneity of these tumors and that tumors can be characterized by being mutated, for instance, in a driver with receptor tyrosine kinase EGFR, and the very common mutation is an EGFR deletion and that gene is referred to as EGFRvIII, variant 3. But a subset of tumor cells in EGFRvIII mutated tumors actually express mutation and there have been treatment trials targeting this mutation using small molecules using immunotherapy. And one can deplete tumors of the cells with this mutation if the tumor occurs anyway. There are other receptor tyrosine kinases, that's -- that are mutated or amplified such as the platelet drive growth factor receptor, the c-MET receptor tyrosine kinase in addition to EGFRvIII. And these -- there are agents that potentially target all these drivers in GBM.

Could you comment on targeted therapy and precision medicine approaches impacting clinical outcomes in GBM?

Right. So this question does overlap what we've been discussing. But I think precision medicine has been effectively applied in certain circumstances to the care of our patients. And I think in glioblastoma, the most common use of molecular diagnostics that drives precision medicine is in the interpretation of MGMT gene methylation -- so MGMT, methylguanine methyltransferase, is routinely evaluated for whether it's expressed in glioblastoma. That is determined by an assay that looks at its gene promoter methylation. And if the promoter is methylated, the gene is silenced and the enzyme is not expressed, that enzyme reverses the effects of our best chemotherapy temozolomide. So finding that the gene is methylated predicts that patients' tumors will be sensitive to temozolomide. And that clearly translates to improved tumor response and improved patient survival. And so that assay is very, very important. And it's also being used in the -- in clinical trial designs that are intended to test other agents in substitution to temozolomide. More specifically, if the MGMT gene is not methylated, the gene is expressed. It predicts that patients' tumors will not be sensitive to temozolomide, then it justifies the elimination of temozolomide to -- from the clinical treatment regimen and substituting temozolomide with an agent that's under investigation.

I would like to add a couple of points that all sort of support what you just said. I think a lot of therapies we had so far were not very precise. So the treatment that's -- the treatment that builds the backbone for our current approach to glioblastomas consists of best possible surgery, followed by radiation and radiation, given to the area of the brain that's involved by tumor, not very specific therapy. You could argue that temozolomide an alkylating drug is also not very specific. So we're not as precise as we want to be. And these biomarkers, MGMT being one example and in context of the help might be the PTGR1 helps us really select patients that might benefit or have a higher likelihood to benefit from a given therapy.

How does LP-184, first of all, how does it work? And why is it so unique? And then how does LP-184 fit into areas of precision medicine for GBM?

Firstly, as I mentioned sometime earlier, LP-184 is a prodrug -- it needs to be activated by an oxidoreductase called PTGR1. PTGR1 is often expressed preferentially higher in many tumor cells. Thus, one property that LP-184 has is that this requirement for activation provides it with a window of tumor specificity. Once activated, the active metabolite of LP-184 goes on to damage DNA. It causes certain lesions in DNA that cannot be repaired by global genomic repair pathways and are dependent upon prepared by a transcription of coupled nucleotide exogen repair. What this means is that if the damage is not repaired, tumor cells will die. Often, tumor cells differ from normal cells because of certain mutations. And therefore, these tumor cells have vulnerabilities that are not present in normal cells. One aspect of this vulnerability is that they are inefficient in repairing the damage caused by LP-184, Thus, while normal cells will recover from this damage, tumor cells do not and therefore, LP-184 can preferentially kill give ourselves.

So that sort of covered some of that. There -- in addition to the oncogenic mutational predictors of sensitivity, there is bioinformatic gene expression data that predicts that LP-184 will be particularly active against tumor cells that are deficient in the transcription-coupled nucleotide excision repair mechanism. And about 30% or so of glioblastoma are -- have low expression of genes required for nucleotide excision repair. And the basis of this is strongly supported by the evidence that cells repair the DNA damage caused by LP-184 through nucleotides as a repair mechanism. And I would add, even in terms of very basic clinical translational aspect of LP-184, -- it is an alkylating agent. And so in that broadest class, it falls within the alkylating agents, which are temozolomide and [Indiscernible] however, LP-184 modified DNA at a different site than those other alkylating agents. So it primarily alkylates at M3 of ADME and that DNA modification is insensitive to the expression of MGMT. And as we've discussed earlier, MGMT expression is one of the major limitations of temozolomide efficacy. So tumors that are predicted to be insensitive to temozolomide due to MGMT expression, and that is approximately 70%, 60% to 70% of glioblastomas may be sensitive to LP-184 therapy.

Okay. Next question is, can you elaborate a little bit on the results from preclinical studies with LP-184 performed to date and their implications on clinical translation, clinical trial design, et cetera.

Yes. So we've worked with Lantern to evaluate LP-184 in what we consider to be state-of-the-art preclinical models, some models in vitro and tumors grown in brain, in animals, in mices in vivo. And so -- and we were excited about doing this based on data initially obtained by Lantern using the NCI-60 cell lines showing that the small number of traditional glioblastoma cell lines that exist in the NCI-60 panel were sensitive to LP-184. In particular, cells that are known to express MGMT and the insensitive temozolomide. And so we've evaluated LP-184 in a number of traditional human glioblastoma cell lines and in more modern models, such as patient-derived GBM neurosphere lines and patient-derived xenograft lines. And we're finding that many of the majority of the 10 to 15 or so models that have been looked -- [Indiscernible] have been looked at have IC50s, -- so inhibitory concentrations [Technical Difficulty] LP-184 in the range of -- certainly in the nanomolar range, which is quite low. And cells that were clearly insensitive to temozolomide, not achieving IC50s with temozolomide at concentrations of hundreds of micromolar have been sensitive to LP-184 in the 100, 200 nanomolar range. So that -- so that was exciting in vitro. And we've evaluated LP-184 in tumors grown in mice subcutaneously and in brain and found the drug to be extremely active in causing tumor regression in subcutaneous glioblastoma models, including lines derived from neurospheres and also traditional cell tumors derived from neurospheres and also traditional cell lines. And that LP-184 also prolonged animal survival in mice bearing preestablished tumors in brain. And so the confluence of this, I think, is quite promising in the potential for this drug to be effective in patients or certainly supports, in my view, the need to proceed with clinical testing of this drug.

Okay. We'll move on to the next question, which is how can LP-184 be leveraged to fill current treatment option voids as a targeted therapy option in select patient groups? Can you define those patient groups and the methods being considered to select them?

Yes, drugs such as this, which is -- which meets basic criteria in terms of preclinical efficacy, a good rationale for drug delivery, and matched with a great need for new drugs is something we take very seriously. And [Indiscernible] clinical trialist working in glioblastoma, I think this is quite an interesting drug to pursue. And they place a new potentially efficacious compound might have in treatment of glioblastomas is certainly quite open. So we do not have a lot of drugs that provide a true benefit. So if this was a drug that showed -- after showing tolerability, if it showed an efficacy signal in recurrent glioblastoma. It would be very tempting to try. So it would be very reasonable to try testing this drug. As an example, in newly diagnosed glioblastoma in combination with radiation in MGMT methylate or unmethylated tumors. Certainly, when early phase studies are done and the first FX trials in recurrent disease, such as within a Phase II prospective study, that would be also important to find out if there are correlative biomarkers that might predict a responsive treatment, what could be the role of MGMT methylation for this cancer where we use it as antitumoral agent in recurrent disease. And what about PTGR1 which is required to activate LP-184, which is a prodrug into its active form. So there are a lot of interesting important questions to answer.

I would just add to that. We just -- we commented earlier on the role for transcription-coupled, nucleotide excision repair as a mechanism for relative LP-184 resistance and conversely tumors that are deficient in expression of the genes that are required for transcription-coupled nucleotide excision repair would be predicted to be sensitive to LP-184. So in addition to PTGR1 expression as a possible predictive biomarker of LP-184 sensitivity component expression of transcription-coupled nucleotide excision paired genes might also be a predictor as well. And there are also agents as we think about how one might ultimately develop LP-184 clinically, there are well-tolerated drugs currently used for other indications that can deplete tumor cells of transcription-coupled nucleotide excision repair gene products and theoretically sensitize tumors to LP-184, so one could imagine once either incorporated into early clinical trials or later-stage clinical testing to consider combinatorial agents that sensitize tumors to LP-184 for these mechanisms.

Okay. I'll move on to the next question, which is what are the clinically relevant molecular or genetic subsets of GBM patients and how can we balance trial enrollment time lines with optimal representation from shrinking subsets of molecular subtype?

The challenge in clinical trial development is to balance the potential benefits of focusing on molecular subsets with practical aspects of successful enrollment over a reasonable period of time and also with the uncertainty, particularly in terms of a drug like this with regard to the ability of molecular subsets to predict drug sensitivity or resistance since this agent has the potential to be broadly effective though, albeit perhaps more effective in some subsets than others. So how do you walk that line when designing a clinical trial was commented on earlier, there's bioinformatics data that predicted an increased GBM sensitivity in tumors that have EGFR activating mutations that have PTEN/AKT mutations. And those mutations are relatively common in glioblastoma. And so certainly, one strategy, at least initially would be in a Phase II trial to power the trial with sufficient numbers of patients to retrospectively determine if there is -- if one of these molecular biomarkers actually associates with a response or not as opposed to preselecting patients with these mutations as part of clinical enrollment criteria. And personally, based on this drug, I feel that a better approach would be to not be selective at time of enrollment, ideally try to power the study higher enough to perform retrospective analysis. And then if there's a suggestion of a signal, then work with that in future trial design.

I would agree with you, John. And this is the drug we have a lot to learn about. The hope is that this drug will serve a broad population of patients that it will not just serve a niche of a certain molecular signature, but that it's considerably nonspecific or limited specific kind of drug along the lines of other treatments that have worked in the past. Starting the efficacy first, looking at subgroups, the second step might be the approach that would be the most fruitful for this drug. If there's a thing molecular marker that's associated with response, certainly, then one would also try to design more focused, more targeted clinical trials based on the biomarker. But we are hopeful that this drug, which does fulfill minimal criteria to make a to clinical trial in brain cancer and only a few drugs do it, we're hopeful that this drug gets the best possible chance to show us true colors and to us whether it can actually support -- whether it can actually be of potential impact for our patients.

Okay. How can LP-184 be used in combination with other agents in GBM, for which GBM setting, would it be most valuable to test a combination therapy approach.

Yes, this is an excellent question. And the way we study new compounds in the setting of glioblastoma is either looking for response signals in recurrent disease. And once we're getting into combinatorial questions, the question is are we thinking about combining with radiation or are we combining with other drugs. So an attractive way to study a possible added benefit to radiation is the population of MGMT promoter unmethylated tumors that overall do not benefit at least for the vast majority to the addition of temozolomide where you could study the safety of combining the drug with patients receiving radiation alone. And that has been an increasingly accepted way to study the combination of radiation and drugs in the newly diagnosed setting. Once that safety is established, you could consider adding broadening that approach and consider adding temozolomide certainly, there are other combinatory options, but that would be a relatively standard way to go about this a systematic way to introducing this drug into the current standard of care into the standard of care treatment framework in glioblastoma.

So I would agree with that, Matthias, and that was a great general discussion of chemotherapy drug development approaches -- and I would add that one, I think, potentially exciting aspect of LP-184 is the defining that deficiency and transcription-couple nucleotide excision repair sensitizes cells to LP-184. And we have preclinical laboratory data that if we pharmacologically deplete tumor cells and tumors in vivo of -- we deplete them of one key component of the transcription-coupled nucleotide excision repair mechanism, then we sensitize cells and tumors to LP-184. And we can do that with an FDA-approved drug that crosses the blood-brain barrier called spironolactone. Spironolactone is a drug that's been used for decades as a diuretic for patients. It's very well tolerated. And importantly, it does cross the blood-brain barrier. Separate from its diuretic mechanism, spironolactone was found to deplete cells of a transmission couple of nucleotide excision repair components, ERCC3 through protein degradation. And we have found that spironolactone can decrease the IC50, the LP-184 IC50 by 4 to fivefold in glioblastoma cells in vitro and treating animals that have glioblastoma tumor xenografts combining LP-184 with spironolactone appears to substantially improve the antitumor response. So one, I think, interesting and good challenge in how we think about clinical trial design for LP-184 is how and/or when we consider a combination strategy using an agent like spironolactone in the clinical trial.

Okay. Last question here. How has Lantern Pharma established a collaboration with neuro-oncology at Johns Hopkins? And what are the next steps in this effort?

When we are looking at collaborators to further develop the potential of LP-184 for glioblastoma, Dr. Laterra's lab and Johns Hopkins were a natural alignment. Dr. Laterra's lab has previously developed several studies in glioblastoma, and therefore, the lab has expertise in areas that would be very useful in this collaboration. This includes the development of neurospheres, intracranial, gemographs, so on and so forth. But as importantly, Dr. Laterra's lab has also conducted studies in various areas of glioblastoma that are essential for the understanding of how LP-184 could be developed further, including the studies on EGFR hyperactivation studies on MGMT, so on and so forth. Therefore, the natural alignment allowed us to approach Dr. Laterra and we had wonderful early discussions. And now we have had this active collaboration that has been very fruitful for the last 2 years. We are now on the path to defining a clinical protocol for the first in-human trial in glioblastoma in collaboration with Johns Hopkins with Dr. John Laterra.

My laboratory at John Hopkins and the Kennedy Krieger Institute has been now collaborating with the team at Lantern Pharma for a year or 1.5 years now. Again, focused on really asking the question does LP-184 fulfill the preclinical requirements that make it exciting enough to really invest the substantial resources to bring it to clinical trial, exciting enough that raises the promise of potentially improving the quality of life and survival of our patients with glioblastoma. And so this collaboration, sort of a standard laboratory pharma collaboration where Lantern Pharma and I had discussions about the key questions, and I proposed some research studies to answer those questions and Lantern Pharma has funded those experiments. We've now been in discussion with the clinical team to -- with regard to clinical trial opportunities in clinical trial [Indiscernible] and that's been done primarily through my clinical colleagues here at Johns Hopkins.

I think this is a really exciting example of how collaboration can become fruitful. Of course, a lot of drugs sort of strand early on, don't fulfill the minimum criteria to be developed. This drug fills the -- make the initial checkboxes for clinical trial involvement. And it's kind of a beautiful story if there's a drug that has been tested within our team members laboratory. And then there's a discussion about this drug. There's some excitement that is developing and then there are people on the clinical side that want to bring this to the bedside. And in many ways, the reason we all go into oncology is to bring new drugs, new compounds from the laboratory into clinic. And this might be one of these examples. And it happens to be a drug that was developed or codeveloped in one of our laboratories -- sometimes it's different. This is, I think, a collaboration that we're all very excited about. And there are many of us that will want to play a role one way or the other. And we have identified a principal investigator within our group, who will be the chef and a lot of us will be sous chefs. We will make -- try to make the best out of this really outstanding opportunity.

Okay. And with that, we'll start with some live Q&A here. We have Dr. Kishor Bhatia with us today to answer your questions. If you have a question, be sure to type it in and using the Q&A tool down below, and I will ask your question. We have some that have already come in here, Kishor, can LP-184 be of use in other brain cancers besides glioblastoma?

Yes. So one advantage with LP-184 is that it has very good activity in several other solid tumors as well. If you couple that efficiency of [Technical Difficulty]

Kishor, we're having a little bit of trouble hearing your audio at the moment.

Can you hear me now?

Yes, much better. Yes. So yes, LP-184 has activity against a variety of other solid tumors. That includes lung, brain, breast, colon cancer. And if you couple this with the ability of LP-184 to cross the blood-brain barrier, clearly, it has potential in the treatment of brain metastasis -- other brain metastases. Okay. Great. We have a few more coming in here. What challenges exist in applying LP-184 to the newly diagnosed glioblastoma setting?

So the standard of care for newly diagnosed glioblastoma is going to be temozolomide. And one aspect of using temozolomide, as we all heard is that it won't work in tumors that express MGMT. And over a period of time, temozolomide treatment will result in resistance due to MGMT expressing clones. So one area to consider which we are discussing further on is to understand if a combination of LP-184 and temozolomide in early tumors might solve this problem.

Okay. We have one additional question that I see coming through here. And some of this may have been answered already, but how does LP-184 compare with temozolomide in glioblastoma?

So both work in a similar fashion. Temozolomide, however, does not have a correlation with certain genomic features LP-184 is far more sensitive in tumors that either under express DNA repair genes or have activation of certain pathways. These are features that are commonly found in many glioblastomas. So in that sense, LP-184 has the ability to be more targeted to specific tumors and can be personalized in that sense. The other major difference is that the D&A region caused by Temozolomide and LP-184 defer considerably. And the N6, the end to adenine lesion cost by LP-184 is not a substrate for MGMT. And therefore, LP-184 is agnostic to MGMT expression.

Okay. And I just saw another one coming through here. Is there any opportunity for immunotherapies to be used with 184 in combination work?

Those are studies that are ongoing, and we don't have the answer as yet, but those as ongoing studies. Okay. Great. Those are all of the questions we have today. Thank you, everybody, for joining, and have a great rest of your day.