Onconova Therapeutics, Inc. (ONTX) CEO Steve Fruchtman on Q2 2022 Results – Earnings Call Transcript

Onconova Therapeutics, Inc. (NASDAQ:ONTX) Q2 2022 Earnings Conference Call August 11, 2022 4:30 PM ET

Company Participants

Bruce Mackle – Investor Relations, LifeSci Advisors

Steve Fruchtman – President & Chief Executive Officer

Mark Gelder – Chief Medical Officer

Mark Guerin – Chief Operating Officer & Chief Financial Officer

Conference Call Participants

Charles Zhu – Guggenheim

Chun Lung – Ladenburg

Robert LeBoyer – Noble Capital Markets

Operator

Ladies and gentlemen, thank you for standing by. Welcome to the Onconova Therapeutics Second Quarter 2022 Financial Results and Business Update Conference Call. At this time all participants are in listen only mode. Following management’s prepared remarks, we will hold a question-and-answer session. [Operator Instructions] As a reminder, this call is being recorded today, August 11, 2022.

At this time, I’d like to turn the call over to Bruce Mackle of LifeSci Advisors, please go ahead.

Bruce Mackle

Thank you, operator, and welcome everyone to Onconova’s second quarter 2022 financial results and business update conference call. Earlier this afternoon Onconova issued a press release reporting its financial results and business progress. If you have not yet seen this press release it is available in the Investors and Media section of the company’s website at www.onconova.com. Following my introduction Onconova’s President and CEO, Dr. Steve Fruchtman will provide an overview of the company’s recent highlights and future outlook, followed by Chief Medical Officer, Dr. Mark Gelder, who will discuss progress across Onconova’s pipeline. And lastly, Chief Operating Officer and Chief Financial Officer, Mark Guerin will report the company’s second quarter financial results. These prepared remarks will then be followed by a question-and-answer session.

Before turning the call over to Onconova’s management team, I’d like to remind everyone that statements made during this conference call will include forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995, which involve risks and uncertainties that can cause actual results to differ materially. Forward looking statements speak only as of the date they are made, as the underlying facts and circumstances may change, except as required by law Onconova disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances. For more information on forward looking statements, please review the disclaimer in today’s press release and the risk factors in the company’s SEC filings.

With that it is my pleasure to turn the call over to Steve.

Steve Fruchtman

Thank you, Bruce, and good afternoon to all our listeners today. This past quarter was an important period of execution for Onconova as we saw progress across our development pipeline. As we advance through the second half of the year, we remained focused internally on the advancement of our lead narazaciclib development program, which as a reminder, consists of two phase 1 alchemer solid tumor studies, designed primarily to evaluate the safety and tolerability of our orally available multi targeted kinase inhibitor. The two administration schemes being tested in these trials mirror those of currently approved CDK 4/6 inhibitors and we’ll identify the best recommended phase 2 dose and schedule of administration of narazaciclib going forward.

We have completed four dosing cohorts in both phase 1 studies, and the safety data continues to look very favorable to date, nurturing our robust preclinical data set. Key components of this preclinical data set were featured in an abstract recently published at the American Society of Clinical Oncology Annual Meeting. These data, which Dr. Mark Gelder will discuss in greater detail showing narazaciclib potently inhibits CDK 4/6 and other kinases implicated in tumor growth, cancer cell survival and metastasis, as well as the immunomodulatory activities. We believe this inhibitory profile may confer narazaciclib safety and efficacy advantages over currently available agents highlighting is best in class potential.

As you are aware, the CDK inhibitors are multibillion dollar franchises to address the need for patients with hormone receptor positive and two negative metastatic breast cancer. Looking forward for narazaciclib, we expect the continued advancement of its phase 1 trials to allow for the second selection of a recommended phase 2 dose, which we anticipate having before the end of this year. We continue to hone in on the indications and treatment regimens. We will pursue a major stage study and will be informed by the results of the phase 1 program throughout this process. To better enable these efforts, we recently amended the protocol of our phase 1 study to allow for the collection of pharmacodynamic data using the cutting edge, the victim assay. This assay is designed to measure thymidine kinase activity and marker cell proliferation that is believed to be predictive of CDK 4/6 inhibitory activity or target engagement. This approach of having a biomarker to determine target engagement rather than the classic phase 1 approach of observing clinical toxicity, and then pulling back to a previous and lower dose for future trials is a methodology that the FDA endorses, and Dr. Gelder will give us great details about this approach.

Though we of course need to finalize the specifics of all of our planned future trials before they are announced, I reiterate that we are interested in multiple indications for narazaciclib potential. These include hormone receptor positive head to negative breast cancer, that is refractory to the FDA approved drugs, multiple myeloma, macro cell lymphoma, and based on the mechanism of action of narazaciclib other potential indications as well. This interest is drawn from both preclinical work and depressing unmet need for improved options in these and additional indications.

Turning our attention now to Rigosertib. I’ll first emphasize that our strategy of utilizing investigator sponsored trials with key opinion leaders to pursue the development of Rigosertib has not changed. This enables us to dedicate our primary focus and resources to our lead narazaciclib programs. As you may recall, Rigosertib can attack cancers with several different mechanisms as it has the ability to modulate to mutate and overexpressed dress pathway, the PLK1 pathway and the tumor immune microenvironment. Our plan investigator sponsored trial in checkpoint inhibitor, refractory metastatic melanoma seeks to leverage Rigosertib role as an immune modulator. This trial, which were evaluated Rigosertib, in combination with the PD-1 checkpoint inhibitor, pembrolizumab builds upon published preclinical data presented at prominent meetings, such as the ACR, and journals that came out of the work at Vanderbilt University that showed Rigosertib promoting the infiltration of T cells into the tumor microenvironment.

Of course, PD-1 inhibitors work by stimulating the cancer killing activity of T cells. Increasing the number of T cells within tumors is expected to enhance the efficacy of these exciting agents. A key goal of the melanoma trial is to demonstrate the answer anti-cancer activity of the Rigosertib loser map combination in patients showing resistance to checkpoint blockade. This is similar to another ongoing investigative sponsored trial, which is evaluating Rigosertib, plus the PD-1 inhibitor nivolumab in KRAS mutated non-small cell lung cancer.

Preliminary data from this trial strongly support the hypothesis behind the scheme to open melanoma study. We look forward to the continued progress of both investigated sponsored studies evaluating Rigosertib with an anti PD-1 agent and anticipate reporting additional data from the KRAS mutated non-small cell lung cancer native this quarter, an abstract that has been submitted to the European Society of Medical Oncology, or ESMO. In addition to these two Rigosertib studies, we are also seeing extremely encouraging results in the investigator sponsored trial evaluating Rigosertib monotherapy in squamous cell carcinoma of the skin associated with the ultra-rare disease dystrophic epidermolysis bullosa or RDEB.

Initial single patient data from this trial showed a sustained complete response in this difficult to treat indication when the patient is still and the patient is still in complete remission today, and continuing on single agent Rigosertib for over one year. This importantly, provides clinical proof of concept for Rigosertib of ability to inhibit the PLK1 pathway, which is a crucial enzyme that is overspread overexpressing odd that associated squamous cell carcinoma, and other more prevalent squamous cell cancers, as well.

As mentioned on our last call, this result is driving conversations, leading clinicians and scientists interested in potentially pursuing additional investigator sponsored trials. This highlights how our collaborative strategy with Rigosertib allows us to increase our avenues for value creation and a capital efficient manner.

With that, I’ll pass the call off to Dr. Mark Gelder to speak more about our clinical programs. Mark?

Mark Gelder

Thank you, Steve. And welcome again to everyone who has joined us this afternoon. As usual, I’ll begin my portion of the earnings call by reviewing the status of our lead narazaciclib program, and its two complimentary phase 1 dose escalation study. These include a US trial, evaluating a continuous daily dosing schedule, and the trial in China, evaluating three weeks on one week off dosing schedule. Both studies are enrolling patients with advanced solid tumors. I am pleased to report this since our last earnings call, the US study has advanced from the fourth to the fifth dose escalation cohort, which is evaluating a 200-milligram oral dose of narazaciclib administered each day.

We have not observed any dose limiting toxicities, or clinically meaningful cases of neutropenia in the trial to date and continue to see anticipated on target effects of the study drug. We’ve remained highly encouraged by these data as a dose limiting factor and therefore tolerability issue of both ribociclib and palbociclib. The most widely prescribed CDK4/6 inhibitors is the bone marrow toxicity or myelosuppression associated with these edges.

This necessitates an interrupted dosing schedule with drugs given three out of every four weeks, so that the bone marrow can recover. If data from our US phase 1 study continues to mature favorbly, we would likely seek to move forward with a continuous daily dosing regimen for narazaciclib. This would clearly differentiate our therapeutic candidate and could potentially contribute to an improved efficacy profile as the one week off require for both palbociclib and ribociclib may permit tumor cell proliferation and therefore tumor growth.

To better inform our development we recently enacted a protocol of men in the US trial that will allow us to assess narazaciclib biological activity in all cohorts moving forward. We will do this using the DiviTum assay Steve referenced earlier, which is a clinically validated blood-based test measuring the presence of thymidine kinase-1. Thymidine kinase-1 or TK-1 is a well-known cell cycle regulated enzyme that is important for nucleotide metabolism during DNA synthesis. PK-1 catalyzes the conversion of thymidine to deoxy thymidine monophosphate, which is then further phosphorylated to die in triphosphates prior to its incorporation into DNA

The activity of TK-1 is very low or absent in resting cells and peaks in the S phase and then disappears during mitosis. Serum TK-1 activity is elevated in cancer patients compared with healthy individuals, and it has been referred to as a liquid AI-67. Prior clinical trials have shown that thymidine kinase-1 or TK-1 activity accurately reflects the biological effects of CDK 4/6 inhibitors. Incorporating assessments of TK-1 into our Phase 1 program is therefore expected to provide valuable data that will enable us to move towards later stage studies with a more thorough understanding of narazaciclib’s maximal, biologically effective dose, and the optimal dose for achieving its maximal pharmacological effect. This will allow us to further de risk narazaciclib’s clinical development, and is clearly in line with the FDA project optimists initiative, which focuses on improving the dose finding and dose optimization paradigm in oncology.

In parallel with our efforts in the United States, our partner HanX biopharmaceuticals continue to advance the phase 1 trial of narazaciclib in China. This study is currently in its fifth dose escalation cohort, which is evaluating 200 milligrams of oral narazaciclib administered each day with three weeks on one week off dosing skeptic. As mentioned on our last earnings call, HanX is working on a protocol amendment to allow for further dose escalation in the study, given the favorable safety data for the Phase 1 program that has been generated to date. Continued progress in the narazaciclib’s phase 1 trials is expected to allow for the identification of a recommended phase 2 dose in the near future, perhaps before the end of the year. Once identified, we plan to utilize this dose in plan later stage studies. As we’ve stated consistently in the past, these trials will include a phase 2 multi-indication basket trial designed to evaluate narazaciclib alone or in combination with other anti-cancer agents.

To expand on a point that Steve made early one indication that we intend to evaluate in our plan’s basket trial is CDK4/6 refractory hormone receptor positive, HER2-negative metastatic breast cancer. Those CDK 4/6 inhibitors are currently approved and generate billions of dollars in annual sales in this indication, virtually all of these patients eventually developers. This leaves a pressing unmet need, we believe narazaciclib can address. We also plan to study narazaciclib indications were CDK 4/6 inhibitors are not approved, both as part of the basket trial and in additional preclinical studies.

Our plans to develop narazaciclib across multiple indications are supported by a robust preclinical data set, which includes data published this past May at the American Society of Clinical Oncology or ASCO Annual Meeting. These data which come from cell base, and in vitro assays, highlight the narazaciclib differentiated inhibitory profile. In cell-based assays narazaciclib demonstrated potent inhibitory activity against ARK-5 and CSF-1 receptor to kinases that are not targeted by any of the three approved CDK for six inhibitors. We believe this finding is significant as inhibition of CSF-1R leads to the activation of anti-cancer immunity, while ARK-5 plays important roles in cancer cells survival in hypoxic environments, as well as metastasis.

The preclinical studies featured at ASCO also compared the narazaciclib to abemaciclib which is the third approved CDK 4/6 inhibitor unlike palbociclib and ribociclib massage is administered on a daily dosing schedule, as neutropenia is not its primary dose limiting toxicity. For abemaciclib, diarrhea is the primary DLT due to its affinity for the kinase GSK, GSK-3 beta. Narazaciclib’s inhibitory activity against GSK-3 beta was found to be approximately 29 times less than that of abemaciclib indicating that it may be i.e., narazaciclib, it may be able to administer at higher, more effective doses before causing any problems with diarrhea.

As I’ve said before, today, we have not seen any dose limiting toxicities in our phase 1 dose escalation trial here in the US, and I can tell you that in terms of adverse events, we have not seen any high-grade diarrhea. Collectively, the results of Onconova disaster suggests narazaciclib inhibitory profile may provide safety and efficacy advantages over currently approved CDK 4/6 inhibitors and complement data discussed on prior earnings calls. These include mirroring data showing the narazaciclib causing less bone marrow toxicity compared to palbociclib. And in vitro data, showing the narazaciclib suppressing the growth of cancer cell lines that are resistant to palbociclib, including those lacking the retinal blastoma or RBG.

Looking ahead, we are eager to continue our work aimed at translating our promising preclinical findings to patients. We believe in narazaciclib has the potential to significantly improve the therapeutic paradigm of several prevalent cancers and look forward to outlining the specifics of our future clinical plans once final.

Moving on, I’d like to briefly discuss progress in Rigosertib investigator sponsored program. I’ll focus exclusively I mean, I’m going to study and the upcoming melanoma study. As Steve has already provided an update on RDEB associated squamous cell carcinoma trial. The first study I mentioned stay is the ongoing phase 1/2a trial evaluating Rigosertib plus the PD-1 inhibitor nivolumab in KRAS mutated non-small cell lung cancer patients. Like the melanoma study, this trial exclusively enrolled patients who have failed prior checkpoint inhibitor therapy. A preliminary readout from the study provided encouraging evidence of Rigosertib’s ability to overcome checkpoint inhibitor resistance, as we observed two partial responses and one instance of stable disease in seven viable patients.

As the mechanism of action Rigosertib predicts just since MOA is not dependent on any one specific mutation Rigosertib responses we’re seeing a problem multiple KRAS mutation variants, which differentiate Rigosertib from agents exclusively focused on patients with specific KRAS mutations, such as G clubs. We view this preliminary data read out as highly encouraging, as it supports our efforts, both in this trial and the melanoma study, given the similarities between the study combinations, and patient populations. Looking forward to additional data from the non-small cell lung cancer trial, we expect to report an updated data via an abstract submitted to the 2022 ESMO meeting, which will take place in Paris, France, in September 2022.

Our goal with this data revamp is to seek further evidence of the study doublets anti-cancer activity and favorable safety profile in this indication. A key point to note about the ongoing KRAS mutated, non-small cell lung cancer trial is that we have yet to reach the maximum tolerated dose of radiotherapy for the combination with the Mepolizumab. Therefore, we may have the opportunity to potentially study increased doses of radiotherapy combined with Mepolizumab that in a future trial in this indication, which remains under considering.

Ultimately, a decision on this front will be based on the final data from the ongoing trial, as well as conversations with experts and key opinion leaders in the field. The second investigator sponsored study out of Scott This is our plan phase 2 trial of radiotherapy plus the PD-1 checkpoint inhibitor, pembrolizumab in patients with checkpoint blockade refractory metastatic melanoma. This trial is supported, as Steve mentioned by the preclinical data and Richmond’s group at Vanderbilt University. The trial seeks to address a key gap in metastatic melanoma current therapeutic paradigm, as roughly half of these patients lack an effective treatment option after progressing checkpoint inhibitors.

Primary our acquired resistance to PD-1 inhibition is no more to occur in 40% to 60% of patients with metastatic melanoma, leaving many in urgent need of a novel therapeutic approach.

Turning now to the KRAS design. It will be a single arm to safe study, with stage one expected to include approximately 10 patients. If pre specified response criteria are met, the study will be cleared proceed stage two where we expect to enroll an additional 19 patients. The trials treatment regimen will consist of Rigosertib 500 milligrams orally administered twice daily, on days 1 to 21 of a 28-week day treatment cycle, plus the Health Authority approved dose of pembrolizumab 400 milligrams administered intravenously every six weeks. The primary endpoint of the study is overall response rate. While key secondary endpoints include progression free survival, overall survival, as well as safety and tolerability assessment. We also intend to collect pre and post treatment biomarker data to better understand Rigosertib effects on the tumor immune microenvironment. While it’s too early to know when we can expect some early interim data from the study, we look forward to providing that guidance in the future as this trial progresses.

With that, I would like to introduce our Chief Operating and Chief Financial Officer, Mark Guerin to report our second quarter financial results. Mark?

Mark Guerin

Thank you, Mark. It’s my pleasure to be speaking on the call today. I’m happy to report that Onconova maintain its strong financial position over the last quarter with cash and cash equivalents of $46.5 million as of June 30, 2022. This compares to $55.1 million as of December 31, 2021. Based on our current projections, we believe our current cash position will be sufficient to fund our ongoing clinical trials and business operations, including the pursuit of corporate development opportunities for more than 18 months. This runway is expected to enable the completion of key value trading milestones across our pipeline. Our research and development expenses for the second quarter of 2022 were $2 million, compared to $1.9 million for the second quarter of 2021. General and Administrative expenses for the second quarter of 2022 were $2.1 million, compared with $2.9 million for the second quarter of 2021. We reported a net loss for the second quarter of 2022 of $4 million or $0.19 per share on $20.9 million weighted average shares outstanding. This compares with the net loss for the second quarter of 2021 of $4.2 million or $0.27 per share on $15.8 million weighted average shares outstanding.

With my financial view complete, I will now hand the call off to Steve to summarize our anticipated milestone before transitioning to question-and-answer.

Steve Fruchtman

Thank you, Mark. Before running through our upcoming milestones, I’d like to congratulate both Mark and our Head of Corporate Development, Dr. Adar Makovski-Silverstein on their recent and very well-deserved promotions. They each have transition into their expanded roles seamlessly. And I look forward to our continued working together.

Turning now to anticipated milestones, we expect to identifying the Rigosertib optimal phase 2 dose the second half of the year. This will inform the design of subsequent studies, including a phase 2 basket trial in multiple indications and doubles. With regards to Rigosertib, we plan to announce additional data in the phase 1/2 KRAS mutated my small cell lung cancer trial via an abstract submitted to the upcoming ESMO meeting in September. Alongside our interactive narazaciclib Rigosertib programs, we continue to evaluate visits develop opportunities that could potentially expand our pipeline. Our guiding principles in this area have not changed. As we are making assessments based on scientific merit, and the size of the unmet need each potential candidate seeks to address. Many companies we interact with are having problems in the current financial climate, to have adequate resources to develop their own new molecular entities.

Based on the financial assessment Mark shared with you, we are confident we have the required financial resources to continue our important work to develop efficacious and safe drugs for patients in need.

With that I’d like to conclude the formal portion of today’s call, by thanking all those who played a role in the progress we have discussed today. This includes Onconova’s employees, collaborators, investigators, and most important of all the brave clinical trial patients.

I’ll now open the call for questions. Operator?

Question-and-Answer Session

Operator

[Operator Instructions] One moment please for our first question. And we’ll take our first question from the line of Charles Zhu was Guggenheim Securities. Please go ahead. Your line is now open.

Charles Zhu

Hey, good afternoon, everyone. And thanks for taking my questions have given us sounds like you’re on track to identify a potential recommended phase 2 dose for narazaciclib as early as the end of this year, and also looks like you’re enrolling dose cohort five for both of the phase 1 study should we interpret that as potentially dose cohorts six to seven as being likely maximum tolerated doses. Thanks.

Steve Fruchtman

Mark, would you like to answer that, thank you.

Mark Gelder

So thank you, Steve. And , as I said so far to date through cohort four, we have not seen any dose limiting toxicity through DLT. We are beginning to see some anticipated expected on target activities. We have incorporated the DiviTum assay into the into the phase 1 study so that we have a good PD-1 mark. With all of that said, I have no idea at what point we might reach our quote unquote dose limiting toxicity or MTD, maximal tolerated dose.

What I do know is that of we will continue to dose escalate until we do reach the maximum tolerated dose or a dose at which, based on the PD-1 marker, we have clear evidence of maximal biological effect whether that’s this dose cohort, i.e., the fifth, whether that’s the sixth or the seventh, I have no way of predicting, but based on the quote unquote, on target activity, we are beginning to see. I think that we probably are getting reasonably close. But what exactly that will be what those said exactly will be and exactly when we’ll get there, I can’t say I am very hopeful it’s before the end of the year, because we have some other studies that we would like to start moving forward.

Steve Fruchtman

Yes. Great, thanks for taking that…

Charles Zhu

Thank you, Mark.

Operator

Our next question from the line of Chun Lung with Ladenburg Thalmann. Please go ahead, your line is now open.

Chun Lung

Hello, thank you for taking my question. And this is Lung Chun on for Ahu Demir. My question is just Mark talk about a future of phase 2 basket trial. If possible, could you please give us more color on the communist plan on or other stock clip and you plan to combine with other drugs and other education besides breast cancer or any specific marker to use? Thanks

Steve Fruchtman

Mark?

Mark Gelder

So, all I can say for certain at this point is that we are putting together a panel a slate of stuff studies that we are very interested in moving forward with the some of them are single agent narazaciclib, others are narazaciclib in combination with other anti-cancer therapies. What I can say is that in the breast cancer space, if you look at the three approved CDK 4/6 inhibitors most all of their approvals are in combination with an anti- estrogen whether that’s an aromatase inhibitors such as Letrozole or Palbociclib, etcetera.

As we’ve said, we are clearly going to move forward in the CDK 4/6 refractory hormone receptor positive HER2 negative metastatic breast cancer space, that will likely be in combination with an anti-estrogen. The exact final decisions on the design of that trial have not yet been made. But we’re 99.9% of the way there. We have a trial designed in mantle cell lymphoma, as we’ve talked about, again, that has not been absolutely finalized. So I don’t want to say much more about that. And, we’re looking at some other trials. So until we get absolutely final, cemented in written in stone trial designs with various combinations. I hate to say anything about it publicly. But that’s really all I can say. Steve, you may or may not say anything more.

Steve Fruchtman

Well, thank you, Mark. I think you’re comprehensive are clearly that these drugs are approved in metastatic breast cancer. As Mark mentioned, eventually, all patients who will come refractory based on a mechanism of action presented at ASCO we believe we have and we have shown you evidence as well cancer cell breast cancer that we are active in situations with palbociclib is not to clearly refractory breast cancer population is a major interest. We also have data in mantle cell suggestive data in myeloma pre clinically. So we have a number of indications we can study. As Mark mentioned some of the combinations with an anti-estrogens clearly, some of the indications additional may include checkpoint inhibitors, BTK inhibitors and thinking about mantle cell. So we have a number of possible studies, we believe that as a psychic, to bring benefit to patients, I need to show that in the phase 2 bucket trials and plan to initiate as soon as we know the recommended phase 2 does.

Chun Lung

That’s great. Thank you so much.

Steve Fruchtman

Thank you.

Operator

[Operator Instructions] We’ll take our next question from the line of Robert LeBoyer with Nobel Capital Markets, please go ahead. Your line is now open.

Robert LeBoyer

Good afternoon. I just want a little clarification on something that that you touched on a little earlier. And with the mesocycle of trial, I understand that you’re the cohorts thus far are looking very good with no dose limiting toxicity, and you’re enrolling more cohorts? Is there any timeframe? You kind of touched on the idea of year end? But in terms of the next cohorts do you have any expectation of you have more guidance on when phase 2 would start?

Steve Fruchtman

So I’ll take that to give Mark Gelder. And we can’t predict when phase 2 will start until we know the recommended phase 2 dose reason, we’re suggesting we may know the recommended phase 2 just before the end of the year, even though we’re not seeing as above highlighted the US study. And he does seven toxicities, we are beginning to see engagement of our targets. As you know the CDK 4/6 inhibitors targets the push rapidly proliferating cell population in our body and that’s the bone marrow. We are seeing some decrease in the white gap and the patients treated in the current cohort with narazaciclib that anything that approaches a serious adverse event. Since we are engaging the target in the marrow, we know we have an active drug the whitecaps have gotten to know up.

And as we continue to dose escalate, we may see more of that. But it is hard to predict exactly when the white couch or some other toxicity will be observed severe enough to call that we have reached the dose limiting toxicity need to pull back. But pharmacodynamic marker and as Mark describe in depth also help us to determine the optimal phase 2 dose. So it is hard to forget, we did try to give some guidance where we suspect perhaps by the end of this year, we will be able to know the recommended phase 2 dose. And once we do that, we will rapidly move on to what we really want to do, which is open the bucket trials for the various indications that we described.

Robert LeBoyer

Okay, great. Thank you very much.

Steve Fruchtman

Thank you, Robert.

Operator

There are showing no further questions in the queue. At this time, I’d like to turn the conference back to the speakers for any closing remarks.

Steve Fruchtman

Thank you, operator, and thanks again to all for listening and for your insightful questions. We have enjoyed updating you on our recent progress. We continue to look forward to making even more progress. And we wish everyone a very lovely evening and thank you again.

Operator

Ladies and gentlemen, thank you for your participation on today’s conference call. This concludes today’s event. You may now disconnect.

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