Agenus Inc Q1 FY2020 Earnings Call

Good morning, ladies and gentlemen. Thank you for standing by. And welcome to the Agenus First Quarter 2020 Conference Call. At this time, all participants are in a listen-only mode. Please note, this event is being recorded. I would now like to turn the conference over to Dr. Jennifer Buell, President and Chief Operating Officer of Agenus. Dr. Buell, please go ahead.

Thank you. Thank you, Ceanne. Today’s call is being webcast and will be available on our website with our accompanying slide material for replay. Before we start, we’d like to remind you that this call will include forward-looking statements, including statements regarding our clinical development and regulatory plan and timeline, as well as timelines for data release and cash projection. These statements are subject to risks and uncertainties, and we refer you to our SEC filings for more details on these risks. As a reminder, this call is being recorded for audio broadcast. I’m Jennifer Buell, President and Chief Operating Officer of Agenus and joining me today are Dr. Garo Armen, Chairman and Chief Executive Officer; Dhan Chand, Head of Drug Discovery, Dr. [Indiscernible], Lead Scientist for Allogeneic iNKT Cells and Christine Klaskin, our Vice President of Finance. I will now turn the call over to Garo.

Thank you very much, Jen. And a special thank you to all of you for joining us during this time, when the world has turned upside down because of the COVID-19 pandemic. I hope you and your families are safe and well. Our team at Agenus has found a productive way to adapt in this new norm. At the earliest signal of the pandemic, our team reacted swiftly and took proactive measures to protect our employees, their families, and our business. As a result, our operations in Berkeley, Lexington, and Cambridge have remained open with a rotating work schedule for safety, and with limited interruption to our key priorities. We operate with approximately one-third of the workforce on site and the remainder working from home. And that has not disrupted any part of our operation so far. Importantly, to the best of our knowledge, none of our employees have been infected with the virus so far, and we’d like to keep it that way. Earlier this year, we projected receipt of approximately $60 million in cash milestone payments for 2020. We’ve already received $15 million based on the sales of Shingrix, which has our QS-21 adjuvant in it. However, given the environment, the remaining $45 million is uncertain because of the disruptions caused by COVID. Hence, we’ve taken measures resulting in annualized cost savings of approximately $50 million. These savings are driven by reductions in both external and internal expenditures, and importantly, they will result in a slowdown of several programs, but we do not expect these steps to affect our near-term or medium-term commercial launch prospects. We also expect that our high-priority clinical development and research programs will proceed as planned. Our proactive measures are designed to deliver our key milestones this year, including plans for our BLA filings, our acceleration of clinical development of our next-gen multipurpose CTLA-4 molecule 1181, about which you will hear much more from Dr. Buell, and our advancing of iNKT cell therapy to the clinic for the treatment of cancer and COVID-19 patients, which you will hear from Dr. [indiscernible]. She will also tell you about the advantages of our iNKT cells, including, for example, substantially reduced costs associated with cell therapy when we practice iNKTs. Additionally, you will hear that we’re advancing important programs like our TIGIT molecules into the clinic. As you know, we started this program a number of years ago, and now we’re ready to take that into the clinic. I will now turn the presentation to Dr. Jen Buell, our President and Chief Operating Officer to provide you with an update on our highest-priority programs, starting with AGEN1181, our multipurpose next-gen CTLA-4.

Thank you very much, Garo, and hello everyone. As Garo mentioned, I’ll start by providing an update on AGEN1181, and there’s a summary of this program on slide 4 that we’ll review today. This molecule is familiar to many of you. As Garo said, it’s our multifunctional T-cell antibody, which also binds to CTLA-4. Importantly, this molecule’s Fc region is engineered. We did this because we knew some key features this engineering could provide. Those features included increased immunogenicity, increased T-cell activation beyond which we see with first-generation CTLA-4, superior combination with PD-1, as you see on slide 4, as well as important potential safety benefits, such as a reduction in endocrinopathies for patients treated. We expect to increase or broaden the patient population of responders, patients who will respond or are unlikely to respond to a first-generation CTLA-4 due to a genetic polymorphism, affecting about 40% of the population. What we’re going to talk to you about today, our data from this trial will show that as the molecule has been designed to benefit patients who harbor this genetic polymorphism, patients are benefiting from AGEN1181. We have also seen no endocrinopathies, none of the safety-related side effects that we see with Yervoy related to hypophysitis or otherwise, which is a very important feature. Fc engineering is something that we know to be really quite important. We’ve published on this technology and our techniques on our AGEN1181 molecule in Can Cell last year. We’ve also, as Dhan will speak to you today, engineered our TIGIT molecule to bring similar enhancements. We’ve shown you data that supports the benefit of this engineering. We’re now seeing data from late-stage clinical trials with an Fc-engineered HER2 antibody called margetuximab. You may be aware of some of that data. On slide 5, I’d like to summarize that AGEN1181 is advancing in a Phase 1 dose-escalation trial. This next-generation antibody has shown profound activity in the form of objective responses, which are unusual to see this early in clinical development. We’re hopeful that based on the current trends, and as patients continue on therapy, we will continue to see more patients with more durable responses. You may have heard that a number of hospitals have been converted to treat patients with COVID-19, and this could impact, of course, some clinical trials as well as patient access or patients with cancer getting access to their therapies. However, in spite of this reality, we continue to recruit to our trials without interruption. Our principal investigators have informed us that based on the data available to date, AGEN1181 has lifesaving attributes that support the continued enrollment of this trial. Today, we have a queue of patients waiting to be enrolled. You may remember, as I mentioned earlier, that AGEN1181 was deliberately designed to improve the efficacy and safety of first-generation CTLA-4. In addition, this antibody is expected to expand the patient population who will benefit. I'm now going to highlight some data that supports the design of this molecule and the activity that we’re seeing. In our dose escalation trial, AGEN1181 alone and in combination with balstilimab demonstrated a clinical benefit rate of 70%. This includes complete responses, partial responses, as well as disease stabilization of patients with late-stage cancer. During our last call, we described a patient with refractory endometrial cancer. This patient had late-stage disease and checked out all prior therapies. Importantly, she had a very poor prognosis based on an available biomarker that helps us determine a patient’s likelihood to respond to therapy. These markers include the patient being negative for PDL-1, the patient having microsatellite stable disease, which is unlikely to respond to immune therapies, and this patient had a genetic polymorphism in her CD-16 allele that rendered her unlikely to respond to a first-generation CTLA-4. In spite of these negative odds, we are thrilled to see that this patient is a confirmed complete responder on AGEN1181 monotherapy at 1 mg/kg. Now, on slide 6, I want to highlight another very exciting case. This patient is also one with refractory endometrial cancer, with a similarly poor prognostic profile, with metastatic disease in multiple locations. This patient is now also a confirmed partial response in her target lesions and a complete response in her non-target lesions. This patient responded to a very low dose of AGEN1181 in combination with balstilimab, our PD-1 antibody. If I can turn your attention to slide 7. Last week we convened with our Advisory Board. This Advisory Board is comprised of top immuno-oncology experts, some of them are specialists in the CTLA-4 mechanism, some of whom were the first to dose patients with a first-generation CTLA-4 over 20 years ago. After an extensive review session, our advisors endorsed our accelerated development path for AGEN1181, which we are now in the process of launching as we speak. For this phase of development, we will pursue a fast-to-market strategy. This means going after cancers where there are limited or no effective treatment options available to these patients. These tumors are highly prevalent or, said differently, represent large cancer market opportunities. These opportunities include PD-1 refractory non-small cell lung cancer, PD-1 refractory melanoma, and microsatellite stable tumors like colorectal cancer, as well as endometrial, which are the two cases I shared with you just a few moments ago. We’ll continue to keep you updated as these programs progress and mature. I’ll now turn to our lead program, our PD-1 program, balstilimab, which we call Bali, and our CTLA-4 program, zalifrelimab, which we call Zali. The results that you see on slide 8 show the evolution of cancer therapies for women with cervical cancer. Starting with chemotherapies on the left and VEGF inhibitors, which are still widely used despite their limited benefit. The data that we’ve presented now from our program, balstilimab and zalifrelimab, are based on a large cohort of 55 patients who had a median of 12 months of follow-up. Importantly, all responses were confirmed by an independent radiology review, which is the gold standard in assessing outcomes in cancer. We summarized our findings in a recent Agenus newsletter, which is available on our website. Notably, we have observed 14 objective responses. These include 4 complete responses and 10 partial responses in these 55 patients evaluated so far. This is a response rate of 26%. As a reference, Merck was granted accelerated approval for their PD-1 antibody based on 11 responses in 77 patients, with a response rate of 14%. As you can see here, our combination has the potential to become the most effective treatment available to patients with metastatic cervical cancer. A few comments regarding cervical cancer patients and our plan: cervical cancer is a horrifying disease, particularly for young women who come from economically disadvantaged backgrounds and have limited access to healthcare. Patients are diagnosed and treated with toxic chemotherapy, which has many difficult side effects and little clinical benefit. Their cancer ultimately progresses with little to no effective treatment options available to them, as you can see here. We’re committed to changing this reality. Data from our cervical cancer clinical trials with the Agenus Bali + Zali, our PD-1 and CTLA-4 antibodies, has shown a near doubling of responses compared to currently available treatments. Most importantly for us is that these responses are durable. These patients are not converting or progressing once they’re responding, which is incredibly important for patients. Additionally, we’re seeing patients with long-term disease stabilization who later convert to response. During our recent year-end call, we mentioned that we received Fast Track designation from the FDA for the investigation of balstilimab alone and in combination with zalifrelimab in relapsed/refractory or metastatic cervical cancer. We plan to submit our BLA filings this year, and we’ll continue to keep you informed on our progress. I’m going to wrap up with a few very exciting programs. During our recent meeting with clinical experts, they noted that we have the most productive research engine in I-O. I agree. Today, I’m joined by two of our lead scientists responsible for our next innovation expected to enter the clinic very soon. Dr. Dhan Chand and Dr. [indiscernible] are leading our TIGIT and our iNKT programs, respectively. They’re joining us here to talk about these programs today. As you know, TIGIT is shaping up as a powerful combination partner with PD-1 antibodies, especially in tumor expressing TIGIT. We’ve designed two different approaches to optimally target TIGIT. First, our Fc-engineered anti-TIGIT antibody has outperformed all tested competitor antibodies and shown superior T-cell activation when combined with PD-1 or LAG-3 antagonists. Our TIGIT bispecific molecule, AGEN1777, has demonstrated potent tumor killing as a monotherapy in difficult-to-treat cancers where PD-1 antibodies alone are ineffective. In addition to these two TIGIT antibodies, we are rapidly advancing our allogeneic cell therapy to the clinic to treat patients with cancer and to treat patients with COVID-19. We expect both INDs to be cleared shortly, and as a matter of fact, one may clear as early as this week. I note that, like us, the FDA has been working through weekends to process applications, which is very heartening during this health crisis. [Indiscernible] will tell you more about T-cells. She is trained in molecular biology and immunology and she joined us from the Harvard Beth Israel Deaconess Medical Center.

Thank you, Garo and Jen. So, in connection to the T-cells – iNKT T-cells have several advantages over other allogeneic approaches in development, including but not limited to their significant expansion capacity, their use in an allogeneic setting without requiring genetic manipulation, and their ability to suppress graft-versus-host disease. I am excited to report that our team filed 2 INDs to advance our iNKT cells to combat cancer and separately COVID-19. iNKT cells are a rare population of lymphocytes. Importantly in late-stage cancer, the frequency and the function of iNKT cells is highly correlated with overall survival. Our modified iNKTs are a natural component of the innate immune system, and their reduced numbers or function is associated with poor immune response to cancer and poor prognosis in patients with late-stage disease. You can see on slide 9 some of the notable advantages of iNKT cells. First of all, iNKT cells can penetrate into the tissue, which gives them a critical advantage to target solid tumors; there are no certified approved cell therapies. Secondly, iNKT cells can kill cancer without requiring genetic manipulation. So, employing iNKTs in an unmodified form allows patients to receive the treatment quickly and at a significantly lower cost. Third, iNKT cells are expected to target SARS-CoV-2 and cells infected with the virus. iNKT should be agnostic to mutations of the current strain and other coronaviruses. While severe complications of SARS-CoV-2 infection are characterized by life-threatening respiratory disorders and other organ failure, our allogeneic iNKT therapy, AGENT-797, is expected to help clear the virus while controlling harmful inflammation caused by the virus. Preclinical data demonstrates that iNKT activation induces a rapid antiviral response and enhances immunity to respiratory and other infections. iNKTs have also been shown to prevent lung injury in preclinical models by reducing the number of inflammatory cells, dampening inflammation and thus preventing or controlling tissue damage. This may be especially important in COVID-19. AGENT-797 could promote long-term immunity against COVID-19, which would be an important outcome to protect both recovered patients from reinfection and to protect healthy individuals from the disease. An important benefit of our allogeneic approach is its scalability. We have demonstrated that iNKT cells from a single donor are manufacturable and scalable. Based on our early process development work, we have developed a scalable process design to manufacture about 1,000 doses from a single donor. Our near-term clinical trials will help to determine the key features of AGENT-797 in cancer and infectious disease, and we are ready to quickly design optimal combinations with our cell therapy and checkpoint antibodies. My colleagues will be presenting data at AACR on our utmost combinations with key insights into the criticality of these approaches and significant differentiation that Agenus has in delivering these combinations. Thank you very much. Now, I will turn it over to my colleague, Dhan Chand, to discuss our TIGIT program.

Today, I’m excited to discuss two of our TIGIT antibodies, why they’re important and how we believe they will change the treatment paradigm. As Jen mentioned, TIGIT is shaping up as a powerful combination partner with PD-1 antibodies, especially in tumors expressing TIGIT. Our portfolio of TIGIT-targeting antibodies includes the Fc enhanced TIGIT monospecific AGEN1327 and our TIGIT bispecific AGEN1777. We believe both molecules have unique advantages over other TIGIT antibodies that are in clinical development. Since TIGIT may be new to many of you, I will describe what TIGIT is, as seen on slide 10. TIGIT is the receptor primarily expressed on T-cells and NK cells. TIGIT attenuates innate and adaptive immune responses by inhibiting the actions of T-cells and NK cells. Additionally, it increases the immune suppressive activity on regulatory T-cells. TIGIT is over-expressed in multiple tumors and is known to be a key player in driving resistance to anti-PD-1 therapy, causing tumors to grow. Locking TIGIT with antibodies like our monospecific TIGIT antibody AGEN1327 or our TIGIT bispecific AGEN1777 unleashes important immune cells such as T-cells and NK cells to kill various types of cancer. Agenus was the first to discover and report at Cancer Cell and at AACR 2019 that TIGIT antibodies require Fc gamma receptor co-engagement to promote optimal T-cell activity against tumors. Our TIGIT AGEN1327 is engineered with this Fc enhancement and has outperformed all tested competitor antibodies, showing superior T-cell activation when combined with PD-1, LAG-3 antagonists, OX40, or CD137 agonists. We presented this data at AACR 2019. Our TIGIT is an ideal combination partner for addressing non-resistance mechanisms to current checkpoint therapy and provides the potential for deeper responses. Our preclinical data with our TIGIT also showed superior tumor killing compared to competitor molecules, as seen on slide 11. We aim to maximize anti-tumor activity, similar to the robust activity observed with our Fc engineered AGEN1181 that has already shown remarkable activity in early clinical trials. Importantly, TIGIT has also been implicated as a significant target for overcoming resistance to anti-PD-1 therapy. Our bispecific TIGIT antibody, AGEN1777, is designed for use as monotherapy for tumors unresponsive to PD-1 antibodies. AGEN1777 is our first-in-class TIGIT bispecific that leverages our internal multi-specific platform to co-target another inhibitory receptor not yet disclosed, but also expressed on T-cells and NK cells. We discovered that co-targeting TIGIT with this undisclosed target using our bispecific approach provides superior immune activation compared to the combination of monospecific antibodies to the same targets. This TIGIT bispecific approach has shown potent tumor killing activity in a colon cancer model where PD-1 monotherapy is ineffective. AGEN1777 can be an important therapy for PD-1 relapsed/refractory tumors. Although PD-1 and PD-L1 antibodies have experienced spectacular commercial success, only a small proportion of patients have had sustainable long-term benefit, creating a substantial need for therapies in those who relapse or do not respond to PD-1 monotherapy. We expect to file an IND for AGEN1777 for the TIGIT bispecific by the end of 2020. There is growing conviction that targeting TIGIT will provide a breakthrough in I-O, and we are uniquely positioned with two distinct molecules on track to be launched into clinical development as early as the first half of 2021. Now, I will turn the call over to Christine Klaskin to provide a financial update.

Thank you, Dhan. We ended the first quarter of 2020 with a cash balance of $92 million, compared to $62 million at December 31, 2019. For the first quarter ending on March 31, 2020, we reported a cash burn from our operations of $32 million. Our net loss for the quarter was $45 million or $0.31 per share, which included non-cash expenses of $16 million. We generated net income for the same period in 2019 of $17 million or $0.14 per share. In the first quarter of 2019, we recognized revenue of $80 million, which included revenue related to the upfront license fee from our transaction with Gilead, in addition to non-cash royalties earned. For the same period in 2020, we recorded revenue of $15 million, primarily related to non-cash royalties earned. I’ll now turn the call back to Garo to close.

Thank you, Christine. And thank you very much to the team who explained our current state of affairs and our prospects very well. Today, we are a company of 260 persons. It’s not the number that matters; we have capabilities to innovate, to develop, to manufacture our discoveries and we’re currently building our commercial capabilities to become a fully integrated company. We have stressed all along, speed and innovation are key in our business, particularly a business that has very exciting prospects going forward. Jen Buell talked about the fact that our external advisors have commented that we may be the most innovative, productive company in the field of I-O. We can do these things because we have end-to-end capabilities from novel target discovery to full GMP manufacturing for antibodies. This has been critical to our productivity. We have brought 14 new discoveries to the clinic and launched 6 clinical trials, and we are gearing up to file our first BLA in the third quarter of this year. We’ve developed our clinical operations team and delivered the full target accrual of our clinical trials in the last three years. These may sound trivial to some, but we have delivered 11 GMP manufactured batches for our own trials and partnered programs at our manufacturing site at Agenus West. The team there has done an absolutely terrific job. As we’ve said before, we’re continuing operations with no interruptions. We have a queue of additional batches to manufacture this year. As [indiscernible] said, we have launched a cell therapy company, AgenTus, which designed a very unique allogeneic cell therapy approach with the kind of advantages we’re discussing, for example, for COVID-19; it offers potentially the capability of being an anti-viral therapy or anti-inflammation therapy, all in one, and do this with a single cell source, which means it’s an off-the-shelf cell therapy that drives costs down and, most importantly, it drives the speed of patient availability up. We’ve also talked about having generated over $540 million in cash from partnerships, collaborations, and transactions with multiple pharmaceutical companies like Gilead, Merck, GSK, and Incyte as well as UroGen, all in the last 4 years. We expect additional partnership transactions this year. We are in term sheet discussions with companies already. Given that my colleagues have done a terrific job of keeping you abreast of everything that is going on, I will stop here and entertain any questions that you may have.

[Operator Instructions] Your first question comes from Matt Phipps with William Blair. Please go ahead.

Hi. This is Hunter on for Matt. Just a couple of quick questions. I was wondering if you could provide some color on the unmentioned part of the TIGIT bispecific. I know you did mention specifically what the other part was, but maybe sort of the mechanism that you’re targeting there. And then, as just to follow up, I think previously you had mentioned that with the lowest dose of 1181, you had a pending response. I was just wondering if that was still pending or a confirmed response. Thank you.

Let me just make a general comment, and then I’ll turn it over to Dhan and then to Jen to address the 1181 question. As some of you may know, we have a very sophisticated competitive intelligence capability at Agenus, and this has been a critical component of our decision-making and strategy that drives from research strategy onwards. I have mentioned that we’ve been working on TIGIT for quite some time, but all along, we have evaluated what is happening with competitors out there in the TIGIT field and what we can add incrementally or leapfrog the other programs, so that we come up with an advantage that offers benefits to our Company, but also importantly to patients. Our TIGIT program has been specifically designed to address what is needed and what advantages we can provide. So, Dhan will answer your question more specifically on that.

Thank you for the question. The second target in our bispecific, which we have not yet disclosed, is a first-in-class target expressed on T-cells and NK cells. We have discovered that the best way to target this first-in-class undisclosed target is to do so in the form of a bispecific that includes TIGIT. Overall, what we have discovered is that when we co-target TIGIT and this yet to be identified receptor, we see superior activity compared to that of monospecific approaches to each of these targets. I would like to emphasize that the second target, which we have not yet disclosed, is a first-in-class target.

Regarding 1181, we presented data on two different patients. Both of the responses have been confirmed by independent radiology review.

I might add, they have been continuing. One of the hallmarks of immunotherapy for everybody is the benefit of having responses last for a long time or convert to a curative outcome. Everything we're seeing from our first-generation products, Bali and Zali, to our second-generation product so far, 1181, are indicative of lasting responses that may convert into a curative outcome. Next question, please?

Your next question comes from Mayank Mamtani from B. Riley. Your line is now live. Please go ahead.

Thanks for taking my question. Congrats team on the progress. And I appreciate the efforts you’re putting in on COVID-19. Just Zali Bali. On the BLA filings, could you just remind us, it seems like the clinical section is full; are you just working on the non-clinical side? What are some of the other things you have to do if there is an FDA meeting before you’re able to submit the BLA? Could you just remind us on the process?

Thanks very much, Mayank, for the question. Nice to hear you. Regarding the process, so we’re pursuing rolling submissions, which include meeting with the FDA to discuss different components of the filings. For elements like our manufacturing component, the quality, the agency has remarked on the quality of our manufacturing and the completeness of our prior interactions for INDs and otherwise. We have already engaged and discussed and are very confident in the completeness of several modules, including manufacturing. On the clinical side, we’re continuing to collect data. We completed accrual. Patients with refractory cervical cancer will progress in a relatively short amount of time. We’ll have a good sense of our complete cohorts very actively, and we’re in the process of analyzing the data for readiness for the submission. We’ve had a series of interactions with the agency because we accelerated this program from a first-in-man study to a Phase 2 expansion in refractory cervical cancer. At that point, we met with the agency and discussed our strategy and trial design. It’s a matter of continuing to engage them to provide updates on each of our molecules, our pharmacology, nonclinical, manufacturing, and clinical, with some of which has been completed, and a couple of which are continuing until our filing date. We’ll be filing in the second half of this year, as Garo mentioned.

Great. On 1181 about the recent Advisory Board meeting you had. Could you just talk maybe qualitatively to the stable disease that you’re seeing? Are these in lung and colon cancers that are informing your next choice to go into these bigger indications? Any color there would be great.

I’ll be thoughtful about my response, because we are anticipating some upcoming data presentations at major medical conferences. What I will share are some observations. This is a solid tumor study, and we have represented cancers in our trial, including lung and melanoma. We’ve seen activities beyond those indications as well, including other gynecologic cancers like ovarian, for example. An important case being described in detail soon is a gynecologic case with long, durable disease stabilization, nearly a year. This is disease stabilization that has not yet met the RECIST criteria for response, but looks very active. Similar trends in other tumor types are also represented, showing disease stabilization in the majority of patients treated. I’ll leave it at that so we don't restrict ourselves to what we can present at upcoming conferences.

I understand and appreciate the qualitative color. One final one on the COVID-19 efforts you have. It seems like you’re nearing IND acceptance. Any color on how you’re thinking to develop and any institutions you may decide to partner with? There are certain hotspots that could benefit from a trial like this. Any color there?

We need to first get signals from the clinic. The objective of our first trial is to look at various blood markers and see how patients respond to therapy in a dose escalation study. It’s premature for us to define next steps beyond this exploratory clinical trial.

To clarify, are these going to be non-severe COVID-19 patients initially?

The cells will be in the New York population. We have collaborators at New York hospitals who have been at the frontline of this. The cells will explore how they can mitigate the virus and dampen harmful inflammation experienced after viral clearance. Both features are critical. We will first explore them in a more severe setting, evaluating cell persistence, activity, and viral clearance.

Great. Just last thing on financials. I believe there were two different tranches of milestones you were anticipating: one Shingrix-related and one related to some pipeline molecules with Gilead. Any color on what you are seeing that might be addressed for the remainder of the year?

We have received the first tranche of the GSK Shingrix royalty milestone of $15 million. However, given GSK's guidance, which suggested a significant downtick in Shingrix revenues going forward, it’s unlikely we will meet the revenue milestone that would have driven the second payment for us. There are two sets of milestone payments associated with separate companies. We’ve adopted a conservative posture and planned for no milestones. This doesn’t mean we won’t receive them; it just means we’re planning conservatively. We have initiated $50 million worth of annualized savings that are already in place. This will provide us with comfort. Regarding new potential collaborations, we are in term sheet discussions with two separate parties. I expect that this will lead to upfront cash payments helping manage our cash for the balance of the year and into next year.

I appreciate the color. Looks like it will be a wash. Thank you.

Thank you very much. Any other questions? That concludes our call. I may want to turn this over to Ceanne, who will do a stellar job of concluding remarks. Ceanne, would you end the conference?

Thank you. The conference has now concluded. Thank you for attending today’s presentation. You may now disconnect.