Welcome to the Cardiff Oncology conference call to discuss the company's MCRC program update and development plan. At this time, all participants are in a listen-only mode. Following management's prepared remarks, we will hold a Q&A session. To ensure that we have ample time to address everyone's questions during the Q&A session, we would ask for a limit of one question and one follow-up per person. To ask a question at that time, please press star followed by one, one on your touchtone telephone. As a reminder, this call is being recorded today, Monday, August 7, 2023. I would now like to turn the conference call over to Laurence Watts of Gilmartin Group. Please go ahead. Thank you, operator. Slides for today's investor call can be found on the homepage and the Events and Presentations tab of the Cardiff Oncology website at www.cardiffoncology.com. Joining us on the call today from Cardiff Oncology are Chief Executive Officer, Mark Erlander, Chief Medical Officer, Fairooz Kabbinavar, Chief Scientific Officer, Tod Smeal, Chief Financial Officer, Jamie Levine, and Senior Vice President of Regulatory Affairs, Chuck Monahan. Please turn to slide two. During this conference call, management will make forward-looking statements, including, without limitation, statements related to guidance, results, and the timing of data readouts for onvansertib clinical trials. These forward-looking statements are based on the company's current expectations and inherently involve significant risks and uncertainties. Our actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties. Factors that could cause results to be different from these statements include factors the company describes in the section titled "Risk Factors" in our annual report on Form 10-K, filed with the SEC on March 2nd, 2023. Cardiff undertakes no duty or obligation to update any forward-looking statements as a result of new information, future events, or changes in its expectations. With that, I will turn the call over to Chief Executive Officer, Mark Erlander. Mark? Thank you, Laurence, and good afternoon, everyone. We're excited that you've joined us today to hear important updates on our clinical development plan in our lead program of RAS-mutated metastatic colorectal cancer, or mCRC. Colorectal cancer is the fourth largest cancer indication in the United States, with annually rising rates among younger adults, and there is a significant unmet need for new approved therapies for mCRC patients. Today, we are announcing our decision to shift our RAS-mutated mCRC clinical program to the first-line setting. This change represents an opportunity to have both a significant impact on this large patient population and to be transformational for our company. Slide three describes the key drivers for moving into the first-line setting. The first factor is our clinical data. Last September, we presented data for the first 48 evaluable patients in our Phase Ib/II second-line trial, including a high response rate in a subgroup population that we refer to as BEV naive patients. BEV is short for bevacizumab, which is the approved drug Avastin. BEV naive patients are those who are not treated with BEV in their first-line therapy before enrolling in our second-line trial. Today, we are sharing an update from the trial that continues to show high response rates, especially in BEV naive patients. Also, for the first time, we were able to share data on the additional 18 patients we enrolled in the Phase Ib/II trial, which we refer to as the expansion cohort. Importantly, the same strong efficacy signal was replicated in the BEV naive patients in this entirely new cohort. Looking at all of the BEV naive patients in our trial, we continue to report strong data with an exceptionally high and confirmed objective response rate of 73% and a median progression-free survival of 15 months. A second reason for moving into the first line is our strong, new preclinical data that establishes a fundamental mechanism for which the BEV naive clinical findings we observed. Specifically, we have discovered a new mechanism of action by which onvansertib inhibits new tumor vascularization and growth, and our data indicates why BEV naive patients may respond better to treatment compared to BEV exposed. The third reason for our decision to move into the first-line mCRC is the constructive and highly encouraging feedback that FDA provided at our recent Type C meeting, and which I'll discuss in more detail on the next slide. In addition to announcing our new clinical program, today, we are also announcing our decision to expand our relationship with Pfizer. In November of 2021, Pfizer invested in Cardiff Oncology through the Pfizer Breakthrough Growth Initiative, signaling the alignment of our development program with Pfizer's strategic priorities. Today, we are expanding this relationship such that Pfizer will provide clinical execution support for our new first-line trial, which we see as continued validation of the high level of strategic interest in onvansertib's potential. On slide four, we show an overview of the resulting first-line mCRC clinical development program. In September of last year, we indicated that the positive BEV naive signal seen in our second-line trial may provide us the rationale to move into the first-line.... In June of this year, we had a Type C meeting with the FDA, where the agency agreed with our proposed first-line program, which includes an initial phase II trial, CRDF-004, followed by a phase III registrational trial, CRDF-005. In our new CRDF-004 trial, we'll enroll first-line RAS-mutated mCRC patients. It's designed to generate preliminary safety and efficacy data, as well as dose confirmation. We expect to begin enrolling patients in the trial this fall and to release interim top-line data in mid 2024. This rapid timeline is supported by a large eligible patient population, a broad enrollment criteria, a lack of any competing trials in RAS-mutated first-line mCRC, and the clinical execution capabilities of Pfizer Ignite. The data from CRDF-004 is intended to support the launch of the CRDF-005 trial, which is designed to be a seamless registrational trial for both accelerated approval based on the interim look at objective response rate, or ORR, as well as full approval based on progression-free survival and overall survival trend. The FDA agreed with our two-trial mCRC program that we are announcing today. On slide five, we show that increased commercial opportunity that results from steps that we are announcing today. With our prior focus on second-line mCRC, we estimated that the addressable U.S. population was approximately 23,000 patients per year, and the strongest responders, the BEV naive patients, are about a third or 7,500 patients of that total second-line population. While this is a significant opportunity, our revised clinical development program will more than double the size of the addressable population to 48,000 first-line patients per year, all of which are BEV naive. It's important to remember that onvansertib targets PLK1, so our addressable patient populations are significantly larger than those for therapies that target a single oncogenic driver mutation. Slide six presents our full development pipeline for onvansertib, and you can now see that the first-line trial in our lead mCRC program at the top, as well as onvansertib trials and other indications. These are not impacted by any of our announcements today. Let's now get into the details. Slide seven highlights the three topics that we will address today. First, we will report new clinical data from our phase Ib/II trial in the second line. Next, we will discuss the scientific basis for our clinical findings, and then finally, we will discuss our clinical development path forward. On slide eight, at this point, I'd like to introduce Dr. Fairooz Kabbinavar, who is our Chief Medical Officer, to discuss the clinical update from our phase Ib/II trial. Because this is his first public presentation since joining Cardiff Oncology in February, I'll say a few words about his accomplished and very highly relevant background. After completing his medical training at Harvard's Beth Israel Deaconess Medical Center, Dr. Kabbinavar brings over 30 years of oncology experience in both academia and biotech settings. He was an academic oncologist at UCLA for 25 years and then joined the biotech industry as the principal medical director in Genentech's immuno-oncology program, after which he held CMO roles at different biotech companies. Dr. Kabbinavar brings deep knowledge of colorectal cancer as well as other solid tumor cancers. Critically, while at UCLA and Genentech, Dr. Kabbinavar served as lead investigator for two practicing- changing trials that led to the approval of BEV or Avastin in metastatic colorectal cancer. As you'll hear, his experience has many direct ties to the strategy we are announcing today. With that, I'll hand over to Fairooz. Fairooz? Thank you, Mark. It's a pleasure for me to share this update on the clinical results today with all of you. On slide nine, we remind you how onvansertib works by inhibiting a key regulator of cell cycle, polo-like kinase of PLK1. Onvansertib is the first oral, well-tolerated PLK1 selective inhibitor, that we believe the properties that impact its tolerability positively are its oral dosing and relatively short half-life of 24 hours, giving us a flexibility in our dosing schedule relative to prior drugs targeting PLK1 that had to be administered by IV, had a longer half-life, and inhibited multiple PLK family members. Onvansertib's selectivity for PLK1 reduces off-target effects that also contribute to its better toxicity profile. Slide 10 shows the current paradigm for treatment in the mCRC setting. Patient's treatment is determined in part by the tumor genetics, and over 50% of patients have a tumor with a RAS mutation, for which there are no currently approved targeted therapies available. The current standard of care consists of chemotherapy, either FOLFIRI or FOLFOX, and the potential addition of BEV, which confers a slight benefit to the patient responses. BEV was approved for use in mCRC based on the pivotal study, of which I'm a senior author, that we published in New England Journal of Medicine in 2004. Since then, there have been no new therapies approved in almost 20 years for this patient population, which underscores the significant unmet need that, that, exists today. One thing to keep in mind from this slide is that BEV is approved for use in both the first and the second-line setting for mCRC. This is an important factor enabling our move to the first-line setting, as I'll discuss later. On slide 11, you will see that in our Phase Ib/II trial, onvansertib was combined with FOLFIRI and BEV in second-line mCRC patients that had a KRAS-mutated tumor. On our slide 12, our decision to target this patient population was driven by the underlying mechanisms, as shown in this slide. First, onvansertib has been shown to have synthetic lethality in RAS-mutated mCRC tumors. Second, onvansertib synergy with DNA-damaging agents, allows us to pair it effectively with second-line standard of care chemotherapy. One additional comment I'll make on this slide refers to the unmet need I mentioned a bit earlier. When we look at drugs under development for these patients, Amgen's LUMAKRAS and Mirati's adagrasib, currently market drugs are limited to G12C KRAS mutation, which represents only about 3%-4% of the mCRC patient population, as you can see on this pie chart. G12C-specific inhibitors provide no benefit for over 90% of the RAS-mutated tumors. In contrast, our trial was designed to explore onvansertib in all KRAS-mutated tumors, and in a few slides, we'll show data that suggests that is the case. Slide 13 shows the design of our Phase Ib/II trial. We enrolled patients with a KRAS mutation who had unresectable metastatic disease. We combined onvansertib with the standard of care treatment of FOLFIRI and BEV. The primary endpoint of the trial was objective response rate, with progression-free survival and duration of response as secondary endpoints. Slide 14 visually represents our enrollment cohorts. In our prior data release, we reported data for 48 evaluable patients in the phase Ib and initial phase II trial. We decided to continue enrolling patients as we transition to the next phase of our program, which resulted in an additional 18 evaluable patients in the trial. Today, we'll include these patients in our results for the first time, allowing us to report data for all 66 evaluable patients enrolled in the trial. Slide 15. As Mark mentioned in his comments earlier, an important element of our data is the strong signal we have seen in our BEV naive patient subgroup. Let me define what we mean by this term in this slide. When we refer to our patients in our second-line trial as BEV naive, we mean that in their first-line therapy, they received FOLFIRI chemotherapy alone without BEV. These patients are therefore BEV naive when enrolling in our second-line trial, where all patients receive FOLFIRI, plus BEV, plus onvansertib. In our trial, 23% of the 66 patients were BEV naive. We refer to the other 77% of patients in our trial as BEV exposed, meaning they were treated with BEV in addition to FOLFIRI chemotherapy in the first-line setting. When we look at the efficacy data on the next few slides, it will become abundantly clear that BEV naive and BEV exposed subgroups patients respond differently to FOLFIRI, plus BEV, plus onvansertib. Slide 16 shows a waterfall chart for all 66 evaluable patients in our trial, split between BEV naive subjects on the left and BEV exposed on the right. As the table at the left shows, we achieved a 29% objective response rate across all patients, and for these patients with a response, the median duration of response is 12 months. These are promising data in this challenging patient population. The most exciting data relate to the 15 naive patients, BEV-naive patients on our trial. We achieved an impressive 73% response rate, including one complete response, a 13-month duration of response, and a 100% disease control rate, meaning none of these patients had a progressive disease as their best response. The 73% objective response rate for our trial compares very favorably to the 23%-26% response rates observed in BEV-naive historical controls. In my 25-30 years of experience researching colorectal cancer, I've never, ever seen a response rate in the 70%+ percent range in the second-line setting of an mCRC. Slide 17 shows the swimmer plot for the 66 evaluable patients on our trial. Again, the BEV naive subjects are on the left, and the BEV, BEV exposed patients are on the right. In the BEV naive plot, you can see the high number of confirmed objective responses. Another important takeaway relates to my comment earlier that all patients in our trial had unresectable disease. As you can see on the left, eight of our 15 BEV naive patients, or 53%, left the trial to pursue surgery or ablation, meaning their disease had reduced to a point where these local treatments or therapies became a potential effective option. once the decision to pursue surgery is made, the patients are censored, and no additional data are reported, which appears on the plot as a teal diamond at the end of these patient swim lanes. You can see how several of the patients with a relatively short time on trial left to pursue surgery, which is a positive outcome for these patients. The remaining four patients who did not have a partial response had stable disease, giving us a disease control rate of 100%. On the right-hand side, you can see that even among the BEV-exposed patient population, many patients remained on trial significantly beyond the four-six month progression-free survival period expected in this broader patient population. On slide 18, I mentioned earlier that onvansertib's mechanism of action allows us to explore efficacy in patients with any KRAS mutation. This slide provides the data to suggest that this is the case. In the table, we show the best response for each patient, separated by individual KRAS mutation. Our 66 evaluable patients are fair representation of the KRAS mutations in mCRC patient population. We see objective responses across most of the KRAS variants in our patient population. On slide 19, we show the progression-free survival curve for all patients on the left and the median progression-free survival split by BEV subgroup on the right. Median progression-free survival for all patients was 9.3 months, as you can see on the left. The more remarkable data is once again for the BEV naive patients seen on the right. These patients had a median progression-free survival of 15 months, which is approximately double the progression-free survival of historical controls shown at the bottom right-hand corner of the slide. Moving on to, to safety, slide 20 shows the basis for my comments earlier that onvansertib is well tolerated when used in combination with chemotherapy. The more severe grade four treatment emergent adverse events are either neutropenia or leukopenia, which are common events in patients treated with standard of care chemotherapy. None of these patients discontinued their treatment due to the side effects, and all resolved without any issue. In all, there were no major or unexpected toxicity seen in our trial. Now, having presented this, our clinical findings, I'm going to hand over the mic to Mark again, take you through the next set of slides. Okay. Well, well, thank you, Fairooz. We're now going to discuss our progress in determining the underlying mechanisms that may explain the strong efficacy data we saw in the BEV-naive patient population. When we first announced the BEV-naive finding last September, we said we had launched a broad preclinical program to explore the mechanisms at work. Our Chief Scientific Officer, Dr. Tod Smeal, will discuss the important and new exciting findings from that process. As a reminder, prior to joining Cardiff Oncology, Dr. Smeal was most recently Chief Scientific Officer at Hexagon Bio, and prior to that, Chief Scientific Officer of Cancer Biology at Eli Lilly, and previously Director of the Oncology Research Unit of Pfizer. Dr. Smeal's 25 years of work in the biopharmaceutical industry, developing cancer therapies, has focused on targeted therapies and their resistant mechanisms, especially in intracellular signaling and kinase inhibitors, which has led to FDA approval of thre cancer drugs. Dr. Smeal brings highly relevant expertise to our leadership team. Tod? Thank you, Mark. Almost a year ago, we set out to determine the basis for the strong clinical signal observed in second-line BEV-naive patients. The results of our efforts show in the following slides align well with our initial hypothesis that PLK1 inhibition can interfere with angiogenesis. We also discovered a new mechanism mediated by PLK1 inhibition responsible for this effect. I'm excited to share the results of this non-clinical work with you today. On slide 22, we describe the four pillars of our work that underlie the basis of the BEV-naive clinical finding. In the preclinical models that we examined, we were able to observe increased efficacy from the combination of onvansertib and BEV, as well as gain insight into the potential underlying mechanism for this effect. I'll describe our work exploring the observed tumor growth reduction and the role hypoxia signaling, angiogenesis, and resistance mechanisms play in this finding on the following slides. Let's look at each of these topics in turn. On slide 23, we show in vivo data in three KRAS mutant xenograft models with eight to nine mice per group. Each model compared four arms, a control arm consisting of vehicle only, an arm that included only onvansertib, an arm that included only BEV, and an arm that included onvansertib and the BEV combination. In all models, the onvansertib plus BEV combination was shown to have significantly superior anti-tumor activity compared to the single agent arms. Slide 24 shows photographs from representative tumors in the study. Data shown from data on the prior slide. At the end of the study, tumors from the LoVo and SW620 models were removed from the mice at the same time point and photographed, providing a view of the gross histology of the tumors. In the photographs, the difference in size of the represented tumors is apparent, what is equally important is the vascularization of the tumors. The control arm tumors show a high concentration of blood vessels indicated by the redness, showing the vasculature that allowed the tumor to grow. As we add onvansertib or BEV, the tumors become paler and smaller as the angiogenic effect takes hold. The tumors treated with onvansertib and BEV combination on the bottom row are not only smaller, but are also paler due to the substantial decrease in vascularity that than either agent alone. Before presenting the next dataset, slide 25 provides some context for the phenomenon we've just seen. This is important because it underlies the claim Mark made at the beginning of the call, that we now believe we've discovered a new mechanism of action for onvansertib. As solid tumors grow, tumor cells become starved for oxygen, a condition referred to as hypoxia, due to the insufficient supporting vasculature. This is one of the hallmarks of solid tumor cancers. In response to hypoxia, cancer cells activate the hypoxia-inducible factor pathway, or HIF pathway. This heterodimeric DNA binding protein promotes tumor angiogenesis, proliferation, and survival by controlling the transcriptional expression of many downstream genes. For example, the HIF pathway, by inducing the expression of proteins such as VEGF, allow the tumor to recruit new tumor vasculature to supply oxygen, nutrients that allow the tumor to survive and grow. BEV is an anti-angiogenic drug that inhibits the growth of new blood vessels in the tumor by blocking VEGF function. Slide 26 demonstrates the new finding that PLK1 inhibition can have an anti-angiogenic effect. If we focus on the data for the LoVo cell line in the upper left and the four lanes within the top rectangle, you can see that in normoxic conditions, where normal levels of oxygen are present, shown as NX on the slide, the HIF-1 alpha protein levels are not significant and are not induced, and we do not detect significant levels of protein, as indicated by lack of signal in these two lanes. Now let's look immediately to the right at the two lanes under hypoxic conditions, labeled HX, which mimics the oxygen-starved microenvironment of the tumor. The dark-colored band of the third lane shows that HIF-1 alpha protein expression was strongly induced by tumors, tumor cells in response to this lack of oxygen, as expected to grow angiogenesis. The fourth lane is the critical finding, showing that treatment of with onvansertib directly HIF-1 alpha expression in hypoxic conditions, and as a result, will be expected to inhibit the creation of new vasculature and the ability of the tumor to survive and/or proliferate in a hypoxic tumor microenvironment. Given that both onvansertib and BEV inhibit angiogenesis, why is the combination more powerful than either agent alone? As you can see on slide 27, the two drugs function at different points in the hypoxia signaling pathway that are complementary. BEV specifically binds the vascular endothelial growth factor, or VEGF-A, inhibiting angiogenesis. Onvansertib inhibits the broader HIF-1 alpha pathway, potentially inhibiting not only VEGF-A induced angiogenesis, but also several other tumor proliferation and survival mechanisms promoted by HIF-1 alpha. This finding represents an entirely new mechanism for onvansertib, inhibiting a survival switch of tumor genesis and suggests the combination of onvansertib and BEV could result from two hits at different steps on the hypoxia pathway. This complementary activity of these two agents may provide additional treatment opportunities in other BEV-responsive cancers. As Bruce said earlier, all patients in our trial received onvansertib and BEV, which we've just shown is a powerful combination. Why was the response of BEV-naive patients apparently so much stronger? Can we find direct evidence in patients on why higher BEV exposure results in less clinical signal than patients without BEV exposure? Does patient data support our initial hypothesis that BEV treatment upregulated pathways that confer resistance to BEV and onvansertib? As depicted on the top half of slide 28, in collaboration with Tempus, we looked at the genes and pathways expressed in tumor cells taken from 135 mCRC patients after they completed their first-line therapy. 71 patients had received only FOLFOX in the first line, and 64 patients had received FOLFOX, FOLFOX and BEV. As shown in the bottom half of the slide, when we compare the two groups, we found that genes and pathways associated with both hypoxia and mitosis were upregulated in the BEV-exposed patients, meaning that the prior BEV treatment in the first line potentially conferred resistance to the combination of BEV plus onvansertib by tumor cells upregulating these pathways. Additionally, modulation of the oncogenic signatures associated with angiogenic factors such as VEGF-A, were observed in the BEV-exposed tumors and may drive resistance to treatment. The findings in this study for 135 CRC patients provide further support for our proposed mechanism underlying the high response observed in the BEV-naive patients within our trial. Altogether, as seen on slide 29, we believe that this work supports the hypothesis that there is a third mechanism of action for onvansertib, inhibiting the HIF-1 alpha survival switch that tumors activate to overcome hypoxia in the tumor microenvironment. This finding suggests that there may be new cancer indications where the treatment of, treatment with onvansertib could be effective, and we're continuing with preclinical work to investigate these opportunities. Having discussed our new mechanisms of action that we, that we have discovered, I'll now hand things back to Mark. Well, thank you, Tod. Now that we've looked at the clinical data as well as the basis for these findings, I'll ask Fairooz to summarize our recent discussions with the FDA and our plans for onvansertib's clinical development path going forward. Fairooz? Thank you, Mark. Slide 31 summarizes the feedback we received from the FDA on our, at our Type C meeting in mid-June. We requested the meeting to discuss a broad clinical program in be and seek the agency's agreement with our strategy. In the meeting, the FDA had a very clear message for us. We should consider shifting our development program to the first-line setting for two very important reasons. First, all patients in first-line mCRC are BEV-naive, as BEV is never used in the adjuvant or neoadjuvant settings. Our data suggests BEV-naive patients may be more responsive to treatment with onvansertib. Second, by shifting to the first line, the absolute number of patients who would benefit from onvansertib treatment is significantly larger, which is an important consideration for the agency. Our discussion during the Type C meeting also addressed the clinical development path we could use in the first-line setting. Given the requirements of Project Optimus and our own desire to generate a safety and efficacy signal before investing in a large registration trial, our program will start with CRDF-004 trial, which can confirm both the efficacy signal we saw in the second-line BEV naive patients and the optimal dose of onvansertib in this setting. The next step agreed with the FDA will be the CRDF-005, a seamless registration trial, which could support both accelerated approval using an objective response rate from an interim readout, then a full approval on the basis of progression-free survival and an overall survival trend. Slide 32. Our shift in the focus to first-line RAS-mutated mCRC is an important one. This slide summarizes all the factors that drove us to this conclusion. The first bullet under clinical factors is that all patients in first-line setting are BEV-naive, which is a catch-all bullet for all the clinical and preclinical evidence we have presented so far on this call. However, there are other clinical drivers for a decision, including the large unmet need of this patient population and the lack of competing trials in RAS-mutated patient population, which could facilitate rapid enrollment in our trial. From a regulatory perspective, we believe the clarity we received in our discussion with the FDA on our first-line plan reduces the regulatory risk and provides a validated, validated pathway to the potential accelerated approval. From a commercial perspective, the larger addressable patient population first-line allows us to provide a potential benefit to many more patients with this devastating disease, which is not only an attractive commercial opportunity, but also allows for an enrolment forecast enables us to announce interim data in mid-2024. Lastly, I'd like to describe the reasons for our decision to stop enrollment and wind down our second-line ENSEMBLE trial. First, our new first-line trial is essentially testing the same clinical hypothesis as ENSEMBLE, that onvansertib, when added to standard of care, improves efficacy in BEV naive patients. Therefore, running both trials is redundant. Second, given our goal of achieving an accelerated approval for onvansertib, all the data and evidence to date confirms that shifting the first-line setting, where all patients are BEV naive, is the best path forward. In summary, we believe these factors indicate that first-line path, when compared to second line, represents a lower clinical risk and a higher probability of success. On slide 33, we highlight the design of our CRDF-004 Phase II trial. The trial will enroll patients with RAS-mutated, unresectable tumors and who have had no prior treatment with FOLFIRI or FOLFOX or BEV. The 90 patients will be randomized across three arms, including two different flat doses of onvansertib, those with standard of care, and a control arm, where patients receive standard of care alone. Standard of care will consist of FOLFIRI plus BEV or FOLFOX plus BEV, because both of these chemotherapies are approved for first and second-line use interchangeably. The onvansertib dosing will follow the same protocol as our prior Phase Ib/II trial. The primary endpoint will be objective response rate, with the duration of response and progression-free survival and secondary endpoints. Our goal is to show an objective response rate greater than 65%. Let me put this figure in some context on the next slide. As I presented earlier in our phase Ib/II trial, we saw an astounding 73% response rate in our BEV-naive patients, which not only compares favorably to second-line historical controls of 23%-26%, but also first-line historical control of approximately 45%. Turning to progression-free survival on the right, in our second-line trial, we saw a 15-month median progression-free survival for BEV-naive patients treated with onvansertib plus standard of care, which is, again, higher than the second-line historical controls of 6.9-8.5 months, and our first-line historical controls of nine-10 months. Summarizing, in our Phase Ib/II trial, we observed an outstanding 73% response rate in the BEV-naive group of patients with an equally impressive median progression-free survival of 15 months in second-line mCRC patients, with a KRAS mutation strongly suggesting that this subgroup needs to be studied in the first-line setting, where all patients happen to be BEV-naive. This strategy was approved by the FDA during our Type C meeting. I will now hand things back over to Mark to conclude the call. Okay, thank you, Fairooz. Before we conclude and take questions, I'll make a few comments about our corporate strategy supporting the clinical and preclinical priorities you've been hearing about today. On slide 35, you can see how we agreed to broaden our partnership with Pfizer to include the clinical execution of Cardiff's CRDF-004 trial. As a reminder, in November of 2021, Pfizer made an investment in Cardiff Oncology through its Breakthrough Growth Initiative, which is a fund Pfizer created to invest in companies that are developing clinical-stage assets aligned with Pfizer's core areas of focus. Today, we are announcing that Pfizer, through its Pfizer Ignite program, will be responsible for the clinical execution of our new Cardiff CRDF-004 first-line trial. The benefit to Cardiff Oncology is that we can access Pfizer's significant development capabilities, scale, and expertise through a fee-based model. Importantly, Cardiff Oncology will maintain full economic ownership and control of onvansertib and all the data we generate from this trial. On slide 36, you can see that as of June 30, 2023, we have $89.4 million in cash, and we expect this provides us with the resources to fund all our operations into 2025. As you can see at the top of the slide, we still plan for important readouts from our ongoing clinical programs within that timeframe. In conclusion, on slide 37, today, we've announced an important transformation for our company, which includes advancing of our lead mCRC program to the first-line setting and an expanded relationship with Pfizer. Together, these achievements reflect the tremendous opportunity we see for Cardiff Oncology to provide immunical benefit to a large number of patients currently fighting cancer. With that, we are ready to take your questions. Operator? Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. One moment for questions. Our first question comes from Marc Frahm with TD Cowen. You may proceed. Hey, yes, thanks for taking my questions. Maybe to start out with on the trial design, how do you plan to account for the physician choice to use FOLFOX versus FOLFIRI in the first line, in terms of-? Oh, thanks- criteria? Yeah, thanks, Marc, for that question. We, in that trial, that phase II trial, we will demand that you have equal proportion of backbone of FOLFOX and FOLFIRI, for each one of those arms. Okay, that, that's very helpful. That's what I was guessing. And then just in terms of the Type C, I mean, it sounds like you, you know, got a good alignment there out of the Type C meeting. Can, can you just walk through the rationale for, why did you request the Type C meeting, you know, given that ONSEMBLE was already kind of underway and, and had been discussed with the FDA previously? Thanks, Marc. You know, as you know, we continued to look at our phase Ib/II data and continued follow-up, and we also saw the data from our expansion of the 18 patients, which also included bev-naive patients. We continue to see and replicate the findings of the bev, bev-naive having high response rates. You know, our focus is really the fastest path to an accelerated approval. When we looked at that, we, we really went back to the FDA showing this data, and that's how we got to a first-line setting where it would be all bev-naive patients. Okay. Thank you. That's very helpful. Thank you. One moment for questions. Our next question comes from Joel Beatty with Baird. You may proceed. Hi, thanks so much. This is Ben on for, for Joel. Thanks for taking our questions. Can you maybe tell us, how Cardiff and then, Pfizer benefit from this, this program you announced? Oh, absolutely. The benefit there, number one, is that we will be able to, in essence, join forces through this partnership to, to move onvansertib much faster through a first-line trial and first-line clinical development. That's simply stated. Got it. Thank you so much. Then, how fast do you think you can move from the CRDF-004 clinical trial to the registrational Phase III? No, we haven't that, you know, publicly talked about that yet. I think we'll be able to say a lot more about that as we get into the phase II trial. One thing that you should keep in mind, though, is that when we went to the FDA and got agreement on the seamless registrational trial, they agreed that we could use ORR as the interim endpoint for accelerated approval. As you know, that it was absolutely critical because that allows the trial as far as the first primary endpoint, to go much faster. Got it. Thank you so much. Appreciate it. Thank you. One moment for questions. Our next question comes from Robert Burns with H.C. Wainwright. You may proceed. Hey, guys, congrats on this new agreement with Pfizer and advancement into the frontline setting. Two questions from me. Considering that the first patient was dosed in the ONSEMBLE trial in late March, I'm curious whether there are any learnings from the two doses that you evaluated in that trial, that can be applied to the new phase II trial in the frontline setting, and then I've got one more. Yeah, great question, Robert. You know, the, the trial itself, it started somewhat slow, but has really ticked up. The number of patients, that are in each arm, is really a handful. We don't see at this point, really, being able to, use that data going forward. Okay. Thank you for that. My last one, since you stated that the benchmark for success in the 004 trial is an ORR greater than or equal to 65%, are you also considering the delta between onvansertib plus standard of care versus standard of care as a benchmark for success should onvansertib not demonstrate a 65% ORR, just slightly below it? Yes. You know, the bottom line there, Robert, is that we're looking for a delta of 20%, so we're looking at a 45% versus a 65%, but really it's the delta that we're looking at. Okay. Thank you, Mark. Thank you. I would now like to turn the call back over to Mark Erlander for any closing remarks. Well, thank you, operator, and with that, I would like to thank all of you, for participating in today's call. Thank you. This concludes today's conference call. Thank you for participating. You may now disconnect.