Earnings Transcript for ADXS - Q2 Fiscal Year 2020

Operator: Greetings and welcome to the Advaxis, Inc. Conference Call to discuss Second Quarter 2020 Financial Results and Business Update. At this time, all participants are in a listen-only mode. A brief 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 Tim McCarthy of LifeSci Advisors. Thank you, sir. You may begin.

Tim McCarthy: Thank you, Michelle, and thank you everyone for joining us for today's conference call to discuss Advaxis second quarter 2020 financial results and business update. If you have not seen today's press release, please visit Advaxis’ website at www.advaxis.com. Before turning the call over to Ken Berlin, Advaxis’ President and Chief Executive Officer, I would like to remind you that during this conference call, Company will make projections and forward-looking statements regarding future events. Any statements that are not historical fact including but not limited to statements that contain words such as will, believes, plans, anticipates, expects, estimates, and similar expressions are forward-looking statements. We encourage you to review the Company’s SEC filings, including without limitation, the Company’s Forms 10-K and 10-Q which identify the specific risk factors that may cause the actual results or events to differ materially from those described in these forward-looking statements. Advaxis expressly disclaims any intent or obligation to update these forward-looking statements except as otherwise maybe required under applicable law. With that, I’ll turn the call over to Ken Berlin. Ken?

Ken Berlin: Thank you, Tim, and welcome everyone to our conference call to discuss Advaxis’ second quarter 2020 financial results and to provide a business update. Joining me on today's call are Dr. Andres Gutierrez, Chief Medical Officer; and Molly Henderson, Chief Financial Officer. We will all be available during the question-and-answer session at the end of our prepared remarks. To start, I'd like to provide an overview of our focused strategy at Advaxis, centered on our proprietary Listeria monocytogenes or Lm based immuno-oncology drug candidates. Our Lm immunotherapy platform utilizes live attenuated Lm, which are bioengineered to secrete tumor-specific antigen/adjuvant fusion proteins to engage the patient's immune system to destroy tumor cells. Our drug constructs developed from this platform have the potential for comprehensive immune stimulation by harnessing a pathogen-like response against cancers. We believe our Lm-based drug constructs attack cancer in three distinct ways. First, our Lm drug constructs alert and train immune system by activating antigen presenting cells or APCs. Second, our constructs attack the tumor directly by generating strong cancer specific T-cell responses. And third, they break down the suppressive tumor microenvironment, enabling activated T-cells to directly attack tumor cells. We have applied our Lm technology platform across a broad range of clinical programs where drug constructs that target certain tumor-specific and viral-specific antigens, as well as new antigen targeted drug constructs that are personalized, based on an individual specific mutations, as well as off-the-shelf tumor type specific. Through these diverse approaches, nearly 500 patients have been dosed across HPV associated cancers, prostate cancer, non-small cell lung cancer and other tumor types. Our results have provided significant learnings in terms of safety, efficacy and mechanism of action that help inform our more focused clinical plan, which maximizes the likelihood of success. We see a significant opportunity to apply our differentiated approach to help a broad range of patients, especially those patients who are non-responsive or refractory to currently available treatments such as checkpoint inhibitors. And we'll continue to exercise strong financial discipline, as we pursue this plan. Later on in the call, Andres will provide more detailed clinical updates. But before that, I'd like to provide some brief program highlights. Advaxis has pursued two main approaches with its Lm technology, single antigen constructs, such as ADXS-PSA and multiple antigen approaches like our NEO and HOT programs. And before I moved to discuss or exciting recent results with the ADXS-503 drug constructs from our HOT program, I'd like to remind you of our early results from our ADXS-PSA and ADXS-NEO programs, which have provided important proof-of-concept for the HOT program. In the Phase 1/2 clinical trial for our ADXS-PSA construct, studied in combination with KEYTRUDA, a leading checkpoint inhibitor, we were pleased to see a prolongation of survival in men with late-stage prostate cancer with a median overall survival of 33.7 months in 37 patients in the combination arm of this study. In a subset of these patients, dosed with prior docetaxel and visceral metastases, we observed a median overall survival of 16.4 months, which compares quite favorably to best supportive care on the one hand and to KEYTRUDA alone on the other hand. In addition, we saw no additive toxicities in this combination. To put these results in perspective, it’s important to note that these meaningful impacts on survival have not been previously observed with immunotherapy in this advanced patient population. These are intriguing results, and we are assessing next steps for the ADXS-PSA program. We will keep you updated as we have more clarity on our path forward with this program. The ADXS-NEO approach on the other hand was designed to present a large payload of neoantigens to stimulate a targeted patient-specific T-cell response against cancer cells. The ADXS-NEO Phase 1 study provided us with immunogenicity data, which showed that a neoantigen approach delivered through our Lm platform was capable of generating specific T-cell responses against hotspot mutations, as well as other personal neoantigens and demonstrated the potential to control tumor growth with our first multi-antigen drug construct. While we ultimately decided not to pursue the ADXS-NEO program due to the limitations associated with truly personalized neoantigen therapies, the NEO study results provided valuable insights and proof of mechanism for how we could apply neoantigen-based therapies to a broad patient population with a particular tumor type, using an off-the-shelf approach. The results from our PSA and NEO studies have laid a strong foundation for our HOT program. First, the PSA study demonstrated safety and clinical activity of one of our Lm-based drugs when combined with a checkpoint inhibitor. Second, the NEO study demonstrated strong and rapid immunogenicity with multiple neoantigens, including hotspot mutations. While NEO therapies, specifically checkpoint inhibitors, have changed the treatment landscape for some solid tumors, the fact remains that the vast majority of patients will not respond to these therapies or will eventually develop resistance to treatment and ultimately progress. There is a tremendous opportunity to both, improve the proportion of patients who may benefit from these treatments and also increase the durability of responses to these treatments. We believe the drug constructs in our HOT program have the potential to help address this large unmet need. Our HOT program consists of more than 10 different drug constructs using a cancer type specific off-the-shelf, neoantigen-based approach, the drug constructs in the HOT program target somatic mutations or hotspots that commonly occur in the cancer types we are targeting. And added to these hotspots are tumor-specific oncofetal antigens and cancer testis antigens or CTAs, which have been modified. With this broad and diverse number of targets in each HOT drug construct, the constructs have a greater likelihood to generate potent tumor-specific and high-strength killer T-cells in nearly all patients with the tumor type being targeted by that specific HOT construct. Because hotspot mutations in OFA, CTA proteins play critical roles in oncogenesis, we believe targeting all of these at the same time, provide the best opportunity to kill tumor cells and improve clinical responses. A real differentiator of our approach is that we combine high avidity targets that are expressed in all or most patients with specific cancer type into an off-the-shelf treatment that can be readily available to a broad patient population. Essentially, we can provide the benefits of a Neoantigen-targeted therapy without the manufacturing challenges and long treatment wait times associated with personalized neoantigen approaches. And now, I will discuss why we are excited about the early results we have seen in our HOT program. Our ongoing Phase 1/2 study investigating ADXS-503, our first HOT candidate in the clinic in patients with non-small cell lung cancer is evaluating ADXS-503 both as monotherapy and in combination with Merck’s anti-PD-1 therapy KEYTRUDA. In May, we reported updated data from the trial, which showed sustained clinical benefit in patients -- in the first two evaluable patients treated with ADXS-503 in combination with KEYTRUDA, including one partial response with tumor reduction of approximately 60% and the other patient achieving stable disease with a 25% reduction in a target lesion. While we were encouraged with our monotherapy data, which showed 3 out of 6 evaluable patients achieving stable disease and a dose escalation part of the study, our combination arm results are particularly exciting. These results have been sustained now out to 26 weeks -- excuse me, now out to 16 weeks and 25 weeks respectively. And these were achieved with a manageable safety and tolerability profile. Most importantly, the responses seen in the combination arm were achieved in patients who had recently progressed after two years of therapy with KEYTRUDA and who had achieved only stable disease as their best response while on KEYTRUDA. These data suggest that the addition of ADXS-503 to KEYTRUDA has the potential to restore or even enhance sensitivity to checkpoint inhibitors. In order to understand the mechanism of action for ADXS-503 drug construct, we are doing comprehensive immune and biomarker profiling. The early results of this work, thus far, support the clinical results we have seen to-date. From an immunogenicity perspective, we have observed activation of cytotoxic and memory CD8+ and CD4+ T-cells. Specifically, in each of the first six patients evaluated in Part A, and in one patient evaluated in Part B of this study, CD8+ T-cells were generated. In addition, antigen spreading was confirmed in 5 of 7 evaluated patients, meaning that for the vast majority of patients tested thus far, we were able to generate CD8+ T-cells against epitopes that were not incorporated in ADXS-503. This is important because antigen spreading improves the potential for killing tumor cells. These results taken together demonstrate on mechanism activity of ADXS-503 and are therefore very encouraging. We're looking forward to exploring this further through our relationship with Personalis, announced in February, under which we will utilize Personalis’ ImmunoID NeXT Platform to conduct comprehensive tumor genomic profiling to enable the identification of predictive composite biomarkers and/or signatures of response, as well as a broad evaluation of potential mechanisms of therapy resistance within the tumor cells. These initial clinical and biomarker data have enhanced our confidence in our strategy to focus on drug candidates within our HOT program. We look forward to moving our next HOT drug construct, ADXS-504 in prostate cancer, into the clinic. The IND for ADXS-504 was cleared earlier this year, and we expect to dose our first patient in this study in the fourth quarter of this year. Before I turn the call over to Andres, I'd like to express my gratitude to the Advaxis team, our partners and trial investigators, and especially our patients who are at the very heart of our mission at Advaxis, which is to improve the lives of people with cancer and their loved ones. The dedication of our team and collaborators to this cause has allowed us to build some very nice momentum in our clinical programs, and we look forward to providing our shareholders with timely updates as we continue to execute on realizing the potential of our Lm platform. Andres?

Andres Gutierrez: Thanks, Ken, and thank you all for joining us today. As Ken described, we are encouraged by the results from our first program in the clinic, the ongoing Phase 1/2 ADXS-503 trial in non-small cell lung cancer. And here, I would like to provide you with an overview of the trial, our results and our path forward with this program. The trial is seeking to establish a recommended dose, safety, tolerability and clinical activity of ADXS-503 administered alone and in combination with KEYTRUDA. The two hypotheses in the study are, first, that the addition of ADXS-503 could reverse resistance in patients with metastatic non-small cell lung cancer taking KEYTRUDA as last therapy; and second, that ADXS-503 could prolong the progression-free and overall survival that is achieved with KEYTRUDA alone as first line therapy in non-small cell lung cancer. Based on our historical results with ADXS-PSA in combination with KEYTRUDA as well as our early results with ADXS-503 in combination of KEYTRUDA from Part B of this study, it is possible that the addition of 503 may improve the clinical outcomes of those patients who would otherwise receive KEYTRUDA alone, if they have a PDL-1 score higher or equal to 50%, or if they are unable to undergo the standard-of-care combination therapy with KEYTRUDA and platinum-based chemotherapy in first line. Going back to the study design for ADXS-503, Part A of the study was the monotherapy arm, which evaluated two-dose levels in patients who have refractory metastatic non-small cell lung cancer. This Part A has been completed with 7 patients treated with ADXS-503 alone. And in this phase, the drug has been safe and tolerable at the tested doses. And as Ken mentioned, 3 of the 6 evaluated patients in Part A showed stable disease, one in dose level one and two in those level two. As expected, ADXS-503 monotherapy induced a specific T-cell reactivity in all patients treated at both levels, as well as antigen spreading in 83% of them in Part A. Part B of this study is examining ADXS-503 in combination with KEYTRUDA in patients who have metastatic non-small cell lung cancer and progressive disease, while receiving KEYTRUDA as last therapy. In this particular setting, ADXS-503 is added on to KEYTRUDA in order to reverse the resistance to the checkpoint inhibitor and to once again achieve disease control. Part B was designed to explore two-dose levels of ADXS-503 in combination with KEYTRUDA, the first of which has been recently completed with three patients enrolled and treated. With the preliminary encouraging safety and efficacy results in the first two evaluable patients in Part B, including a partial response and a stable receipt for 16 and 24 weeks, respectively, we have decided to expand Part B at the first dose level to enroll up to 15 additional patients in the first stage of a Simon two-stage study design. In both patients, previous best responses with KEYTRUDA alone were stable disease during the two-year treatment period, it's possible that the clinical benefit achieved with the addition of ADXS-503 after immediate prior progression on KEYTRUDA may be due to reversing the system and complementary activity to KEYTRUDA warranting the expansion to evaluate additional patients in this part of the study. We will provide additional clinical and immunogenicity updates on patients from Part B as they become available in the fourth quarter of this year. In addition to our recently announced data in Part B, we also share our plans to begin Part C of the study, which we evaluate in ADXS-503 in combination with KEYTRUDA as a first line treatment for patients with metastatic non-small cell lung cancer that either have a high PDL-1 expression score and can receive KEYTRUDA alone, or for patients who are ineligible to receive the standard-of-care regimen of KEYTRUDA in combination with platinum-based chemotherapy in first line. As previously mentioned, the decision to evaluate the combination regimen of our ADXS-503 with KEYTRUDA as a first line treatment in patients is a strategic decision driven by [Technical Difficulty] and from taking the Keynote-046 study where ADXS-PSA plus KEYTRUDA prolonged survival in patients with metastatic castration-resistant prostate cancer. The encouraging safety, tolerability, immunogenic profile and clinical activity from Part B of our ADXS-503 study with no dose limiting toxicities observed suggests that our combination immunotherapy regimen may represent an important new option for patients that are ineligible to receive chemotherapy in combination with KEYTRUDA as well as for those patients who would ordinarily receive KEYTRUDA alone in first line. It's important to note that the two evaluable patients treated in Part B were elderly with very advanced disease and still they have clinical benefit with the combination therapy that has lasted up to six months while also being well-tolerated. Now, based on the well-characterized effects of Lm vectors on innate and adaptive immunity and within the tumor microenvironment, our results are suggestive that ADXS-503 may be restoring sensitivity to KEYTRUDA in patients refractory to this drug may and also enhance responses in patients undergoing therapy with KEYTRUDA in first line therapy. Assessing this potential enhancement in a patient population that is ineligible for standard of care chemotherapy or who would already have received KEYTRUDA alone in the first line therapy is a logical next step that also brings the potential to improve outcomes in these patients without adding significant toxicity. It has been observed with the current dual immunotherapy combinations. The full characterization of the immunogenomic profile of our patients will further help us understand the reasons behind these encouraging outcomes. I'm pleased to note that Part C is currently open to enroll patients. And we're looking forward to evaluating ADXS-503 with KEYTRUDA as a new regimen that may have a very positive benefit risk ratio in this particular population. I will now provide some information on the immunogenicity data we've obtained from both, our neoantigen programs, NEO and HOT. ADXS-NEO, a personalized Lm-based immunotherapy is a bioengineered bacteria vector that secretes an antigen/adjuvant fusion proteins consisting up to 4 unique personal neoantigens and a truncated fragment of listeriolysin O, which has adjuvant properties. Preliminary immunogenicity results from our Phase 1 trial exploring two dose levels of ADXS-NEO found that regardless of the dose level tested, ADXS-NEO induced in all patients, one activation and proliferation of CD4 CD8+ T-cell to neoantigen specific T-cell responses after only one week of the initial priming dose. And three, antigen spreading with T-cell responses to neoantigens not selected to be part of the NEO construct, as Ken mentioned before. Biopsies taken at baseline and on therapy in two patients in the NEO study also documented increased T-cell integration in the tumor microenvironment, suggesting the induction of our HOT tumor phenotype with these vectors. So, this study provided strong evidence that the neoantigens in Lm vectors induce a robust and quicker specific immune response and favorable changes in the tumor microenvironment or anti-tumoral effect. In the ADXS-503 program in non-small cell lung cancer, we're reproducing the new correlative results already documented across all the clinical studies with Lm vectors, including those in the NEO program. So far, as Ken mentioned, a total of 7 out of 9 patients have been evaluated, 6 in monotherapy and one partially evaluated in combination therapy. In all patients, we have documented transient increase secretion of cytokine/chemokine several hours after infusion, consistent with immune activation. Furthermore, the activation of cytotoxic and memory T-cell has been documented in patients treated with monotherapy, as well as in the first patient receiving combination therapy with ADXS-503 and KEYTRUDA. So, far there has been efficient priming for antigens in ADXS-503 in all 7 patients with CD8+ T-cells generated against hotspot mutations and/or other tumor-associated antigens found in the ADXS-503 vector. Additionally antigen spending was augmented in 5 out of 7 suggesting induction of a specific T-cell activity against a secondary typical pool, not incorporated in ADXS-503 and which maybe an advantage in using a very strong anti-tumoral response. We will continue to advance our ADXS-503 program in non-small cell lung cancer, while in parallel moving our next HOT drug construct, the ADXS-504 into the clinic in the setting of early prostate cancer. In this study, ADXS-504 will be administered in the adjuvant setting for patients with prostate cancer who have experienced biochemical recurrence after radical prostatectomy or radiotherapy. We will be looking to provide long-term disease control with only a few doses of ADXS-504 in these patients as the tumor burden in the adjuvant setting is lower than in the advanced metastatic setting, the setting in which ADXS-PSA was studied. We will provide updates on status of our trial as they become available. So, with drug constructs from our HOT program, we are hopeful that this novel approach will provide off-the-shelf neoantigen-based therapies that can be applied broadly across solid tumors. With that, I'll turn the call over to Molly for a review of our financials. Molly?

Molly Henderson: Thanks, Andres. Before getting to our financial results for the second quarter ended April 30th, I'd like to make a couple of comments on our capital market strategy for 2020. We started the year on a solid note by strengthening our balance sheet with a completion of a $10 million public offering of our common shares in January. We have also continued our efforts to reduce operating expenses through increased fiscal responsibility in support of our focused clinical strategy, as outlined by Ken and Andres. To further add flexibility and optionality for financing our clinical programs, we've put in place at-the-market or ATM in May of this year. We believe this will be an efficient and cost-effective solution for issuing equity over time. And turning to our financial results for the second quarter 2020, R&D expenses were $3.9 million compared to $5.9 million for the same period in 2019. This decrease in research and development expense is mostly attributable to the winding down of our HPV-associated cancer and personalized neoantigen clinical program. General and administrative costs for the second quarter were $2.6 million as compared to $3.1 million for the same period in 2019. This decrease in expenses is attributable to the lower legal fees, reduced employee and business development costs in support of our tighter fiscal oversight. Our net loss for second quarter 2020 was $6.3 million or $0.10 per share, compared to a net loss of $9.4 million or $1.59 per share in the same period of 2019. As of April 30, 2020, we had approximately $28.2 million in cash and cash equivalents on hand. With our continued reduction in operating expenses, including the winding down of non-strategic clinical programs, our current cash without taking into consideration any potential cash inflows to the Company will provide the runway till at least August of next year. Now, I'd like to provide an update on our contract dispute initiated by Stendhal, one of our partners and our former Phase 3 AIM2CERV study. As noted in our public filings, in September, 2018 through a demand of arbitration, Stendhal alleged that Advaxis breached our agreement, when we made certain statements regarding the potential winding down of our AIM2CERV program. The evidentiary hearing of the arbitration was held in October of 2019. And on April 1st of this year, the arbitrator issued a final award denying Stendhal’s claim in full. The arbitrator found that we had not repudiated the agreement and did not owe Stendhal damages fees or interest associated with the arbitration. The parties are ordered to bear their own attorney fees and evenly split the administrative costs of the arbitration. We are glad that this matter has been settled and that no payments are owed to Stendhal as a result. Before we turn it over to questions, I'd like to take a moment to acknowledge the ongoing COVID-19 pandemic. So far, we've been fortunate to have experienced minimal impact on our personnel and clinical progress, but are aware that there may be potential delays in patient enrollment in our ADXS-503 clinical program as we expand into Part B and begin to enroll patients in Part C. Our top priority is safety, and we're working closely with our clinical sites, as well as evaluating potential new sites to ensure that our work continues with minimal disruptions. And lastly, I would like to thank our investors for their continued support and confidence in our program. I also want to thank the entire Advaxis team for their hard work and dedication to our mission. We look forward to continued momentum and progress through 2020. Thank you. And with that, we will now open the call up for questions.

Operator: [Operator Instructions] Our first question comes from the line of Jim Molloy with Alliance. Please proceed with your question.

Jim Molloy: Hi, good morning. Thanks for taking my question. I had a question on how long the Part A, B, C, given it's hard to know for certain on how the trial will go and obviously the patients surviving longer pushes out the trials. But, has Part A informed what you guys think Part B might run until, the timelines on that, and then sort of how Part C might enroll as well going forward?

Ken Berlin: Good morning, Jim. Thanks for your question. I'll give some preliminary responses and then I'll turn over to Andres. So, Part A was important and that it demonstrated that there was clinical activity. We had some stable disease in some very fast progressing, heavily pretreated patients with late stage lung cancer. I think, the other important part of Part A was that we're able to get a clean look at the immune correlative and biomarker data in these monotherapy patients to see exactly how ADXS-503 was engaging the immune system, and we're still collecting that data. But as Andres detailed in his comments, it's clear that the construct is acting on the immune system as it's intended to do. And it supports into the clinical data that we see both from Part A and Part B. In terms of timing, I think, it really depends on the data that we see. We were very excited and are very excited to continue to see these first two patients from Part B, the combination arm, doing well on treatment. Remember, these two patients had progressed previously just before getting on 503; they had progressed previously on KEYTRUDA after having been on KEYTRUDA for three years with best response being stable disease. And so, to actually have achieved a partial response in the second patient, which has been sustained now after greater than 16 weeks, clearly signals that we are adding something to the mix. Now, we need to make sure we can demonstrate that over a larger patient population. So, as Andres outlined, we plan to expand Part B to add an additional 15 patients. And obviously timing on that comes down to enrollment and any potential impacts that COVID-19 might have on enrollments. We currently have five very-high caliber sites that were part of the initial program and now we're adding sites. And so, we are looking at concerted efforts to accelerate enrollment, to see if the data hold up over a larger end. We expect to have some additional data from Part B by the end of the year. And then, as it relates to Part C, we expect to have some data from our Part C patients towards the end of this year and into the following year. Does that answer your question, Jim?

Jim Molloy: It does. Thank you. And I guess, related partially as well. What is the -- the three patients enrolled, the two are evaluable as the third probably hasn't been in long enough, are there any similarities between the third and the first two that might give hope that perhaps when they are available, we'll see something similar?

Ken Berlin: So, we are continuing to evaluate all aspects of these patients try to understand who and how and why certain patients are responding. So, it's still early days and we still are assimilating all the data that we're collecting both from the immune correlative front and a biomarker front. COVID has impacted that a little bit as one of our collaborators has been shut down until recently. So, we're looking forward to getting data from them. And we expect to have some additional data on the biomarker front in the combo arm by the end of July, early August if things go well. So, it's too early to tell what's similar and what's different between the different patients. So, we want to enroll more patients, gather more data, understand a bit more as to the mechanisms and why we're seeing the responses that we're seeing. We are pleasantly responding to these responses. Really Part B was a means to get to Part C initially. So, initially the plan was let's show that the combination of ADXS-503, which hadn't been in patients before was safe in combination with KEYTRUDA, we've done that. And now, we've seen this clinical activity which merits further investigation. And that's what we're doing with the expansion of Part B by adding the additional 15 patients and then we're moving to Part C, which is first line, which is very intriguing. Just a word on Part D. So, what -- to give some color to the data that we have to date, it's important to note that when people progress on checkpoint inhibitors, people with late stage lung cancer, like the patients we have in our in Part B of our study, only 10% to 15% are able to recover, if you will, respond again to some new therapies, right? So, the fact that we're seeing the stabilization of disease, which was the durable in the first patient and how the sustained partial response in the second patient is meaningful. So, if we can establish that we have a 20%, 25% response rate in these patients who fail KEYTRUDA, we think that's a pathway towards a potential approval down the road. I don't want to get ahead of ourselves. It's still early days, but that's why we're very excited, right. Because really nothing has helped these patients once they progress on KEYTRUDA, very little. So, only 10% to 15% of patients are able to be helped by other treatments, other experimental treatments and other things that are available. So, we believe that the bar that's achievable, again if these data hold up over the larger data sets. So, we'll have much better information about the potential for our ability to desensitize patients to KEYTRUDA through this combination arm in Part B by the end of the year.

Jim Molloy: Thank you. Yes. That actually leads into the next question I was going to ask you and it was answered it. So, it seems that what's these sort of aha data points that you need and things like if you can maintain the 20% to 25% response rate in these failures, KEYTRUDA failures and that's really you need to be finding, right, or that or better?

Ken Berlin: Right. So, as Andres mentioned, we've done a lot of modeling. And through our modeling, what we need to see in the next 15 patients is -- or are two more partial responses to give us a high level of confidence that this thing, the response that we're seeing is real to move to the next phase, which would be the second stage of this Simon two-stage design that Andres has mentioned in his comments. Andres, could you elaborate?

Andres Gutierrez: Yes. So, that's what I was going to say. So, once we get the 15 additional patients, we get two additional responses, they were confident that we can move on to stage two of the Simon two-stage design. And again, the target rate of response is 25% in both parts. So -- but there's that go no go criteria, very hard solid -- go no go criteria from stage one to stage two, which is three or more partial responses. It's a very high bar considering as Ken was mentioning, what we have seen with other immunotherapies trying to rescue checkpoint inhibitor failures, the responses are not better than 10%, 12%, 13%. That's what we get to see with trying to rescue these kinds of patients and at the expense of a high toxicity, whereas you see here from what we have seen in the PSA program, that it's very safe and tolerable to combine Lm vector and a KEYTRUDA. So, now we are not expecting to see any kind of major safety concerns either. So, we have not seen that in the first three patients in Part B of this study. So, we are hoping to really progress quickly in the enrollment of the traditional 15 patients. The environment is not the best environment to do so. It's a very competitive landscape. And COVID is also kind of a slowing down activities in some sites. However, we get to see that they're starting -- sites are starting to work again back to normal speed.

Jim Molloy: And then, my last question is for Molly. I know that the spend came down pretty dramatically with the exiting of those other programs. As you’re ramping up into the second half Part B and the Part C and I guess whatever happens with the PSA, is this the level we should expect for the rest of the year or should we see this sort of move up or down?

Molly Henderson: Yes. We've been open and giving guidance as far as what we expect the 12-month spend to be kind of around that $23 million to $25 million. But as Andres just said, some sites are pulling back, other sites are ramping back up. So, we're looking to increase the amount of sites to be able to pull in more patients. So, we're assessing that now. Right now, I’m so confident that we're still in the August effects your timeframe from a runway. And certainly we’ll be opportunistic and look for other sources of non-dilutive financing in the mean time. But, at this point, yes, I think that's probably a safe assumption, based upon run rate we're seeing for the rest of this year and into early next year.

Jim Molloy: And this last question I guess for Ken. So, you hinted at the start of the call, the PSA, stay tuned for clarity and path forward. Is there any timeline or potential guidance or what's sort of path forward we might be anticipating? Is that non-dilutive financing that was just alluded to potentially?

Ken Berlin: Right, Jim, it's a good question. So, I know a number of folks are certainly interested to hear what's going to happen with that program. Yes. So, the next study which would be a randomized control study to generate proof-of-concept data probably requires about $20 million to $25 million to complete. And we are looking for non-dilutive financing to help fund that, in other words partner funding. And partnerships take time. And we had hoped to be at a place now to announce that but we're not. So, there's still some work to do. I can't give you a timetable. But, we continue to look at potential opportunities to fund that study through non-dilutive financing, i.e. partner funding. And like I said, these things take time. It's hard to predict when we're going to reach a conclusion on that. But, the data are intriguing. But, when you think about 503 versus PSA, we believe 503, because we're seeing already a partial response in the combo arm, is a quicker path to proof-of-concept and a less expensive path to proof-of-concept and potentially to an accelerated approval. Right? When you think about those two programs, you can get an accelerated approval based on response rates in non-small cell lung cancer whereas in prostate cancer, we didn't see response rates, but we did see this nice survival benefit. So, survival studies by their very nature take longer and therefore more expensive. So right now, we’re prioritizing 503 over PSA. If we can get some more funding, non-dilutive funding around PSA, we'd like to embark on that next study.

Jim Molloy: Great. Thank you very much for taking the questions.

Ken Berlin: Thanks, Jim.

Operator: Thank you. There are no further questions at this time. I'd like to turn the call back over to Mr. Berlin for any closing remarks.

Ken Berlin: Thank you all again for joining our call today. We're proud of our momentum and confident about the path forward with our HOT program and look forward to providing clinical updates in the coming months.

Operator: Thank you. This concludes today’s teleconference. You may disconnect your lines at this time. Thank you for your participation and have a wonderful day.