Greeting and welcome to the Cue Biopharma First Quarter 2020 Earnings Call. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. [Operator instructions] As a reminder this conference is being recorded. It is now my pleasure to introduce your host Ashley Robinson, Investor Relations.

Thank you. You may now begin..

Thank you, Dough and good afternoon everyone. This is Ashley from LifiSci Advisors and thank you for joining us on today's investor and analyst update call. Joining me on the call today is Dan Passeri, Cue Biopharma's CEO; Dr. Anish Suri, President and Chief Scientific Officer; Dr.

Ken Pienta, Acting Chief Medical Officer and Kerri-Ann Millar, Vice President of Finance and Principal Financial and Accounting Officer. Before we begin, I'd like to remind you that during today's call the company will be making forward-looking statements.

Various remarks that the company makes during this call about the company's future expectations, plans and prospects constitute forward-looking statements for purposes of the Private Securities Litigation Reform Act of 1995.

Actual results may vary materially from those indicated by these forward-looking statements as a result of various important factors including those discussed in the Risk Factor section of the company's annual Form 10-K report filed with the SEC on March 12, 2020 and quarterly report on Form 10-Q filed with the SEC on May 7, 2020 as well as other filings made by the company to the SEC from time to time, which can be accessed on the EDGAR database at www.sec.gov.

In addition, any forward-looking statements represent the company's views only as of today, May 19, 2020 and should not be relied upon as representing the company's views as of any subsequent date.

While the company may elect to update these forward-looking statements at some future point, the company specifically disclaims any obligation to do so even if the company's views change. These forward-looking statements should not be relied upon as representing the company's views as of any date subsequent to today.

Please be advised that today's call is being recorded and webcast. I'd now like to turn the call over to Cue Biopharma's CEO, Dan Passeri.

Dan?.

Yeah. Thanks Ashley and good afternoon everyone and thank you for joining us today for a review of our ongoing progress and first quarter financial results which are available in more detail in our form 10-Q, which was filed with the SEC on May 7.

As a reminder, the slides we're presenting today, as well as a recording of our call will be available on our website for the next 90 days. Also, as a reminder, those of you listening in, you can advance the slides from your computer and we'll notify you and what slide we're addressing at that time.

We will also be available via the email provided on our website for questions that may not be addressed during today's call and you may want to ask subsequently. Beginning with Slide 3, which shows our agenda for today's call, I'll provide a brief overview and update of our pipeline, with an emphasis on our lead program CUE-101.

And that will be followed by Dr. Ken Pienta, our acting Chief Medical Officer, who will provide further details on our most recent observations from our ongoing Phase I CUE-101 mono-therapy dose-escalation and expansion study. Following Dr. Pienta's update, Dr.

Anish Suri, our President and Chief Scientific Officer will further describe our continued innovation and additional progress that we've made in advancing our Immuno-STAT and Neo-STAT platforms. He'll underscore how our rationally engineered IL-2 based CUE-100 series is differentiated.

And finally highlight the rest of our expanding pipeline that now includes CUE-102, KRAS, Neo-STAT as well as the CUE-200 and CUE-300 programs, the latter being in a collaborative partnership with Merck.

Our progress with all of these programs demonstrates focused execution towards platform validation, especially through the ongoing Phase I trial with CUE-101 and for the pipeline and platform developments. Following Anish's update, Kerri-Ann Millar, Cue Biopharma's Principal Financial and Accounting Officer will review our current financial status.

And I'll then provide concluding remarks followed by a Q&A session. To begin, I'd like to thank our dedicated employees for their focus and consummate professionalism in diligently working under these challenging and stressful conditions from the COVID-19 pandemic.

Through their efforts, we have been able to keep our lead drug candidate CUE-101 on track in our first inhuman mono-therapy dose-escalation Phase I trial in HPV positive head and neck cancer. Now moving on to Slide 4, which shows an overview of our core strategic objectives and progress in the first quarter.

In summary, our core objectives have been to one, validate our Immuno-STAT platform through the ongoing generation of data from our CUE-101 clinical dose-escalation study; two, expand our pipeline by selecting additional epitopes with the CUE-100 series and developing other disease applications including autoimmune diseases.

That's for the CUE-300 series and three, to accelerate and enhance our productivity through further development of our Neo-STAT platform.

To date, we have dose-escalated through the first four cohorts and continue to generate translational data and corresponding clinical data essential in providing proof of concept of our IL-2 based CUE-100 series of Immuno-STAT.

And as a reminder, CUE-101 represents the first of what we believe will become a broad set of biologic drug candidates from the CUE-100 series, targeting tumor associated antigens linked to a variety of cancers.

To this point, our near term goal is to de-risk 101 by demonstrating safety, tolerability and clinical activity which will thereby reduce the risk profile associated with the CUE-100 series per se, as well as our follow on CUE-200 and 300 series of biologics.

As a reminder, we have also been developing our Neo-STAT platform to significantly enhance our productivities and provide cost efficiencies to fully exploit the potential de-risking and validation of the Immune-STAT platform, which we are in the process of generating data to demonstrate that.

Anish is going to elaborate upon NEO-STAT later on in the call.

Importantly, in the ongoing CUE-101 Phase I clinical dose-escalation study, favorable characteristics and drug properties including dose proportional PK, early signs of relevant PD activity and growing evidence supporting that the drug appears to be clinically active, have emerged to date from our first three cohorts.

I want to emphasize that we are conducting the dose-escalation study of CUE-101 in a mono-therapy trial in second-line and beyond resistant metastatic HPV positive head and neck cancer patients.

In this highly challenging setting, while still quite early in our clinical study of the drug, we have observed data supporting an apparent increase in the levels of HPV reactive effective T cells and the peripheral circulation in several patients. Moreover, we have observed preliminary evidence of single agent clinical activity of CUE-101.

As we continue to build data with the objective of demonstrating single agent activity in this challenging patient population, it is our hope that we may be able to define a clinical and regulatory path forward for mono-therapy providing benefit to patients who currently have no effective alternative.

Taken together, we interpret these highly encouraging albeit early results as evidence supporting the prospects of CUE-101 single agent activity that needs to be further confirmed in additional patience.

We also recently announced the establishment of a clinical collaboration agreement with Merck for a combination study with KEYTRUDA, which is an anti-PD-1 biologic agent, as a first-line therapy in patients with advanced HPV16 positive head and neck cancer, and a planned dose-escalation Phase I study to be called KEYNOTE-A78.

This collaboration allows us to expand our patient coverage by moving CUE-101 upstream into the first-line therapy where KEYTRUDA is approved as a standard of care.

The rationale of a combined CUE-101 with an anti-PD-1 agent is based on our robust preclinical data which demonstrated that our promising mono-therapy activity with CUE-101 was further enhanced when combined with an anti-PD-1 agent.

The progress we've made in the clinic to date with CUE-101 with early emerging mono-therapy data gives us bolstered confidence in moving forward with our current ongoing mono-therapy trial, as well as the planned Phase-I trial in combination with KEYTRUDA that has the potential of expanding the application of CUE-101 into the frontline therapy setting for recurrent or metastatic HPV16 positive head and neck cancer patients.

Additionally, we continue to make solid progress on the development of our pipeline of drug candidates advancing through the modularity of the platform with CUE-102 targeting WT-1 or Wilms' Tumor-1 and CUE-103, which is presently being reviewed with our Asia partner LG Chem.

We also have generated supportive preclinical data for our KRAS CUE-100 drug candidate, and Anish will follow Ken's 101 update with a review of the progress made in these various programs, as well as an overview of the core competitive features of our platform to remind everyone, and for those of you who are first listening in.

Ken will now provide further details regarding the progress of our clinical development for CUE-101, which is our first clinical drug candidate. I'll now turn the call over to Ken.

Ken?.

Thanks Dan and good afternoon, everyone. I'd like to first remind you about the tremendous commitment we have from the participating clinical centers and associates and oncologists, shown here on Slide 5.

Throughout the COVID-19 pandemic this group of highly respected and dedicated oncologists have remained focused upon screening and enrolling HPV16 positive head and neck cancer patients to participate in our study.

Our investigators enthusiasm for the CUE-101program reflected that and the fact that today we've been very successful in our pre screening process to determine eligibility for the trial.

Recognizing that current therapies are not or rarely curative, we put into place a system whereby patients on first-line or second-line therapy for HPV driven head and neck cancer are pre-screened by HLA type and confirmatory HPV status to determine eligibility for future cue-101 therapy.

The demonstrated demand of patients for pre-screening underscores the significant unmet medical need in this indication. Next, on Slide 6, we show a high level summary of the design for our ongoing Phase I trial of CUE-101.

As Dan mentioned, we're very pleased with our progress of dosing patients in this trial and are highly encouraged by observations to date. As a reminder, we are enrolling post first-line patients with recurrent or metastatic squamous cell carcinoma driven by HPV, specifically HPV16.

This represents approximately 70% of all head and neck cancers occurring in the oropharyngeal region, accounting for an estimated 13,500 patients annually in the US alone. This Phase I trial is to find molecular inclusion criteria to include head and neck cancer patients that are HLA 0201 positive and whose tumors are confirmed to be driven by HPV16.

Through these specific inclusion criteria, we are ensuring that only patients with the potential for clinical benefits are enrolled and treated really a translational precision medicine approach whereby each of our Immuno-STAT drug candidates is intended for patients with a specific molecular fingerprint.

This trial is designed to provide insights into safety, mechanistic activity and potential anti-tumor efficacy. The trial is a standard two part study with the first Part A designed as a typical three plus three mono-therapy dose-escalation trial; patients receive CUE-101 and once every three weeks via IV infusion.

However, we've also provided the opportunity to dose up to nine patients in any given cohort, where we see evidence of clinical activity or PD effect. This strategy allows us to further explore PK/PD effects, as well as build supporting data for determining the most appropriate dose for the part B expansion.

Based on the safety PD and efficacy data from the dose-escalation part we will secure additional patients at that dose level during the Part B expansion phase to confirm the recommended Phase II dose in a total of 20 patients.

Therefore, in summary, both Parts A and B of the trial will evaluate the safety and tolerability of CUE-101 with biologic activity and anti-tumor responses also being followed.

The expansion cohort is designed to confirm the safety biologic activity and anti-tumor activity at the effective dose in additional patients to provide further support and confidence as we move into the later phases with more patients.

To evaluate on target activity, we're measuring several translational biomarkers including T cell expansion in peripheral blood and measuring cytokine production by antigen specific T cells. For anti-tumor activity, we're looking for objective responses by resist criteria at six week intervals or after every two cycles of CUE-101.

I'm very pleased to report that after initiating dosing of cohort one and late September last year, we successfully move forward to cohort two in December and cohort three in March. And we've now enrolled three patients in cohort four during the first two weeks of May.

Again, to reiterate an earlier comments, the fact that we continue on schedule and made such good progress, despite the COVID-19 pandemic, which has shut down multiple clinical trials that are now closed to accrual, we view this as an important metric of the commitment of our clinical collaborators and the enthusiasm they have for our approach to potentially provide clinical benefit to their patients in need.

As a reminder, our preclinical modeling led us to initiate dosing with cohort one and what we believe is a low biologically active dose and then a biologically and clinically active dose maybe achieved starting cohorts three or four. Shown in Slide 7 are the dosing groups for our patient cohorts.

We initiated the trial at 0.06 mg/kg with a threefold expansion up to cohort three, and then a two fold increase for subsequent cohorts. As noted on this slide, we compared the absolute dose by mass as well as molar content of IL-2 to the approved dose of Proleukin which is 0.037 mg/kg.

Proleukin is the wild type IL-2 a molecule generally known as aldesleukin. In the second cohort on a molar basis, we were already above the approved dose of Proleukin and by the 34th cohort we are approximately four to eight fold in molar access.

Today, the 12 patients in cohort one through four have received a total of 31 infusions of CUE-101, three weeks apart with what appears to be an attractive safety profile with limited toxicity.

One patient in cohort four at the one mg/kg dose, having infusion reaction that resolved quickly and we call that we have shown that this dose is about eight fold higher in terms of administered IL-2 than the IL-2 delivered by an approved dose of Proleukin. With this data, we are confident that we can deliver high doses of IL-2 on target safely.

We continue to be highly encouraged by our early progress in observations, including early evidence suggesting biologic activity. We have observed preliminary signs of T cell expansion and activation in our initial PK/PD results that we plan on confirming and extending in future analyses coupled with clinical evaluations.

Importantly, we have now observed early signs of biologic and clinical activity. In cohort one a patient inadvertently received five times the prescribed dose or a CUE-101 dose between the doses intended for cohort two and three.

This patients demonstrated early signs of T cell expansion as well as tumor regression on scan after receiving this dose, but also developed worsening of a pre-existing bullous pemphigoid rash. CUE-101 was discontinued but the patient remained was stable disease off therapy for several months before eventually progressing.

One patient in cohort two demonstrated early signs of T cell expansion and had stable diseases at first scan but did not sustain a continued response. Another patient from cohort two has confirmed stable disease with tumor regression of the target lesion.

This heavily pretreated patient progressed well on therapy with a checkpoint inhibitor continues on study. Also a patient in cohort three has demonstrated activation and expansion of T cells and remains on study.

We note that we are still in the dose-escalation stage of our Phase I trial and continue to monitor the five patients we're continuing to treat. We will provide further details as they become available over the course of the study.

Based on the totality of these metrics, we will continue to evaluate report on the emerging data as we prepare to advance to the dose-expansion Part B of the current study.

In addition to the ongoing immunotherapy trial of CUE-101 and HPV positive head and neck cancer, we show in Slide 8 our collaboration with Merck to initiate and have submitted to the FDA, a concurrent study to evaluate CUE-101 in combination with pembrolizumab or KEYTRUDA as frontline therapy for the same indication in patients who are also HLA 0201 positive.

Our intention is to continue moving forward with the mono-therapy trial for second-line or later HPV positive refractory metastatic, head and neck cancer patients and the cancer patient reach by moving into frontline patients in combination with KEYTRUDA, which is the current standard of care.

In this trial referred to his KEYNOTE-A78, we intend to translate our preclinical findings demonstrating a highly significant synergistic anti-tumor activity with CUE-101 combined with an anti -PD-1 antibody.

These data along with the Q CUE-101 mono-therapy activity in the preclinical tumor model were recently published in a manuscript in clinical Cancer Research last month. We intend to convince this trial in the second half of this year, once we've confirmed the safety of CUE-101 in the Phase I trial.

Furthermore, Slide 8 also shows that we have the option of evaluating CUE-101 in the Neoadjuvant setting in patients newly diagnosed with localized head and neck cancer.

And finally, once we have established clinical proof of concept for CUE-101 head and neck squamous cell carcinoma, we may expand opportunistically into other HPV driven cancers, for example, cervical and anal cancers. I will now hand the call over to Anish to discuss other advances in our pipeline and platform.

Anish?.

Thanks Ken and thank you to everyone listening in. I hope all of you and your families are safe and well through these times. I'd like to remind everyone of the scientific version that has underscored our focus and efforts from the very start.

A vision that was centered on a singular all important question which is how does one take advantage of the selectivity and specificity of the immune response while not breaching patient safety.

We believe our Immuno-STAT framework as exemplified by the CUE-100 series, as shown in Slide 9, of which Cue-101 is representative is a rational solution anchored on sophisticated protein engineering. From an elegant perspective, the best map of the landscape is the landscape itself.

To that end, the landscape of T cell modulation and cancer immunotherapy can involve many elements. However, the key fundamental signals for specificity coupled with controlled activation are what ultimately govern the outcome of the immune reaction. These very core elements are incorporated into the molecular framework of the CUE-100 series.

The two key signals on the 100 series as shown in Slide 9 consist of stabilized peptide HLA molecules to engage the tumor specific T cells via the T cell receptor, thereby locking in the specificity combined with rationally engineered IL-2 molecules that selectively act upon those T cells to control their activation.

We believe this control mechanism is an obligatory prerequisite for T cells and cancer immunity.

In other words, an absence of the appropriate anti-tumor T cell repertoire the application of a T cell modulating approach via a singular cytokine therapy like IL-2 or its variants, or antibodies targeting checkpoint molecules is likely going to be suboptimal or futile endeavor.

From the earliest approval of Proleukin and IL-2 has been a validated target for T cell activation. The challenge for broad application of Il-2 has pertained to safety liabilities, due to cytokine release and vascular leakage and indiscriminate activation of immune cells in broad T cell subsets, including regulatory T cells, or Treg.

We evaluated the incorporation of IL-2 in the CUE-100 series guided by structure based rational protein engineering solutions. From the very beginning, we sought to achieve two key objectives.

One was to generate an IL-2 that avoids the safety liabilities, and Treg engagement properties of wild type IL-2 and two, ensuring that the IL-2 was selectively delivered to tumor relevant T cells. The output of these efforts resulted in the generation of the CUE-100 series framework, as you see here in Slide 9.

The top-down view of the ribbon diagram of the Cue-100 series, as shown here provides a good contextual perspective for the spatial engagement of these molecules by tumor specific T cells. Note there are two modifications to the IL-2 molecule that are important for specificity and selectivity.

The first is abrogation of binding to IL_2 receptor alpha subunit in order to avoid Treg engagement. The second modification is the attenuated binding to the IL-2 receptor beta subunit, such that the IL-2 activity is biased to those T cells that are docked to the specific peptide HLA complex via the T cell receptors or TCRs.

We believe this engineered biologic framework allows us to maintain specificity and selectivity while avoiding the systemic toxicities associated with indiscriminate IL-2 dependent activation of many different cell types.

And indeed, as you've heard from Ken, and as you've seen the dose cohorts, the initial clinical data sets suddenly appeared to support this thesis. Several key points should be emphasized. First we have a normal biologic scaffold that demonstrates exposure and dose proportionality in line with projections, which is highly encouraging.

Furthermore, we have not seen major safety liabilities that doses were in a molar content comparison IL-2 were significantly higher than the approved dose of Proleukin. For example, at the dose level in the fourth cohort, CUE-101 has approximately eight times the molar content of IL-2 compared to Proleukin.

In addition, the early PD data seems to suggest that we have activity in engaging and expanding the targeted T cells based on Tetramer and ELISpot analysis. These are early data at early time points that will be confirmed and extended as we obtain additional patient samples.

But perhaps most encouraging is the composite view from the clinical experience thus far. We design a novel biologics platform that appears to possess favorable properties pertaining to drug exposure in PD and also appears to be demonstrating mono-therapy clinical activity. As we continue to obtain further supporting data from CUE-101.

We are highly enthusiastic about the broad possible applications of the CUE-100 series. The data generated from CUE-101 clinical experience has the potential to de-risk the entire CUE-100 series since the core IL-2 elements coupled to the peptide HLA framework remain constant.

Okay, I'd like to now move on to Slide 10 to remind you of the key features that we believe underscore the superior differentiation of the IL-2 based CUE-100 series over other IL-2 modalities that are out there.

This slide has been presented before as a part of our corporate deck and highlights the important fact that the CUE-100 series can selectively deliver IL-2 to the relevant T cells that is the tumor specific T-cells, while minimizing the safety liabilities and broad effects and other types of subsets, both the Tregs and the vast majority of the non-tumor reactive, effective T cell repertoire that all of us harbor.

This is in stark contrast to the not alpha IL-2 variants that minimize the activity in Tregs but still act with equal opportunity on all other T cells, the vast majority of them have no relevance to tumor specificity.

Furthermore, the core framework of the CUE-100 series can prime and expand T cells from a naive T cell repertoire, as also reported in our recent publication in Clinical Cancer Research last month. While the not alpha IL-2 variants rely upon a pre-existing anti-tumor T cell repertoire that must be present within the patient to derive benefit.

The next slide, Slide 11 highlights our immune-oncology development strategy to exploit the fullest potential of the CUE-100 framework.

The present clinical trial with CUE-101 provides us with a foundational proof of concept in an indication of unmet medical need, and as mentioned previously, 101 is positioned to potentially de-risk the entire 100 series.

We have thus positioned ourselves to maximize success for the CUE-100 series by exploiting the key strength of the Immuno-STAT platform, which is modularity and flexibility that allows us to target different tumor antigens, along with distinct HLA alleles for global patient populations.

This strategic growth opportunities is exemplified from our current ongoing work with CUE-102 and beyond where we have focused on tumor antigens like Wilms Tumor 1 or WT-1 and KRAS and have initiated programs with additional alleles besides HLA-A02.

These include HLA-A24 and A11, both being dominant in Asia, which was the primary reason for our LG Chem partnership for our first three programs. We have made strong progress with our CUE-102 programs and have generated pilot data demonstrating ex vivo expansion of human T cells, poly functionality and the killing of target cells.

These data were recently presented at an invited talk at the frontiers in cancer immunotherapy meeting, organized by the New York Academy of Sciences on May 12. We will also look forward to other avenues and forums to disclose these promising datasets, including the upcoming AACR Virtual Conference on June 22, where we will be presenting a poster.

Okay, so based upon the foundational work of our Immuno-STAT platform, we have further developed our next generation platform referred to as Neo-STAT, which greatly accelerates our scalability in generating new clinical candidates.

The Neo-STAT framework specifically enhances the productivities and efficiencies, both from a time and cost perspective and builds upon a versatility to target multiple tumor antigens including post translational modifications and personalized Neo antigens in the future.

The next slide, Slide 12 focuses a bit more on the Neo-STAT platform, a key intellectual leap here was to design a platform enhancement that significantly expanded the reach into diverse tumor antigens. To remind you, the current Immuno-STAT platform incorporates singular primary tumor driver antigens.

This is great for examples like the HPV16, E7 protein, as in our lead molecule CUE-101 or targets like WT1 or KRAS and such. In these cases, the immune assault to a dominant human driver antigen is likely to provide meaningful clinical benefit.

Indeed, with all of the examples mentioned above data from cell therapy based clinical studies utilizing either TCR T cell therapy or TIL based adoptive cell therapy have demonstrated clinical responses. However, looking into the future, we want to be positioned to capture the vast landscape of available tumor antigens.

Tumor sequencing and profiling data emerging in real time is providing us a continual source of new antigens that can be effectively deployed using our CUE-100 series.

This is the thinking that – is what propelled the Neo stock platform, wherein we can generate the entire CUE-100 series scaffold without any specific peptide attached to the HLA molecule.

And again, this is in stark contrast to the current minister platform where each T cell epitope is an integral part of the Immuno-STAT, meaning it's incorporated into the molecule as a fusion protein at the time of synthesis. Immuno-STATs are synthesized without a peptide epitope.

Instead, the peptide epitope is actually attached subsequently using sophisticated attachment chemistry, as shown in the current figure with examples of three different peptides bound to the Neo-STAT scaffold.

This advance allows us to generate the co-generic scaffold for any HLA allele via a single cell line and then use the same product to conjugate to different tumor antigens to expand our reach.

The fact that only a single scaffold needs to be generated will save us significant resources and both time and cost, but generation of clinical grade material, and in doing so, provides us essentially with an off the shelf biologic to target T cells directly in the patient.

We have generated early proof of concept data supporting the biological activity of molecules generated via the Neo-STAT platform. And an example of one such data set is shown in the following Slide 13.

Additional data underscoring the protein engineering efforts were disclosed at a talk at the World Vaccine and Immunotherapy Congress meeting about six months ago, in December 2019 in San Francisco. So moving on to Slide 13, the top panel here shows the expansion of CMV specific T cells from three human donors.

The bottom panel shows expansion of MART-1 specific T cells. From additional three human donors, MART-1 is a known antigen in melanoma.

In each case, the PBMCs from human donors were expanded with Immuno-STATs were in the CMV or MART-1 T cell epitope is made as a fusion protein or with Neo-STATs within the respective T cell antigen is chemically conjugated to the scaffold. As you can know, the expansion of relevant T cells specific CMV or MART-1 one was very comparable.

The Immuno-STAT expanded T cells are shown in solid lines, while the NEOs that expanded T cells for each specificity are shown in dotted lines. These data provide enormous confidence that the Neo-STAT platform can be developed for future therapeutic applications, and will complement and extend the current application of the Immuno-STAT platform.

Note that the scaffold of the Neo-STAT described in the current slide is essentially the CUE-100 series without an antigenic peptide, but the same core configuration and valency of IL-2 molecules. Next slide. Slide 14 highlights our pipeline progress.

We've made significant progress with CUE-101 in the mono-therapy trial, as discussed by Ken and Dan, and are positioned well for the combination study with pembrolizumab for later this year. CUE-102 with WT1 continues to make strong progress.

To remind you this program is being prosecuted with two different HLA alleles, HLA-AO2 and HLA-A24, which is a dominant allele in Asian populations. CUE-103 is being bettered currently with LG Chem our Asia partner and will be disclosed in the near future.

And as listed here, we've also made meaningful progress with our KRAS programs for the CUE-100 series. We will hopefully find an appropriate forum to share those data in the near future.

We continue to extend the application of our platform with the CUE-200 series wherein we have early datasets with cell surface receptors like CD80, which is B71 that binds to CD28 in T cells and 4-1BB Ligand.

And finally, as disclosed recently, we continue to make strong progress in autoimmunity in our alliance with Merck using the CUE-300 series, wherein we have successfully generated Immuno-STATs incorporating class two HLA molecules to selectively target or reactive CD4 positive T cells in human patients.

Select the modulation of an apparent immune response and autoimmune diseases without broad immunosuppression, as is the case with current therapies is likely to bring superior clinical benefits to patients. We believe this goal can be achieved with a platform like ours.

In conclusion, and as I've stated in prior presentations, the Immuno-STAT and by extension the Neo-STAT platform address that fundamental immunological challenge which is how does one maintain selectivity and specificity of a desirable immune response without breaching patient safety or creating toxicities.

We believe our approach that is built upon rational protein engineering and is bolstered by supporting data sets may offer a unique solution to patients suffering from cancers, autoimmune diseases and threats from chronic pathogenic infections. Okay with that I'll now turn the call over to Carrie to review our financial results. Kerrie. .

Thank you, Anish. Turning now to Slide 15, I'd like to provide a brief update on our financial results for the first quarter ending March 31, 2020. We finished the quarter with approximately $48.7 million in cash and cash equivalents, 60.6 million in total assets and working capital of approximately 39.1 million.

Revenue generated from our collaboration with Merck and LG Chem in the first quarter of 2020 were 9.9 million as compared 0.4 million for the same period in 2019. For the quarter ended March 31, 2020, research and development expenses were 9.9 million as compared to 8.4 million for the same period in 2019.

The increase in research and development expenses was primarily due to clinical trial costs related to our ongoing CUE-101 mono-therapy trial that was initiated in the latter part of the third quarter of 2019, as well as manufacturing costs for CUE-101 to supply our recently announced combination trial of CUE-101 with Merck's KEYTRUDA.

General and administrative expenses were 3.9 million for the quarter ended March 31, 2020, as compared to 3.4 million for the same period in 2019. This increase in general and administrative expenses was primarily due to an increase in stock based compensation expenses and legal and accounting fees incurred in the first quarter of 2020.

In April 2020, we extended our cash runway through an at-the-market equity offering sales agreement for aggregate proceeds of 34.3 million, net of commissions paid to Stifel who acted as sales agents.

The successful deployment of the ATM facility in April has enabled us to strengthen our cash position to further support the development of our Neo-STAT platform and associated pipeline, including the clinical development of CUE-101 as both in mono and combination therapy.

Based upon our current forecast, which includes the further build out of our ongoing clinical studies, our current cash position is estimated to take us into the fourth quarter of 2021. With that, I'll turn the call back over to Dan for closing remarks. Dan. .

Yeah. Thanks, Kerry. Yeah, since our last call, and despite the challenges we continue to face by the COVID-19 pandemic, we've made significant progress across our platform and associated programs, as shown here in Slide 16.

Having raised additional capital in April and having enrolled and treated patients through cohort three and now into cohort four in our CUE-101 Phase I trial we're better positioned strategically to continue advancing CUE-101 for determining a recommended Phase II dose as a mono-therapy and into a combination trial with KEYTRUDA, as well as further advancing our platform and the associated programs As just described above our lead program CUE-101 is well positioned to generate a body of data including PD biomarker activity, and patient scans that demonstrate biologic and clinical activity.

In this patient setting these data would significantly de-risk and validate our approach, allowing us to further build our pipeline based upon the same foundational principles upon which we brought CUE-101. Forward.

With CUE-101 now being dosed at what could be biologically active and clinically relevant levels, we believe we're very well positioned to establish Cue Biopharma as a differentiated leader in immunotherapy with a potentially disruptive breakthrough therapeutic platform.

A couple of our key accomplishments in Q1 include, continued and timely enrollment of cohorts one through four in the CUE-101 mono-therapy trial, along with demonstration of favorable safety and tolerability, dose proportional exposure in line with preclinical projections and early signs of PD activity in emerging clinical activity.

Our guidance for 2020 milestones, as shown on Slide 16 are unchanged from our last call. And principally they are PK and PD results from the Phase 1 CUE-101 clinical trial in the second quarter of 2020 and we've demonstrated that is on track today. Clinical responses in Phase I for CUE-101 via resist criteria in the second half of this year.

We're already beginning to see what appears to be emerging data supporting that. Initiate a combination trial with KEYTRUDA in first-line, head and neck squamous cell carcinoma patients in the second half of this year, and we're on track with that with the announcement of the consummation of the partnership with KEYTRUDA.

Initiate and extend IND enabling activities for CUE-102 in the second half of this year, we're on track. And selecting a defined target for CUE-103 in the second quarter of this year and we are on track for that and discussions with our partner, LG Chem, demonstrate Neo-STAT manufacturability and efficiencies in the second half of 2020.

And as you heard from Anish, we've made quite significant progress towards that objective. And then finally, identify potential clinical candidates in our auto immune collaboration with Merck in the second half of this year.

So with that, I'd like to once again thank our employees for their hard work and commitment to advancing our science forward during these challenging times. And finally, I'd like to thank our shareholders and our board of directors for continued support, enabling us to advance Cue Biopharama's platforms towards validation.

In the clinic we're also moving our preclinical assets closer to IND enabling studies. We look forward to providing further updates on the validation growth and expansion of our pipeline, including our CUE-101 Phase I trial. And most importantly, we're grateful to all who enable us to pursue this noble mission to serve patients in need.

I'd like to now open the line for questions.

Operator?.

Thank you. We will now be conducting a question-and-answer session. [Operator Instructions] Our first question comes from line of Boris Peaker with Cowen. Please proceed with your question..

Congratulations on the progress you guys are making in this environment..

Thank you, really appreciate it Boris. .

So my first question is so in the party of the study – the design allows you to expand doses out to nine patients if you see activities, just curious if you've expanded any or if you plan to expand any of doses based on the initial activity that you're observing. .

Sure.

Ken, would you take that?.

Yeah, thanks for the question, Boris. So yes, we're planning to expand based on our Bayesian approach.

We have not yet started to expand because we've been focusing on escalation since we have not reached the DLT, we've made the conscious decision to continue to dose escalate prior to expanding at any given dose level, but we're constantly evaluating that. But the short answer is we have not started to expand any of the lower cohorts as of yet..

Got you and my second question in terms of the dose-escalation, I mean, your plan has seven cohorts right now, kind of estimated, or I guess, per protocol.

I'm just curious, at some point, if you get to the seventh cohort and the drug is still tolerated is there thoughts of going higher? Or how do you kind of think about the highest dose level worth testing and dose range you consider you have an agonist versus most of the time we're used to thinking of antagonist?.

Yeah, so that's a great question and that's why we really built in this Bayesian approach to look – to really evaluate what types of responses we're having both clinically as well as by PB biomarkers.

And we fully expect that by dose seven, we're going to be seeing those types of biologic and clinical markers that would allow us, even if we haven't seen toxicity to expand out at these lower cohorts, I'm – I seriously doubt we'll have to go higher than dose seven, but we're prepared to.

But the reason we built in this overlying Bayesian approach over the three by three design was really to – because we were concerned that we would not see a dose limiting toxicity. And we want to be able to pick a rational dose for the Part B dose expansion.

So I think before – as long as we're seeing PD and clinical effects, we're likely to use our expansion of these lower cohorts to allow us to pick a Phase II, what we think is going to be the recommended Phase II dose without going necessarily higher..

Great, thank you very much for taking my questions..

Thank you..

Thanks Boris..

Next question comes from the line of Stephen Willey with Stifel. Please proceed with your question..

Yeah. Good afternoon. Thanks for taking the question and congrats on all the progress and the incremental information on some of the early cohorts. Maybe a couple questions for Ken, so you mentioned I guess an infusion reaction is happening. I think it was maybe cohort three. .

That was cohort four..

So cohort four, so can you maybe just talk about the severity of the AE that was observed there and do you think you might have to pre-medicate as you as you move higher?.

Yeah, so it was an SAE and not in another deal too. And the patient was – he would rapidly resolved over the space of an hour basically. And required – the patient did get some ibuprofen. But there was – we – the investigators have discussed it, we've discussed it.

At this point we don't believe – we're not planning on pre-medicating at the next dose level and have no indication right now that we would have to do that. Again, this was not a sustained SAE that leads – would lead us to you change what we're doing at this point..

Okay, no, it's helpful.

And then just curious as to when in the time course of treatment are you evaluating T cell expansion and activation in these patients? How soon after administration?.

So we're looking at – we look at – I'm not quite sure I understood the question. I'm sorry..

So just curious as to when you're assessing these patients for peripheral T cell expansion and activation, how soon after administration, are you looking?.

Right, so maybe I can comment on that. This is Anish, Steve. So the first – as you will remember the cycle is a three week cycle. So the drug is given and the first analysis is after the first couple of weeks, then at each of the cycles before the drug is given. We're able to look at the T cells.

So there's a couple of weeks time lag between the dose of the drug and the time we get the blood for the analysis. And again, as Ken pointed out, and as I stressed, these are early time points. So we need to build this out with additional time points and additional doses and additional patients.

So these are early signals that we started to measure at this point..

Okay. And then you mentioned that you're continuing to treat five patients. I think I heard, so it sounds like that might be the one cohort two patient that's had a confirmed stable disease.

Can you maybe just kind of directionally point as to where those other patients are in terms of cohorts?.

Sure. So we have one patient from cohort two, we have another patient from cohort three and then the three patients from cohort four. .

Okay.

And then maybe just lastly, you kind of feel like you have enough information at this point just based on where you are dose-escalation to initiate the PD-1 combo dose-escalation in parallel or do you want to push those a little bit higher before you get that going?.

Well, we really want to push the doses a little higher before we get that going. We wanted to be sure that we have enough information in the mono-therapy arm to be able to pick a dose because we would like to pick a dose that's high enough that we can start to see early and immediate effects in the combo.

And so we did offset the combo to start in the second half of this year, rather than right away. We did suggest that we would start at least at a minimum of cohort three with the combo, but it may – we're hoping that we can potentially even go higher.

So in our submission to the FDA, we said at least that we would – we put in cohort three, but we also have the option of changing that..

Right. That's really helpful. Appreciate the answers and congrats again. .

Thanks Steve. T.

Thank you, Steve..

Our next question comes from the line of Mark Breidenbach with Oppenheimer. Please proceed with your question..

Good afternoon guys and congrats on forward progress with dose-escalation and especially on the early signs of tumor regression in – sounds like some of the patients. Let me ask for the patients who have shown some early indications of tumor regression.

Have they all progressed on prior PD-1 therapy or were any of them only previously treated with chemo?.

Yes, Mark. Thanks for the question. This is Ken. All the patients have been heavily pretreated including checkpoint inhibitors, so they've all progressed on checkpoint..

Okay and so can you comment, is there a protocol mandated PD-1 washout period? And maybe can you just give us some color on the interval between the last PD-1 and the start of CUE-101 for these patients?.

Yeah, so that's a really great question and there is no mandated washout period, per se. All we're requiring is that patients are progressing. The different – so every patient has a different length of time that they've been off PD-1 checkpoint type therapy. In general that's at least two to four months off from their last dose..

Okay, okay, that's helpful.

Maybe a quick one for Dan, I'm just wondering if we can expect the more fleshed out PK/PD data to make an appearance at a medical meeting in second quarter or are you thinking this will be delivered by a press release once you have enough follow up on these patients?.

Sure. I'll answer that sort of as an overview and I'll ask Anish to elaborate, but look, we're going to be opportunistic about it. We're not going to hold on data waiting for a conference unless we already have it lined up and the timing aligns. And we won't put out a press release unless we think it substantively warrants that type of a release.

So our intention is to compile data as we've been doing. Obviously, we're using the quarterly calls as a venue. But at various conferences and also we have investor conferences that we have the opportunity to update on an intermittent basis.

So in this sort of COVID-19 new normal that we're dealing with we'll use virtual venues where applicable or webpage and press releases as appropriate.

I don't know if you want to elaborate?.

So I think that's right Mark. I mean, we – ourselves getting acquainted to the new normal. As I mentioned, even with the WT1, for example, we had that at AACR, that's not going to happen in June, but we will certainly be looking for appropriate forums where we can thoughtfully compile the data and share at these meetings.

And of course, later in the year, we've got opportunities with SITC and such, but we'll look at ones before that too. And that's something that we continue to discuss amongst ourselves with Ken that we'll find those opportunities..

Okay, and just a quick follow up on the AACR presentation on, I guess, CUE-102. Are we going to see any data in that presentation that might give us more of an indication on which types of tumors you initially intend to focus clinical development on for CUE-102? Thanks. .

So the AACR presentation Mark with WT1 is focused on characterization of the molecules and the early data that we've seen with primary human T cells and the downstream effect or responses which are very encouraging.

As for the indications, this is something that Ken and the team are – this is a sort of one of our core priorities this year is to align and define those and as you will know, in contrast to HPV driven head and neck cancer, where he E7 stratify nicely, WT1 has a spectrum of hematological and solid cancers.

And there's a few of them that stand out and the team is continuing to sort of flesh that out. And we'll be able to hopefully share with those sort of thoughts in the latter half of this year is what I'd imagined. We'd have that plan sorted out for a total clinical development strategy and how we apply this molecule.

Also in contrast to 101, where the allelic variant is AO2, the WT1 program is being developed with AO2 for this part of the world, but A24 for the Asian territories, as I mentioned with obviously different T cell epitopes that also provides a breadth of opportunity in different geographies..

Understood and thanks for taking the questions. .

Thank you, Mark. .

Thank you..

Our next question comes from the line of Madhu Kumar with Robert W. Baird. Please proceed with your question..

Well, hey everyone, thanks for taking our questions. So I think our first one is kind of maybe scientific and philosophical for Ken and Anish.

So how long do you think it practically takes to educate T cells we have activated against HPV E7 from CUE-101? And then kind of following from that, do you think the timeline for T cell activation that you're observing so far is consistent with kind of naturally already present HPV directed T cells kind of emerging out of the naive or representative of kind of people that really haven't been kind of trained into 102 to engage with and going after HPV E7?.

Yeah, I'll take a crack at it Madhu, that's an excellent point, which is the kinetics of the evolution of a T cell response as a function of the pre-existing repertoire. So the point that you brought up is a very important one. And it entirely depends on what the baseline composition is.

If you haven't sensitized and you're going from a naive virgin repertoire, then obviously, the time to effect is going to be longer than if you're going to be expanding from a pre-primed repertoire. And that was the case.

We also stressed in the paper that we published last month, where you could see nuances and intensity and present depending on whether you had a pre primed repertoire or not. My bias as an immunologist is these first signals that we've seen from the patients after the first few doses are likely from ones that have some presence in the periphery.

And I think that goes to say that on the longer run, there may be patients that may need a little bit more time on drug to perhaps exhibit similar peripheral signals. That's just the periphery and again, I come back to the central question that this is – we look at the peripheral blood as a surrogate for the lesional tissue.

In case there are scenarios where you have resident populations that have honed in to the tumor and not so much present in the periphery, one may expect to disconnect where you may not see much in the periphery, but you may start to see certain tumor lesions as specific as activities and that's something we've got to just keep an open mind because ultimately, what the effector site is harboring is still an open question.

And you could have resident cells against the very dominant antigen that are parked there that are held back for whatever local resistance mechanisms are there that could be engaged by the drug, we know that the molecule can get to the tumor effective side in a preclinical models, the degree of tumor, resident expansion was significantly higher when we measured the tumor specific T cells as opposed to the periphery, but all those would you bring up excellent nuances of experimental immunotherapy that we're aware of, and as the data emerges, we'll be able to sort of, hopefully put some solid cohesive structures around these thinking..

Okay, also following from that question, to think about the kind of molar equivalences – have you done that kind of exposure equivalent, given that your drug is much more persistent than Proleukin is kind of in circulation..

So we just – we need to get some more exposure data, these early points Madhu and we'll be able to put that in perspective. And that is the intention. We were very encouraged to see that the early exposure looks in line with what was projected, but the Proleukin exposure is very different than ours.

And that's a factor that needs to be further fleshed out as we get additional exposure data from the higher dose groups, but that's a very good point..

Yeah, we also recognize that these doses that we are showing are based on a single dose of Proleukin and of course, much of the toxicity of Proleukin is due to the multiple doses that you need to give to get exposure..

So that's a very good point. .

Great, thank you for taking my questions..

Our next question comes from the line of Reni Benjamin with JMP Securities. Please proceed with your question..

Hey, good afternoon, guys. Thanks for taking my questions. That's on the progress. Hi there.

Maybe just starting off a question for Ken, if I just look at cohorts like one through three, nine patients, if I heard you right there were two SDs and two patients with T cell expansions or activations and I'm – and if that's right, I'm kind of curious why wouldn't, why wouldn't the two patients with the T cell expansions also be the ones who are getting the SDs, just kind of your thoughts on that and what's the longest SD that you've recorded to date?.

So I think that some of these patients we've – what we've seen is that these patients are all rapidly progressing and the fact that we've seen anything at all, at these low doses is pretty tantalizing to me personally, and to all of us.

And I think what we've seen is that we've started to see some TV effects and what looks to be early expansion activation, but that is just not been enough to overcome patients with basically exponentially growing tumor, and at the low doses, we just haven't been able to see a sustained response, even in the patients who are starting to show us some biologic activity.

So if you look at our longest stable disease patient, what we've had is exactly, we have one patient who is through cycle – he's cycle five. And we have to get to at least – to confirm a response we have to get at least through cycle four. So we've had two patients that have made it through to cycle five dosing..

And, and I know it's early days, but I'm kind of curious when you look at the other patients, are there any negative selection metrics or biomarkers that maybe you're starting to pop out or you guys are starting to evaluate? May be even something like T cell exhaustion markers right that that you might be able to utilize moving forward or do you kind of feel that once we start moving into less heavily pretreated patients, we think that the repertoire is going to be healthy enough that that it's not really going to be an issue in terms of patient selection..

Yeah, that's a great question. I think we just – we don't have enough data yet on exhaustion. And we're certainly looking into and have plans in the protocol to evaluate those types of biomarkers to try to understand who is not responding.

I do think moving into earlier grips like we are with the combo study, which will be also a dose-escalation study, by the way. We'll be able to see patients who don't have exponentially growing tumor and we'll have a little bit more time with those patients to have an effect. And I think that's going to be critical.

But I also think that, again, choosing – why don't – trying to understand why the checkpoints fail. And in combination if we're not having a good response, I think we are going to see some using TPS scores, et cetera, we're going to be able to start to get a feel for why CUE-101 might not be working.

So we're thinking hard about that, we've got some biomarkers built in and we're looking forward to treating earlier patients. .

Yeah. Reni, just to add on to what Ken said, I think one of the parameters of immune fitness in terms of looking at the repertoire the induction part of our biomarker panel that will we'll get to that. It's just a point of collecting and having more data.

I think fundamentally what's quite remarkable is you've got a normal protein framework going for the first time in man. And the fact that it is inducing the appropriate what we think is the right repertoire to us is very encouraging.

Obviously, the fact that IL-2 at these high doses is being sustained and tolerated with the appropriate safety parameters, again, becomes very important. And as you well pointed out, whether that also then co-emerges with other metrics that we've started to see is a component that we are very much looking forward to studying.

The relationship between the PD metric and clinical response in terms of absolute numbers, I mean, I just want to be very careful there because ultimately, what's going to matter is, what is the infiltrate at a tumor lesion side, what is the phenotype of the infiltrating repertoire, what may be local resistant mechanisms, we may need to come consider.

To that end, the combination with pembro makes very good sense. But I think as we gather more data in all of these wonderful irrelevant immunological parameters, I think will hopefully get addressed..

Got it and just regarding the PK/PD results that we're still expecting this quarter, I know originally, correct me if I'm wrong, I thought originally, we were thinking about cohorts one and two, but enrollment seems to be going so well, is it fair to say that when we're looking at these PK/PD results, it'll likely be cohorts one, two and three, or not be expected?.

Yeah, I think so. I think our expectations and the way – this is something that's ongoing when we can share that our exposure data, the early exposure data from cohort three, we anticipate to have it by the end of this month.

So our hope is and as you pointed out, the fact that we've continued to see enrollment and we will continue to sort of dose-escalate that as we start to gather more of these data and put it out that it should have a composite body that goes beyond one and two. We're very excited about that..

I was just going to add in here that we are so grateful, again, as I mentioned in the call that we're so grateful that we've been able to continue to enroll. We are hyper aware that 90% of all cancer trials are not enrolling right now across these academic institutions.

And again, the fact that we've been able to – our investigators have been convinced their institutions that we are a critical drug that should be allowed to enroll is a real testament to the – how important they think this is and I am just as an academic investigator myself, I am thrilled that we've been able to enroll through this. So thanks..

That makes sense. And thanks to that. I guess one last question. I want to leave Dan out of the discussion here, but you've got a really nice significant cash position now.

And you can – I guess, I can sort of think about it in two ways, one is, it could result in an acceleration of the pipeline and things that we were expecting might take a year or two, coming in a little bit earlier, or that at this stage in the game, there are enough kind of rate limiting steps like maybe manufacturing where no matter how much cash you throw at it, it's not necessarily going to speed up, the timelines.

How should we be thinking about kind of the usage of cash and the acceleration of the pipeline?.

Yeah. It's a really important question Reni. And by the way, I appreciate your perspective on no matter how much you throw out of these, a lot of companies think by just hiring more people they can increase output. Scale requires rigor, right. And that's what we've been putting in play, laying the foundation over the past year plus.

And we look at the data emerging from 101 as a validator of what the 100 series could represent. So, as we continue to generate more data such as what you've heard today, but on a going forward basis with more patience, our intention is to then we can expand out with 101, we have to advance 102.

And as Anish described earlier, Neo-STAT is meant to be a platform advancement to be able to exploit these observations in a, let's say, more productive, cost efficient manner. So it's a hybrid between what you articulated, we're not going to be conservative and just continue systematically building data on 101 and weight on everything else.

But we're also not just going to start increasing our burn rate. We're going to do this in a very deliberate, purposeful trajectory. The first thing is to generate de-risking validating data with 101, which can then justify increasing expenditure on other assets that benefit from that de-risking. So that's the way we're basically approaching this..

Great, thanks for taking the questions and congrats again on the progress. .

Thanks, Reni. Really appreciate it..

Our next question comes from the line of Tom Schrader with BTIG. Please proceed with your question..

Good afternoon. Thanks for squeezing me in. So going back to what was a very interesting line of discussion about the T cells may actually need to be in the periphery for you to have time to work.

Do you measure that? Can you get an accurate read on the T equals zero T cells that might respond to your antigen?.

Yeah. Tom, so whenever these analysis are done, they're always compared to the baseline from the blood pre-dose. So you have a sense of what that snapshot looks like. You're using that as the baseline to judge an uptick. And that's how you're going to be quantifying it just to get a sense that have you induced the right kind of repertoire or not..

But can you sort of back extrapolate now that it has to start here to have a chance at being an anti-tumor response given the thought?.

That actually is – those sorts of hard numbers can be put in bred species in experimental animals but in – when you get to the population, at the level of the species of humans, those numbers are all over the place simply because you have different levels of sensitization, you have different diversity of the repertoire.

And don't forget through the treatment regimens that these patients have been through the immune competence and fitness criteria's are –may be quite variable. So that – you can do it on a per individual basis, but it is – I think it'd be very difficult to bracket it as a group basis..

And then put maybe the same question, were your people that you treat it all over the place in terms of their prior PD-1 response, and is there anything interesting to think about between what they got out of PD-1 and what they got out of your approach?.

So, I think Ken mentioned that although – I think Ken mentioned this just a few moments ago that almost all of them are prior checkpoint failures.

And again, that comes back to the central point, Tom, which is if you fundamentally don't have the right effector repertoire or the appropriate specificity locked in the application of a checkpoint is not very relevant.

I mean, the checkpoint is working with the assumption that you've got the repertoire in, so one of the questions for us as we gather more data is to understand those varied relationships. And hopefully, as some of these clinical responses solidify, one can perhaps establish those relationships.

And if that's true, then the combination with KEYTRUDA should further build upon that and should have what we think could be quite a remarkable outcome in the sense that you've got an agent that's inducing the right repertoire, in a very selective stable manner, coupled with if they should up-regulate PD-1, they should gain benefit from that angle, but having just a PD-1 blocker in absence of the repertoire doesn't do much..

Okay, got it. Thank you. .

And I would just – this is Ken. I would just note that none of the patients had a sustained checkpoint response before going on study..

Okay, so they were like primary failures, they just blew right through PD-1?.

Pretty much blew right through. Yeah. .

Okay..

There are no further questions in the queue. I'd like to hand a call back to management for closing remarks..

Okay, thank you very much. I also want to thank everyone for your time and attention and for your interest in support of Cue Biopharma. We look forward to giving you continual updates as they become available, and most importantly, we hope everyone stays safe and healthy during these challenging times. So thank you very much and take care everyone..

Ladies and gentlemen, this does conclude today's teleconference. Thank you for your participation. You may disconnect your lines at this time and have a wonderful day..