Cue Biopharma, Inc. (NASDAQ:CUE) Q3 2022 Earnings Conference Call November 14, 2022 4:30 PM ET
Company Participants
Dan Passeri – Chief Executive Officer
Anish Suri – President & Chief Scientific Officer
Ken Pienta – Acting Chief Medical Officer
Matteo Levisetti – Senior Vice President of Clinical Development
Kerri Millar – Chief Financial Officer
Conference Call Participants
Reni Benjamin – JMP Securities
Operator
Greetings, and welcome to the Cue Biopharma Update Call. A question-and-answer session will follow the presentation. [Operator Instructions] As a reminder, this conference is being recorded.
I would now like to turn the conference over to Dan Passeri, Cue Biopharma’s Chief Executive Officer. Thank you, sir. Please begin.
Dan Passeri
Thank you, and good afternoon, everyone. Before I begin, I’d like to remind everyone that you have the slides in front of you that you need to operate manually, and we will notify you what slide we are on. Joining me on today’s call is Dr. Anish Suri, our President and CFO; Dr. Ken Pienta, our Acting Chief Medical Officer; and Dr. Matte Levisetti, our Senior Vice President of Clinical Development; as well as Kerri Millar, our Chief Financial Officer. This conference is being recorded and will be available on our website for the next 30 days.
As a reminder, and as shown here on Slide number 2, this presentation and overview may contain some forward-looking statements, and any forward-looking statements made during this call represents the company’s views only as of today, November 14, 2022. Our agenda for today’s call is shown on the next slide, Slide 3.
I’ll begin by providing an overview of our competitive and strategic positioning based upon data from both our monotherapy trial of CUE-101 as well as the data just recently reported at SITC from our CUE-101 and KEYTRUDA combination trial. Mateo and — can will provide this — a review of this data in further detail momentarily. But first, I want to provide context pertaining to the underlying implications and importance of the data sets observed to date. As you are aware, the ultimate promise of immunotherapy is to enable the intrinsic potential of a patient’s immune system to recognize and kill cancer. We believe through our representative data generated from both our monotherapy trial and combination trials of CUE-101, our IL-2-based Q100 series is now well positioned to become a first-in-class selective T cell engager and best-in-class IL-2 for cancer immunotherapy, as shown here on Slide number 4.
The data bolsters our belief that the demonstrated mechanism of action and resulting in activation and amplification of cancer-specific T cells will mechanistically complement and enhance therapeutic benefit derived from checkpoint inhibition, such as PD-L1 inhibitor KEYTRUDA. We believe the compilation of data — from both the monotherapy and combination trials supports our central thesis of selective activation of cancer-specific T cells while avoiding systemic immune activation will enhance the desired antitumor efficacy. The recent data presented at SITC positions us well to push forward and potentially transform cancer therapy where patients in our own immune systems can be harnessed to the fullest extent to eradicate cancer.
I’m now going to turn the call over to Anish who will provide a brief synopsis and overview of the key mechanistic features of our selective T-cell engager, the IL-2-based CUE-100 series, and I’ll then turn the call over to Ken and Matteo to review the supporting efficacy data that has emerged from the monotherapy trial and provide an update from our recent SITC presentation pertaining to the current efficacy data from our combination of CUE-101 with KEYTRUDA in frontline HPV positive head and neck squamous cell carcinoma patients.
Anish?
Anish Suri
Thanks, Dan, and welcome to all listening to this update. As noted in the next slide, we all appreciate the fact that selective activation of tumor-specific T cells is central to successful outcomes for cancer immunotherapy. However, there are biological constants that nature has imposed that must be considered when thinking about tumor-specific T cells. One, the frequency of tumor-specific T cells in the patient is extremely low. — greater than 99.9% of T cells in the patient have no relevance to Kansas. So how does one go about selectively activating tumor-specific T cells while sparing the broad activation of all other T cells?
Another biological constant is the fact that the only unique marker on an antitumor T cell is the tumor-specific T cell receptor or TCR. There are no other cell surface markers that exhibit an absolute fidelity to the anti-tumor T cell repertoire as the tumor-specific TCR. For example, PD-1 expression is a shared phenotypic marker or CD8 expression is a shared lineage market, but neither are unique to an antitumor T cell. Hence, to exploit this unique selectivity, we’ve developed the Immuno-STAT platform to harness the TCR specificity to activate tumor-specific T cells. We believe, as supported by our clinical data that this approach is differentiated in terms of both safety and efficacy outcomes over other modalities that attempt to activate the immune system in a nonselective manner.
The next slide, Slide 6 depicts the core structure of an immuno-STAT molecule derived from our IL-2-based CUE-100 series, which is the major focus of today’s presentation. As shown here, the CUE-100 series immuno-STAT harness the TCR selectivity via the stabilized peptide HLA molecule to target an affinity attenuated IL-2 variant selectively to tumor-specific T cells. The co-signaling via the TCR and IL-2 receptors on the right antitumor T cell results in T cell activation and expansion. In contrast, of this molecule encounters the vast majority of irrelevant T cells in the patient that is a greater than 99.9% of irrelevant non-tumor-specific T cells. The attenuated IL-2 on its own is very weak. Hence, with this unique bias, we have created a therapeutic index for IL-2.
We have selective focusing on tumor-specific T cells over all other cells. This strategy also forms the mechanistic basis for targeting numerous other activation signals, including other cytokines such as IL-12 IL-15, IL-21, etcetera. Two additional aspects of the CUE-100 series are important to appreciate. While the primary core IL-2 framework is largely conserved between different therapeutic candidates. The primary difference from 1 therapeutic candidate to the next is a 9 to 10 amino acid T cell epitope depicted by the yellow circle in the diagram on the slide. Due to this conserved structure, we believe the clinical proof of concept with our first clinical candidate, CUE-101, has devised the entire platform.
This conclusion is supported by the IND approval by the FDA earlier this year for our second clinical candidate, CUE-102, where based on the clinical safety data from CUE-101, we did not need to perform any additional IND-enabling toxicology studies and were allowed to start the CUE-102 trial at 1 mg/kg dose, which is a clinically active dose from our experience with CUE-101. Both CUE-101 and CUE-102 or 99% sequence identical except for the 9 to 10 amino-acid selepitope. CUE-101 targets a T cell epitope from human paplomavirus for HPV-driven cancers, such as head and neck cancer, while CUE-102 targets a T cell epitope from Wim Tumor 1 or WT1, and oncofetal antigen widely expressed by many solid and hematological cancers.
The other key aspect of the CUE-100 series Immuno-STATs pertains to their favorable stability and manufacturability metrics as a biologic platform. These are antibody Fc fusion proteins that follow established manufacturability and CMC protocols from many decades of commercial monoclonal antibody production. The shelf stability for the CUE-101 GMP drug product, our first clinical candidate is greater than 36 months, which underscores the robustness of rational protein engineering.
Let’s move to the next slide, Slide 7. Based on the generation of a therapeutic index for IL-2 by selective targeting of Teva-specific T cells, we believe that the CUE-100 series has the potential to be the best-in-class IL-2 modality for cancer immunotherapy. As shown here, the improved safety and tolerability coupled with the antitumor T cell selectivity possessions the CUE-100 series in a significantly different bracket when compared to all other IL-2 variants that are being pursued, none of which are selected for the tumor-specific T cells. In fact, most of the focus of other IL-2 variants has been on modulating IL-2 receptor interactions with little thought towards antitumor T cell selectivity. This lack of biological relevance will continue to generate suboptimal clinical outcomes as recently evidenced with the clinical data sets from the recent trials from the PEGylated IL-2 and the non-alpha IL-2 modalities.
Finally, let’s move to Slide 8 that highlights supportive data for biological selectivity and activity of the IL-2-based CUE-100 series. The panel on the left shows selective engagement of the CUE-100 series immuno stat with an antigen-specific T cell. These data were generated by the lab of Dr. Michael Dustin at the University of Oxford. Dr. Dustin has been ion in describing the T cell immune synapse that leads to downstream activation and effective function. As shown here, the CUE-100 series immuno-STAT only forms an immunological synapse shown in green with the antigen-specific T cells were in both the TCR and IL-2 signals are operational. The same molecule with an irrelevant T cell as shown in the bottom left panel demonstrates no immune synapse in absence of TCR engagement.
The middle plan note shows selective expansion of tumor-specific T cells from primary human blood samples, while no off-target effects are noted with irrelevant T cell specificity. This is exactly in line with the molecular design of the drug that is selective expansion of tumor-specific T cells while sparing all other nonspecific T cells. The panel on the right shows intratumoral infiltration and expansion of tumor-specific T cells in an HPV-driven cancer model in mice. Note that in this study, not many T cells are evident in the vehicle-treated mice or in mice treated with the anti-PD-1 antibody alone.
In contrast, a significant number of T cells are present after monotherapy with CUE-100 series Immuno-STAT and this population is further enhanced in combination with anti-PD1 antibody treatment. We believe disability of the CUE-100 series molecules to turn a cold tumor hot by selectively activating the right T cells is a key differentiating feature of our drug design. Similar observations are also evident from the early emerging data from the ongoing mechanistic clinical trial with CUE-101 in a neoadjuvant setting in locally advanced head and neck cancer patients.
With that background on our differentiated mechanism for IL-2 targeting, I’d like to now pass the call to Ken Pienta and Matteo Lebeseti to share the exciting clinical data from the ongoing trials with head and neck cancer patients with our lead clinical candidate, CUE-101.
Ken?
Ken Pienta
Thanks, Anish. As shown on the next slide, data from the ongoing clinical trials with CUE-101 as monotherapy and in combination with pembrolizumab have provided clinical proof-of-concept or POC and derisking of the Immuno-STAT platform. We’re pleased to be presenting our updated data from the ongoing CUE-101 Phase I trial, as both a single-agent monotherapy and third line and beyond patients as well as the encouraging emerging data from the combination study with pembrolizumab in first-line patients.
As previously and consistently stated by us, we believe CUE-101’s mechanism of action as evidenced by the ongoing data generated to date provides effective and tolerated dose levels enable selective stimulation of tumor-specific T cells. — recurrent head and neck cancer is a tough and curable disease. The data we have observed throughout the monotherapy trial enhances our confidence that CUE-101 is stimulated cancer-specific T cells in a subset of these patients with resulting antitumor effect. Furthermore, and more importantly, we continue to observe an evolving trend of enhanced survival.
Key observations in patients treated with CUE-101 monotherapy in third line and beyond include as detailed on Slide 10, and demonstration of a single agent — a demonstration of single-agent antitumor efficacy, evidenced by RECIST based PR and durable stable disease in third line and recurrent metastatic head and neck squamous cell carcinoma and a median overall survival benefit emerging from the survival follow-up in the RP2D cohort. The robust data on CUE-101’s activity in monotherapy and in combination with pembrolizumab has triggered the granting of Fast Track designation status for the treatment of patients in both first and third line setting.
As shown on Slide 11, CUE-101 demonstrates well-behaved pharmakinetics with low interpatient variability at the recommended Phase II dose of 4 mgs per kg. Exposure is maintained throughout multiple cycles of treatment without any attenuation of PK parameters consistent with the lack of clinically relevant immunogenicity. CUE-101 treatment results in sustained increase in NK cells, a positive attribute of an antitumor response as the NK cells may assist in tumor killing. And as you can see in the lower left panel with only a modest and transient increase in Tregs.
As shown in the middle panel, we have observed robust expansion of tumor-specific E7 reactive T cells in the peripheral blood of patients as early as 1 week after administration of CUE-101. In the right panel, paired and post-treatment biopsies demonstrate an increase in tumor-infiltrating T cells and tumor necrosis. In addition to the favorable PK and PD just described, patients with advanced HPV-positive head and neck squamous cell cancer, we are experiencing treating in patterns of clinical benefit.
The examples are shown in the next slide, Slide 12. Patient A experienced a durable partial response with an approximately 60% reduction in tumor burden that was evident starting at 6 weeks after 2 cycles of CUE-101. And lastly, close to 1 year. Patient B who remains on treatment at the present time, has had stable disease with tumor burden reduction of approximately 20% observed at week 48 and notably complete disappearance of HPV cell-free circulating tumor DNA in the blood observed at week 6 and maintained. — the undetectable HPV CD&A is an increasingly recognized biomarker of disease activity and suggests the possibility of a pathologic complete response and cure in this patient who will likely have a surgical resection of their solitary cancer lesion early next year.
Patient C has experienced tumor reduction after a prolonged period on the drug, where no resist based objective response was initially observed by Imagin. And this patient treated with C101an2mg/pkg, we can see that the first several months appear to demonstrate tumor growth even beyond the 20% terrestrial used by RECIST criteria. However, based upon the overall clinical status, the patient continued on treatment. After approximately 6 months, the tumor began to shrink and the patient remains on therapy 14 months after starting treatment with CUE-101. This observation consistent with observations made by others that demonstrates that the kinetics of T cell antitumor activity may manifest over a long period of time.
The next slide, Slide 13, conveys our ongoing survival swimmer plot for the 20 patients dosed at the RP2D of 4 mgs per kg. The emerging ethylene Myer estimate of a median overall survival of greater than 13 months compares favorably to the survival of approximately 8 months observed in patients treated in the second line in OE the KEYNOTE-040 trial of pembrolizumab. As any experienced oncologist understands the survival in third line treatment is expected to be less as the disease is further developed and become more unstable. Our continued evolving data supports the premise that treatment with CUE-101 is clearly trending to increase survival in the third-line setting for patients with head and neck cancer. This data has encouraged our principal investigators, and they are certainly aligned with our position that this provides us with a promising path forward to a registrational trial.
The demonstration of monotherapy activity bolsters our belief that we should see complementary mechanistic effects in combination with pembro. As a reminder, the data from is treated in monotherapy clearly supports that CUE-101 increases the number of antigen-specific T cells. It is likely that these T cells will have greater freedom to kill with concurrent inhibition of the PD-1 pathway, a major mechanism used by cancer cells to prevent immune mediated killing.
I will now pass the call to Matteo to provide an overview of the exciting emerging data and clinical efficacy of CUE-101 in combination with pembro. Matteo?
Matteo Levisetti
Thanks, Ken. As shown on Slide 14, even at our starting dose of 1 mg per kg, we observed a patient with durable stable disease. At 2 milligrams per kilogram, we observed a patient with durable stable disease and a patient with a deep partial response who continues on therapy today. At the presumed recommended Phase II combination dose, we have not only not observed any DLTs. We have observed a 40% objective response rate with 4 now confirmed partial responses and another 4 patients with stable disease that are currently being monitored on the trial. This compares favorably with the reported overall response rate of single-agent pembrolizumab of 19% in the first-line treatment setting as observed in the KEYNOTE 48 trial.
Let me show you 2 examples of these partial responses. Slide 15 shows the patient from Cohort 2, demonstrating a decrease in all 4 of their target lesions, including 2 liver lesions as seen on the 2 scans on the left. I want to emphasize that this is not just shrinkage in lymph nodes, but shrinkage of visceral metastatic tumor disease in the liver. On the upper right side, the graph depicts the absolute measurements of the 4 target lesions with the best overall response of approximately 70%. To any oncologist, this is a significant and meaningful response. This patient has also demonstrated a clearing of the circulating cell-free HBV DNA, which is ongoing. As mentioned before, circulating cell-free HPV DNA continues to be developed and used by our principal investigators as a potential surrogate for response.
As shown in Slide 16, one of the patients with a confirmed partial response from Cohort 3 also demonstrated reductions in all 4 target lesions, including 2 prince lung lesions as well as clearing of their circulating cell-free HPV. As you can see on the scans on the left, target lesions 3 and 4, both are very substantial parental metastatic disease lesions in the lung, decreased in size by greater than 60%. The absolute measurements of the 4 target lesions are depicted in the right upper panel. And as we have seen in the last patient, this patient completely cleared their tumor DNA from the blood at a time concurrent with the observed RECIST response.
In the next slide, Slide 17, we see that all of the patients treated in the combination trial are still alive, 5 of whom have already passed the median overall survival observed in the KEYNOTE-48 trial, which was 12.3 months. We also anticipate an increase in progression-free survival as the data from the 4 mg per kg plus pembrolizumab cohort matures. Taken together, the observed doubling of overall response rate, 40% compared to the historical 19% observed in KEYNOTE-48 with pembrolizumab monotherapy, along with an increase in median PFS will expand patient reach and may provide an attractive therapeutic option for patients with the recurrent metastatic head and neck squamous cell carcinoma in the first line setting.
A high-level perspective of study designs to support approval of both monotherapy in combination with pembrolizumab is presented on Slide 18. We are excited by the preliminary data in the ongoing monotherapy and combination trial and plan to get clarity on the registrational path to approval for both lines of therapy. The recent granting of Fast Track designation further underscores our confidence in realizing successful regulatory interactions. I’m also happy to report that we have treated our first patient with CUE-102, which targets Wilms tumor 1 positive tumors in the trial that is enrolling patients with advanced colorectal, gastric, pancreatic and ovarian cancers.
As shown on Slide 19, CUE-102 and CUE-101 shared 99% amino acid sequence identity. This enabled us to significantly decrease the development time and cost of CUE-102 as we were not required by the FDA to repeat IND-enabling toxicology studies for CUE-102, and we are also able to initiate the Phase I dose escalation study at 1 mg per kg, the dose at which we observed clear signs of biologic activity with CUE-101.
As Slide 20 shows, we are performing the CUE-102 dose escalation study in colon, gastric, pancreatic and ovarian cancers. This design offers us the ability to do monotherapy expansion studies in any or all of the indications being evaluated in the dose escalation phase of the trial. The trial is actively accruing and will be open at 15 sites around the United States. We plan to present additional data at an upcoming medical meeting.
I will now turn the call over to Anish to talk more about our pipeline. Anish?
Anish Suri
Thanks, Matteo. And moving on to the next slide. As you heard from the clinical update, and as shown on this slide, we believe the clinical derisking by CUE-101 has essentially derisked our entire platform. As noted by Matteo, the recent IND acceptance for CUE-102, targeting Western underscores the strategic advantages of platform derisking accomplished by CUE-101, which also highlights the resource time and operational efficiencies. Furthermore, we believe the modularity of our platform, coupled with the clinical validation positions us to generate a rich repository of therapeutic molecules targeting many cancers. Some examples of additional tumor antigens that can be effectively targeted such as mutated KRAS or MAGE-A4 or pram are shown here.
Furthermore, to extend the application of our platform to incorporate multiple T cell epitopes or even personalized neoantigens we have created the NeoStat framework with an empty HLA molecule to which we can chemically conjugate any given tumor epitope. Here again, the core IL-2 variant and valency is conserved. — the Neosat platform expansion realizes significant time and cost efficiencies by having an off-the-shelf approach to selectively target multiple tumor antigens across many cancers. As one evaluates the potential of IL-2 for cancer immunotherapy, we believe our platform has cracked the code for selective targeting of this important cytokine to the tumor-specific T cell repertoire.
With that, I’ll now turn the call over to Kerri to give a brief financial update. Kerri?
Kerri Millar
Thanks, Anish. Turning on to Slide 22, I’d like to provide a brief update on our financial results for the 3 months ended September 30, 2022. The company reported collaboration revenue of approximately $68,000 and $2.4 million for the 3 months ended September 30, 2022 and 2021, respectively. Research and development expenses were $7.6 million and $11.3 million for the 3 months ended September 30, 2022 and 2021, respectively. The decrease was primarily due to green cases in laboratory and drubsextons manufacturing costs, employee compensation, licensing fees and rent. General and administrative expenses were $3.5 million and $4.1 million for the 3 months ended September 30, 2022 and 2021, respectively. This decrease was due primarily to a decrease in stock-based compensation and rent professional and consulting fees incurred during the third quarter of 2022 as compared to the same period in 2021.
We ended the quarter with approximately $59.1 million in cash, cash equivalents and marketable securities and working capital of approximately $51.5 million. Earlier today, we announced that we had entered into a securities purchase agreement with certain accredited investors for $30 million private investment in public equity or a pipe financing. We believe our cash and cash equivalents and marketing securities as of September 30, 2022, along with the $30 million that we will receive from the pipe financing will allow us to support the development of our Immuno-STAT platform, including the clinical development of CUE-101 and CUE-102 into 2024.
I’ll now turn the call back over to Dan for closing remarks. Dan?
Dan Passeri
Yes. Thanks, Kerri. With the recent financing, extending runway upon closing, combined with the supportive and promising data from our ongoing clinical trial, we’re now able to focus on core strategic initiatives to further enhance our competitive positioning to optimize shareholder value.
The clinical data recently reported at SITC enhances our confidence in the breakthrough potential of our platform and the transformative nature of our approach to selectively modulate disease-relevant T cells directly in the patient’s body. We believe we’re now very well positioned to take the company to the next level and emerge as a leading provider of effective and well-tolerated T cell engages with the potential of transforming cancer therapy. In the near term, we’re focused on several core corporate development catalysts and strategic initiatives to further enhance our competitive positioning — primarily among these core initiatives, the following milestones to enhance shareholder value, as shown on the next slide.
With CUE-101 monotherapy expansion cohort and third line and beyond refractory and metastatic HPV positive head and neck cancer patients will have mature median overall survival data by the end of this year with a potential registration trial being defined mid-next year. With CUE-101 plus pembrolizumab combination expansion cohort, we anticipate reporting on preliminary overall response rate in the second quarter of next year. On the full 20 patients with a potential registration trial being defined in the second half of the year. We are highly encouraged by the data reported at SITC on the first 10 patients and look forward to reporting on the full 20 of the 4 mg per kg cohort.
Again, to remind you, we believe the data reported to date supports the premise that CUE-101 as representative of the Immuno-STAT platform CUE-100 series demonstrates the potential of expanding patient reach and therapeutic benefit of checkpoint inhibition, placing us in a strategic position for corporate partnering. The Q102 monotherapy dose escalation trial is ongoing with 102 targeting Wilms Tumor 1 expressing cancers. The evidence of clinical activity should be a catalyst for further validation and value enhancement of our platform. Data from this dose escalation should be reported by mid-2023, with significant potential market opportunities and WT1-positive cancer indications.
We believe the differentiated therapeutic potential of the IL-2-based CUE-100 series as evidenced by our current data sets will further catalyze significant business development and corporate development opportunities for pipeline expansion addressing hematologic and solid cancers. We look forward to providing ongoing updates in the coming months and want to thank our shareholders for their support and shared vision and the potential of Cue Biopharma to transform the treatment of cancer, and we want to extend our gratitude to our employees, the Board of Directors and most importantly, we want to thank the patients and their families for participating in our trials.
Thank you all very much for your attention and interest, and I’d like to now turn the call back to the operator for questions. Operator?
Question-and-Answer Session
Operator
Thank you, sir. [Operator Instructions] The first question we have is from Reni Benjamin from JMP Securities.
Reni Benjamin
Congratulations on the data update at SITC. Maybe just to start off, can we talk a little bit, especially in the combination study, what are the typical treatments that you’re seeing kind of post progression? And are you seeing in these first 10 patients any sort of recycling of checkpoint inhibitors and potentially getting a subsequent response in patients who maybe didn’t have that before.
Ken Pienta
So Ren, this is Ken. Thanks for the question. So the reality is it’s — we don’t know. What’s going on with those folks. This data we’re collecting, but we really can’t give you an update on what other therapies they might be getting afterwards. It’s across multiple sites, and there’s no specific regimen that these folks are going to.
Reni Benjamin
Got it. And then either for the monotherapy or the combination study. I don’t think I saw this number, but I’ll just ask it anyway. Do you have a median duration of response for either of those two?
Ken Pienta
No. We don’t — we haven’t calculated that because we won’t calculate that until we get the final survival data in the monotherapy, and it’s just too early to do that in the combo.
Reni Benjamin
Got it. And then just switching gears real quick to the neoadjuvant study. Can you talk a little bit about maybe how many patients have been enrolled? And have you been successful in obtaining biopsy samples. And is there any color that you might be able to provide from sort of the initial — or any initial takeaways?
Matteo Levisetti
Yes. So the neoadjuvant study is really a spectacular opportunity for us to really examine in the tissue itself, the effects of CUE-101 therapy. So we’re obtaining in the neoadjuvant setting pre- and post-treatment biopsies. We’ve treated close to 10 patients to date. The preliminary data that we have in these paired biopsies demonstrates some of the findings that we’ve observed in patients i.e., we have observed increases in NK cells, pre and post treatment. We also observed findings consistent with the increase in TIL, or tumor infiltrating lymphocytes that we’ve observed in the paired biopsies obtained in the patients in the CUE-101 trial.
Reni Benjamin
I’ll jump back in the queue.
Operator
This concludes our question-and-answer session. I would now like to turn the conference back over to Dan Passeri for closing remarks. Please go ahead, sir.
Dan Passeri
Okay. Again, we want to thank everyone for your time and interest in our ongoing progress, and we look forward to providing you with updates in the coming months. Thank you, again, and take care, everyone.
Operator
Thank you, sir. Ladies and gentlemen, that then concludes today’s conference. Thank you for joining us. You may now disconnect your lines.
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