Good afternoon. My name is Diego, and I will be your conference call operator today. At this time, all participants are in a listen-only mode. After the speaker's formal remarks, there will be a question-and-answer session. If you would like to ask a question during that time, simply press the star key, then the number one on your telephone keypad. If you would like to withdraw your questions, please press the star key and the number two. If you should require operator assistance during the conference, please press star zero. As a reminder, this call is being recorded. I would now like to turn the conference call over to Mariann Ohanesian, Senior Director of IR for Puma Biotechnology. You may begin your conference. Thank you, Diego. Good afternoon, and welcome to Puma's conference call to discuss our exclusive license agreement with Takeda for the development and commercialization of alisertib, an investigational aurora kinase A inhibitor. Joining me on the call today are Alan Auerbach, Chief Executive Officer, President, and Chairman of the Board of Puma Biotechnology, and Dr. Alvin Wong, Chief Scientific Officer. As a reminder, this call is also being webcast. The webcast will be archived on our website and available for replay for the next 90 days. Before I turn the call over to Alan, I would like to note that during this conference call, we will make forward-looking statements within the meaning of federal securities laws. All statements other than historical facts are forward-looking statements and are based on our current expectations, forecasts, and assumptions. Forward-looking statements involve risks and uncertainties that could cause our actual results to differ materially from the anticipated results and expectations expressed in these forward-looking statements. These risks and uncertainties are identified in our annual report on Form 10-K for the year ended December 31, 2021, and any subsequent documents we file with the SEC. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this live conference call, September 20, 2022. The company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call, except as required by law. I will now turn the call over to Alan. Thank you, Mariann, and thank you all for joining our call today. In prior earnings calls and in meetings with investors, Puma has received inquiries as to whether or not the company was looking at bringing in any additional drugs to diversify the company and not just be a one-product company. On its recent earnings calls, Puma has stated that it is indeed looking to bring in additional assets, and we are pleased to announce today that we have in-licensed the anticancer drug alisertib from Takeda. In clinical trials to date, alisertib has shown single-agent activity and activity in combination with other cancer drugs in the treatment of many different types of cancers, including hormone receptor-positive breast cancer, triple-negative breast cancer, small cell lung cancer, and head and neck cancer. The drug has also shown activity in previous clinical trials in peripheral T-cell lymphoma and non-Hodgkin's lymphoma. Takeda's previous clinical development program with alisertib was extensive, and due to this, there's a large, well-characterized clinical safety database with over 1,300 patients who were treated across 22 company-sponsored trials. On today's presentation, Dr. Wong will present the preclinical data showing alisertib's mechanism of action, as well as data from preclinical studies of the drug. I will then present the clinical data that has been generated to date in the indications that Puma is interested in pursuing, and then we will open the call up to questions from investors. I will now turn the call over to Dr. Wong for his presentation. Thank you, Alan. Alisertib is a reversible ATP competitive inhibitor that is highly selective for aurora kinase A, a protein kinase and transcription factor. This inhibition of aurora kinase A leads to the disruption of mitotic spindle cell apparatus assembly and disruption of chromosomal segregation, leading to inhibition of cell proliferation. In hormone receptor-positive cancer cells, aurora kinase A induces the transition from epithelial to mesenchymal phenotype, as characterized by the loss of CD24 surface receptor, decrease in estrogen receptor expression, and upregulation of HER2. Alisertib reversed this transition. Targeting aurora kinase A in vivo also restored a CD24-positive epithelial phenotype. A study of meta-analysis of 39 solid tumor clinical studies included more than 5,000 patients, reported that high aurora kinase A expression levels was a poor prognostic indicator. The forest plot at the right shows a significant association with shorter overall survival. The study also found that there was a shorter progression-free survival and shorter disease-free survival in these patients with overexpression of aurora kinase A, regardless of disease state, tumor stage, or methods used in detection of aurora kinase A expression. Focusing on breast cancer, alisertib treatment in representative hormone receptor-positive, HER2-negative, or triple-negative breast cancer cell lines. Block cell cycle progression and stimulated both apoptosis and autophagy. At the top left, alisertib induced accumulation of cells at the G2M cell cycle arrest as measured by flow cytometry. Below, the Western blots show a corresponding decrease in protein expression of cell cycle regulators CDK1 and cyclin B2. The upregulation of p21 and p53 were also observed. The percentage of both apoptotic as well as autophagic cells also increased upon increasing concentrations of alisertib as seen on the right side of the screen. RB1 is a gene that instructs the protein production of retinoblastoma protein that acts as a tumor suppressor. The loss of RB1 is a common event in cancer and can emerge as a mechanism of resistance to EGFR, CDK4, and estrogen receptor-targeted therapies in breast and lung cancers. RB1 controls entry into S phase of mitosis, and the loss of RB1 function leads to a hyperactivated primed spindle assembly checkpoint. These hyperactivated cancers depend on aurora kinase A in order to overcome spindle assembly checkpoint priming, which leads to stalled mitosis, therefore a potential for synthetic lethal lethality of RB1 loss and inhibition of aurora kinase A. Indeed, in a panel of lung cancers, cell lines on the left, alisertib inhibited those with RB1 loss, in red, to a much greater degree than the wild type, which is in blue. Alisertib strongly inhibits the cell line model of RB1 mutated triple-negative breast cancer, but not when transfected with wild type, RB1, which is in blue. Aurora kinase A and c-MYC, which is another gene transcription factor called cellular mitochondrial mitosis oncogene, upregulate each other, suggesting the existence of a positive feedback loop. c-MYC upregulates cyclin complex, which leads to cell proliferation. Inhibiting aurora kinase A with alisertib would decrease cell proliferation. In fact, the panel of the thyroid cancer cell lines, protein expression levels of aurora kinase, c-MYC, and phosphorylated MYC all tended together on the top left of the western blots. On the bottom left, alisertib inhibited growth of cells with c-MYC overexpression. To the right, xenograft models that expressed higher levels of c-MYC in tumor growth was inhibited, but tumors that had low expression were not. That concludes my part of the break, and I'm gonna turn it back to Alan. Thank you, Alvin. I will now discuss the clinical data that has been generated with alisertib to date in two solid tumors that Puma is interested in continuing the development of alisertib in small cell lung cancer and breast cancer. In a phase 2 trial that was published in The Lancet Oncology in 2015, alisertib was tested as a single agent in several cohorts of patients with solid tumors. These included small cell lung cancer as well as breast cancer. To first discuss the monotherapy data in small cell lung cancer, the study design involved the administration of alisertib to patients with small cell lung cancer who had previously received up to 2 prior cytotoxic regimens in the metastatic setting. Patients were administered alisertib monotherapy at a dose of 50 milligrams BID for 7 days, followed by a 14-day break. As you can see on the table on the right, in patients with chemotherapy-sensitive disease, alisertib resulted in a response rate of 19% and a duration of response of 3.1 months. For the patients with chemotherapy-refractory disease or chemotherapy-resistant disease, alisertib resulted in a response rate of 25% and a duration of response of 4.3 months. We note that the results in patients with chemotherapy-resistant disease compare favorably to results with recently approved drugs in chemotherapy-resistant small cell lung cancer. On this slide, you can see the waterfall plot for the patients treated in the trial with small cell lung cancer treated with alisertib monotherapy. On this slide, the light blue bars represent the chemotherapy-sensitive patients, and the red bars represent the patients with chemotherapy-refractory or resistant relapse. The adverse events in the trial are shown in slide 15. The AEs for alisertib are similar to what one would expect for a drug that targets the cell cycle. The main grade three or higher AEs in the trial were neutropenia, anemia, leukopenia, and thrombocytopenia. The table on slide 16 compares the AEs profile from the study of alisertib with the most recently approved drug in small cell lung cancer, lurbinectedin. As one can see, the side effect profiles of the drug are very similar, with a slightly lower rate of grade three or higher neutropenia and leukopenia for alisertib and slightly lower rates of grade three or higher anemia and thrombocytopenia for lurbinectedin. Alisertib was also tested in a randomized phase 2 trial of paclitaxel plus alisertib versus paclitaxel plus placebo in patients with second-line small cell lung cancer, which was published in the Journal of Thoracic Oncology in 2020. Alisertib was dosed at a different dose than in the monotherapy trial, with alisertib being administered at 40 mg BID for 3 weeks on days 1 to 3, 8 to 10, and 15 to 17, plus paclitaxel dosed at 60 mg/m² IV on days 1, 8, and 15, whereas the comparator arm received placebo plus paclitaxel, with paclitaxel given at 80 mg/m² IV on days 1, 8, and 15 in 28-day cycles. Randomization was stratified by type of relapse after primary treatment based on the common definition for each type, with sensitive defined as relapsed greater than 90 but less than 180 days after primary treatment, and resistant or refractory defined as relapse less than or equal to 90 days after primary treatment. The protocol was initially written by the sponsor to record relapse type at the time from initial response. A protocol amendment was done midway through the trial, which corrected the stratification definition of relapse type after primary treatment so that relapses were recorded from last administration of platinum-based chemotherapy, which is in line with the NCCN treatment guidelines and clinical treatment practice. To maintain balance the primary endpoint of PFS was analyzed by using the original stratification definition of relapse type. In addition a sensitivity analysis, which used the corrected stratification definition, was also performed. The trial also incorporated an extensive biomarker analysis with pre-specified analysis of c-MYC expression and a retrospective analysis of genetic alterations in ctDNA with clinical outcome. The primary endpoint in the trial was progression-free survival, or PFS. For the intent-to-treat population, the hazard ratio using the original definition was 0.77, with a P value of 0.113. Using the corrected definition, the hazard ratio was 0.71 with a P value of 0.038. For the patients with chemotherapy-resistant or refractory relapse, the hazard ratio was 0.66 with a P value of 0.037. For the ITT population, the OS showed a hazard ratio of 0.87 with a P value of 0.714, and using the corrected definition, that hazard ratio was 0.79 with a P value of 0.209. As mentioned previously, there was an extensive biomarker analysis done in the trial with prospective testing for c-MYC. For the patients in the trial who were found to be IHC positive for c-MYC expression, the hazard ratio in the trial was 0.29, with a median PFS for the paclitaxel plus alisertib arm of 4.64 months and a PFS for the placebo plus paclitaxel arm of 2.27 months. The trial also incorporated an analysis of patients with alterations in cell cycle genes, including CDK6, RBL1, RBL2, and RB1. Of note, RB1 mutations were the most frequent mutation with approximately 60% of the patients having RB1 mutations, while CDK6, RBL1, and RBL2 mutations were found with very low frequency. As shown in the slide for patients with cell cycle mutations, the PFS in the paclitaxel plus alisertib arm was 3.68 months, while the placebo plus paclitaxel arm was 1.8 months, and the hazard ratio was 0.395 with a P value of 0.003. The overall survival in the subgroup of patients was 7.2 months for the alisertib arm and 4.47 months for the placebo arm, with a hazard ratio of 0.427 and a P value of 0.00085. Slide 19 shows the AE profile for the trial. Higher rates of grade 3 or higher AEs were seen in the alisertib arm for neutropenia, anemia, and decreased neutrophil count, which would be expected based on the prior phase 2 trial of alisertib monotherapy. There were also drug-related fatalities in the trial due to neutropenic sepsis, febrile neutropenia, and septic shock. We will now move to the clinical trials that have been done with alisertib in breast cancer. In the previously mentioned phase 2 trial of alisertib monotherapy that was published in Lancet Oncology in 2015, alisertib was also tested in patients with HER2-negative hormone receptor-positive breast cancer, HER2-positive breast cancer, and triple-negative breast cancer. Patients were administered alisertib monotherapy at a dose of 50 milligrams BID for 7 days, followed by a 14-day break. In a cohort of patients with HER2-negative hormone receptor-positive breast cancer, treatment with alisertib resulted in a response rate of 23% with a progression-free survival of 7.9 months. The waterfall plot for the trial is shown in slide 23. The red bars represent triple-negative breast cancer patients, the blue bars hormone receptor positive HER2 negative breast patients, and the green bars HER2 positive breast cancer patients. The adverse events seen in the trial, in the patients with breast cancer is shown in slide 24. The AE profile for the drug in breast cancer patients was similar to what was seen in small cell lung cancer patients with the main grade 3-4 AEs being neutropenia, leukopenia, stomatitis, and fatigue. alisertib was also tested in a randomized phase 2 trial in hormone receptor positive HER2 negative metastatic breast cancer patients that was presented at the San Antonio Breast Cancer Symposium in 2020. In this trial, alisertib was dosed at 50 milligrams BID on days 1 to 3, 8 to 10, and 15 to 17 on a 28-day cycle, while fulvestrant was dosed at its approved dose of 500 milligrams IM on days 1 and 15. The baseline characteristics from the trial were well-balanced, although a higher percent of patients with prior therapy were seen in the metastatic setting in the patients with alisertib plus fulvestrant. Of note, patients were required to have continued the treated with prior fulvestrant as an inclusion criteria for the trial. The results from the trial showed a response rate of 17.8% in the alisertib alone arm and 20.0% in the alisertib plus fulvestrant arm. The PFS was seen to be 5.6 months in the alisertib alone arm and 5.1 months in the alisertib plus fulvestrant arm. The lower PFS rate in the combination arm may have been due to the higher% of patients with prior chemotherapy administered in metastatic setting. The fact that no difference in PFS was seen between the alisertib monotherapy and the combination of alisertib plus fulvestrant arm may be due to the fact that all patients had previously received fulvestrant, and we are not aware of any clinical trials that have shown the activity of fulvestrant in patients who've received prior fulvestrant. The AEs from the trial are shown in slide 26. The main AEs seen in the trial were similar to prior monotherapy trial, with neutropenia, anemia, and decreases in white blood cells and lymphocytes seen. Alisertib was seen to be well-tolerated in the trial, with the majority of patients discontinuing due to disease progression and a relatively small percent discontinuing due to tolerability issues. Alisertib was also tested in a randomized phase 2 trial in hormone receptor-positive HER2-negative metastatic breast cancer and triple-negative breast cancer patients, which was published in JAMA Network Open in 2021, where patients were randomized to receive either paclitaxel plus alisertib or paclitaxel alone. In this trial, alisertib was dosed at 40 milligrams BID on days 1-3, 8-10, and 15-17 on a 28-day cycle, while paclitaxel was dosed at 60 milligrams per square meter on days 1, 8, and 15 of a 28-day cycle. In the control arm, paclitaxel was dosed at 90 milligrams per square meter on days 1, 8, and 15 of a 28-day cycle. As is seen on the KM curve on the right, for the cohort of patients with hormone receptor positive HER2 negative metastatic breast cancer, the combination of paclitaxel plus alisertib resulted in a statistically significant improvement in progression-free survival with a hazard ratio of 0.56 and a P value of 0.005. The median PFS in the paclitaxel plus alisertib arm was 10.2 months, and the median PFS in the paclitaxel alone arm was 7.1 months. Treatment with paclitaxel plus alisertib resulted in a higher but not statistically significant improvement in overall survival, with a median OS for the paclitaxel plus alisertib arm of 26.3 months versus 25.1 months for the single-agent paclitaxel arm of the trial. This resulted in a hazard ratio of 0.89 and a P value of 0.61. As investors are aware, the standard of care for the frontline treatment of hormone receptor-positive HER2-negative metastatic breast cancer in the U.S. is treatment with CDK4/6 inhibitors. In a cohort of patients in the trial that were treated with the prior CDK4/6 inhibitor palbociclib, the combination of paclitaxel plus alisertib resulted in a median PFS of 13.9 months, while the paclitaxel alone arm resulted in a median PFS of 5.6 months. The hazard ratio was 0.59, with a P value of 0.19. We believe that there is preclinical data to support the role of alisertib in patients with hormone receptor-positive breast cancer who've progressed on palbociclib. The data on the slide shows that both the loss of RB1 and upregulation of c-MYC correlate with resistance to palbociclib. As you will see on the left, the loss of RB1 in hormone receptor-positive breast cancer cell lines that are resistant to palbociclib. This finding was confirmed by immunohistochemistry, as shown in the middle. On the right, you will see upregulation of c-MYC in the same palbociclib-resistant cell line. There's preclinical data demonstrating alisertib's activity in tumors with RB loss and c-MYC overexpression. We believe these preclinical findings may be the reason for the efficacy seen in the patients with prior CDK4/6 inhibitors in the alisertib trial. We also note that in the previously mentioned clinical data from the phase 2 randomized trial in small cell lung cancer, it was also demonstrated that the activity of alisertib in patients with RB1 mutations and high c-MYC expression. We believe this provides further support for the findings seen in these breast cancer patients who were previously treated with palbociclib. For the cohort of patients with triple-negative breast cancer, the combination of paclitaxel plus alisertib resulted in an improvement in progression-free survival with a hazard ratio of 0.35 and a P value of 0.022. The median PFS in the paclitaxel plus alisertib arm was 9.6 months, and the median PFS in the paclitaxel arm alone was 5.7 months. Treatment with paclitaxel plus alisertib resulted in a higher but not statistically significant improvement in overall survival with the median OS for the paclitaxel alisertib arm of 16 months versus 12 months for the paclitaxel alone arm, which resulted in a hazard ratio of 0.51 and a P value of 0.09. Slide 31 shows the AEs that were seen in the trial. Similar to what was seen in previous trials, higher rates of grade 3 or higher AEs were seen in the paclitaxel plus alisertib arm for neutropenia, leukopenia, diarrhea, mucositis, and stomatitis. This slide summarizes alisertib's clinical activity in breast cancer. We believe that this summary slide well demonstrates alisertib's efficacy in both HR-positive HER2-negative breast cancer as well as triple-negative breast cancer. We believe that this efficacy compares favorably to both the current drugs approved in treatment of these tumor types as well as the drugs that are currently in development in these indications and is supportive of the future development of alisertib in these tumors. As has been previously mentioned, the main AE of alisertib is neutropenia. Slide 33 compares the grade 3 or higher neutropenia as well as the febrile neutropenia rates of alisertib with other drugs that are currently approved for either hormone receptor-positive breast cancer or triple-negative breast cancer. As is seen on the slide, the rates of grade three or higher neutropenia and febrile neutropenia seen with alisertib, either as monotherapy or in combination with fulvestrant or in combination with paclitaxel in breast cancer, are well within the range of the rates of these AEs for the other drugs currently approved for breast cancer. As noted at the bottom of the slide, in clinical trials to date, the neutropenia with alisertib appears to be cumulative, and the company believes it may be able to reduce the rates of grade three or higher neutropenia and febrile neutropenia by using the prophylactic treatment with GCSF as is recommended in the NCCN guidelines for hematopoietic growth factors. This prophylaxis with GCSF has not been used in clinical trials to date, but Puma is looking to implement this prophylaxis with GCSF in future trials of alisertib. Puma is interested in pursuing the development of alisertib in hormone receptor-positive breast cancer as well as small cell lung cancer based on the prior clinical data that has been generated. We are also keenly interested in studying the drug in biomarker-focused populations where the drug has shown a higher degree of activity, such as patients with c-MYC amplification and RB1 loss or RB1 mutations, as we believe that this may provide a point of differentiation from the other drugs being developed in the treatment of these diseases. Puma plans to meet with the FDA in either the second half of 2022 or the first half of 2023 to discuss the alisertib clinical development plan. The company also plans to discuss the FDA's Project Optimus with the FDA as it relates to the current dosing schedule for alisertib. We believe that there will be several clinical milestones for alisertib program in the coming months. This includes the publication of biomarker studies from the randomized trial of alisertib plus fulvestrant versus alisertib alone in hormone receptor-positive HER2-negative breast cancer, which we expect by the end of the year, biomarker data from the randomized trial of alisertib plus paclitaxel versus paclitaxel alone in hormone receptor-positive HER2-negative breast cancer, which we anticipate in the first half of 2023, and data from an ongoing investigator-sponsored trial, which is a phase 1/2 trial of alisertib plus pembrolizumab for the treatment of patients with RB-deficient head and neck squamous cell cancer, which we anticipate sometime in 2023. To briefly discuss the treatment landscape for the indications that we are looking to pursue with alisertib. In the U.S., the incidence of hormone receptor-positive HER2-negative breast cancer is 40,000 patients per year, with 29,700 deaths per year. As discussed previously, there are two biomarkers of interest that we are looking to study with alisertib, elevated c-MYC and RB1 mutations or deletions. According to the published biomarker analysis from clinical trials, approximately 50% of hormone receptor-positive breast cancer tumors may have c-MYC elevations, and approximately 2%-9% of hormone receptor-positive HER2-negative breast cancer samples have RB1 mutations detected at the time of resistance to CDK4/6 inhibitors. We believe that these represent meaningful commercial opportunities for Puma with alisertib in hormone receptor-positive HER2-negative breast cancer. The current treatment paradigm for HR-positive HER2-negative breast cancer is shown on this slide. For the combination of alisertib plus fulvestrant, as is shown on the slide, we believe there's an opportunity to develop the drug in patients who are PIK3CA wild type as a second-line treatment in patients who have failed first-line treatment with a CDK4/6 inhibitor and who are chemotherapy naive. We also see an opportunity to develop the combination of paclitaxel plus alisertib in the same PIK3CA wild type patients in patients who have already been treated with chemotherapy. In both of these patient populations, there is a further opportunity to differentiate the drug by developing it in biomarker-defined populations such as elevated c-MYC and/or RB1 deficiency. We are aware that there are two new drugs, Enhertu and Trodelvy, which may be approved in the future for the treatment of HER2-negative hormone receptor-positive breast cancer as well. We therefore believe that focusing on these biomarker-defined populations would be helpful to differentiate alisertib in the treatment landscape for HER2-negative hormone receptor-positive breast cancer. In the U.S., the incidence of small cell lung cancer is approximately 31,000-33,000 patients per year, with approximately 17,000-18,000 deaths per year. As discussed previously, there are two biomarkers of interest, elevated c-MYC and RB1 mutations or deletions that we are looking to study with alisertib based on the previous clinical trial results, which may provide further differentiation from the other drugs in development. According to the published biomarker data from the alisertib clinical trial, approximately 72% of small cell lung cancer patients have c-MYC elevations, and approximately 60%-80% of small cell lung cancer patients have RB1 mutations. We believe that these findings represent meaningful commercial opportunities for Puma with alisertib in patients with small cell lung cancer. There are currently a limited number of drugs being developed for the treatment of small cell lung cancer. We recognize that lurbinectedin received accelerated approval for small cell lung cancer, and is currently in a phase three confirmatory trial in small cell lung cancer. However, there are not many other drugs in the later stages of development for small cell lung cancer. The licensing terms for the drug, Puma paid Takeda an upfront payment of $7 million, and Puma will pay Takeda a total of $287.3 million upon the achievement of future regulatory and certain one-time sales-based milestones for alisertib. There are no milestone payments due to Takeda during the clinical development of alisertib. The regulatory milestones are spread out over certain geographic regions and are split by indications, and it is fair for investors to assume that the magnitude of the sales-based milestones comprise more than half of the total stated milestone amount. Puma will also pay Takeda a tiered royalty based on net sales of alisertib. Importantly, as there are currently no Takeda-sponsored trials of alisertib that are currently ongoing, and the only ongoing clinical trials are investigator-sponsored, this licensing deal is not anticipated to have any impact to Puma's previously stated R&D budget or expense guidance for 2022. For fiscal year 2022, Puma reiterates its previous guidance that net product revenue will be in the range of $180 million-$190 million. In addition, we continue to expect full year net income to be in the range of $6 million-$10 million. We also continue to anticipate that for Q3 2022, NERLYNX net sales will be in the range of $44 million-$47 million, and we continue to anticipate a Q3 net loss of between $1 million and $2 million. In the Q4 of 2021, Puma implemented a reduction in expenses with the goal of reducing expenses in order to maximize operating cash flows. In the Q2 of 2022, we reported positive net income and are projecting positive net income for the year for 2022, which we believe was a direct result of these expense reductions. The company remains committed to continuing to achieve these operational cash flows, even with the addition of alisertib, and will continue to reduce expenses if needed to achieve this. We look forward to updating investors on this in the future. In summary, we believe that alisertib has demonstrated substantial clinical activity in phase 2 trials of hormone receptor-positive, HER2-negative breast cancer, triple-negative breast cancer, and small cell lung cancer. The drug has clear synergy with Puma's existing business, and we believe that the drug represents a novel mechanism of action from other drugs in development and provides an opportunity for differentiated commercial opportunities in biomarker-directed populations. This concludes today's presentation. We will now turn the floor back to the operator for Q&A. Operator? Thank you. We will now begin the question-and-answer session. If you wish to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. If you wish to withdraw your request, please press star two. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment please while we pull for questions. Our first question comes from Yigal Nochomovitz with Citigroup. Please state your question. Hi, Alan and team. Thank you very much for taking the question. I just had a couple. So for small cell lung cancer, for ER-positive HER2-negative breast, and for triple-negative breast, could you comment on the% of those populations that have the RB1 tumor suppressor gene loss, which would take advantage of the synthetic lethality with aurora kinase A inhibition? The second question is, could you just briefly comment, there's a competitive aurora kinase A inhibitor from Eli Lilly called LY3295668. Any thoughts on the differentiated profile that you have with your asset from Takeda? Thank you. Hi, Yigal. Thank you for the questions. Your first question is the percent of patients with small cell lung cancer, ER positive, HER2 negative breast, and triple negative breast with RB1 mutations. Yeah. We had a slide on this, but I will be more than happy to go over this with you. Okay. In terms of the market size, for small cell lung cancer, it's somewhere between. There have been two studies that have been done. One is obviously the alisertib study. There was another one which is escaping my memory, so I apologize. It was, I believe it was a European study. It was somewhere between 60%-80% of the patients, so the small cell lung cancer patients, that had RB1 loss of function mutations. In terms of ER positive breast cancer. Sorry, go ahead. Okay. In terms of ER positive. Sorry. Yigal, go ahead, sorry. No, no, it's okay. I'll go ahead. I wasn't saying anything. Okay. In terms of ER-positive breast cancer, you know, looking at the patients who have failed CDK4/6 inhibitors, it's somewhere between 2%-9% of hormone receptor-positive, HER2-negative breast cancer patients that have RB1 loss of function mutations. In triple-negative breast, I will have to get back to you. I don't think I have that data. I don't have that handy. Let me get back to you offline on that. Sure. Okay. Your second question, in terms of the competitive landscape, the Lilly assets, we are aware of. We have seen the clinical data for. I am not, you know, from a mechanistic standpoint, there's only so much that's been published on it, but the data is published. I don't remember seeing that there was any responses in their trial. If I remember correctly, I think it was presented at ASCO, and I believe they just saw stable disease. And I believe it right now is. I don't believe they're testing it in small cell lung or breast. I thought for some reason they were just going after it in one of the neuroblastomas, a rare neuroblastoma. Okay. Gotcha. Just one more kind of, like, big picture question. With this in-licensing, should we view this as sort of the, you know, the beginning of a wave of in-licensings from Puma, or is this more of a, you know, a one-off? You got very interested in this asset, fits into your pipeline well, and it's more of a one-off, or should we expect, you know, start to see more deals from you guys? Yeah. Look, first of all, you know, we were very, very pleased in the Q2 of 2022 to be able to be, you know, a net income positive company. We are very, very committed to being a net income positive company. Now, as we move forward and you see NERLYNX sales grow and royalties grow into 2023, 2024, et cetera, we obviously want to protect that. Now, there is obviously an opportunity with alisertib, and it fits in well with, you know, what we're doing to do great things for cancer patients and also to add value to the shareholders and still maintain that net income positivity. If there are other assets out there that we think are interesting and that we can in-license and still maintain that net income positivity, we would certainly be open to that as well. Got it. Thank you, Alan. Thank you. Our next question comes from Divya Rao with Cowen and Company. Please state your question. Hi, Alan. This is Divya Rao on for Mark. Congrats on the deal and thanks for taking our question. Just curious on the small cell lung cancer. I know that you haven't talked to the FDA or anything like that, but just based on the data you have generated, that Takeda has generated so far, is there any kind of plan or have you thought about maybe enriching or screening patients who are MYC positive or RB1, or have the RB1 deficiency, as a way to, like, enrich your population to maybe get a little bit more potency or a higher RR in the trial? Yeah. Divya, absolutely. That's why we, in the presentation, we reiterated many times the focus on biomarker-directed population. Yes, absolutely. We are absolutely interested in either, you know. Again, you know, both, patients with c-MYC elevations and with, you know, RB1 mutations, you know, are present in quite high you know, percentages in small cell lung cancer patients. Do we see it as a way to, you know, enrich the population so that you maximize the activity and hence maximize the risk benefit? Absolutely. Do we also see it as a way from a commercial standpoint of differentiating the asset as well? Absolutely. Definitively, absolutely, we are interested in that. Thank you. That's helpful. Then I guess, more of a, you know, a little bit of a broad question, but just based on the three indications that you are going after, are there any that you think just based on your experience is a little bit more straightforward in terms of registrational, given that all three indications have some level of phase 2, maybe not all randomized, but some level of phase 2 data? Yeah. I don't think I can adequately answer that question till we talk to the FDA. But I think they all have. I mean, there is no question they all have a very straightforward path in terms of, you know, the route to approval. Now, I would say, you know, for hormone receptor positive, HER2 negative breast cancer, I'm not aware of the FDA approving any drug on an accelerated approval basis. You have always had to do a randomized. For small cell lung cancer, obviously there is the precedent with, you know, lurbinectedin, so there might be that opportunity. In triple negative, there might be an accelerated approval opportunity, but, you know, obviously already having positive randomized data there, you know, helps us as well. I think, you know, there is clearly a straightforward pathway in all three tumors, and I think we're interested in having the conversation with the FDA to explore that. Great. Thank you so much. Thank you. Our next question comes from Geoff Meacham with Bank of America. Please state your question. Good afternoon. This is Hal calling in for Geoff Meacham, and thank you for the question. First, congratulations on the deal. I think I have two questions. The first one is really some expectation for the biomarker data in Q4 and also the first half of next year. Are we expecting to see maybe some of the response rate in, you know, RB1 deficiency-engaged patient population? What should we sort of expect to see in those data? And then the second piece is more about the combo strategy. Is it more about the pembro trial that ongoing or what may be some other opportunities that in your hand that you think will have opportunity to explore? Yes, thank you for the question. On your first question, which is the biomarker data, I'm talking off the top of my head here, I think my memory is correct. In the combination of the alisertib plus fulvestrant, I don't remember if RB1 is one of the mutations they're looking at, I don't recall. It's not striking my memory that it is. In the data, which is the paclitaxel plus alisertib, I believe they are looking at the RB1 mutation there we would see that data. In terms of your second question on the combination, to clarify, the combination of pembro plus alisertib is not in small cell lung or breast. It's actually in RB1 deficient head and neck cancer, and that's an investigator-sponsored trial. That is the only study ongoing testing alisertib and pembro. In terms of the combinations we would be interested in taking forward, I think that, you know, there's clearly single agent activity in small cell lung cancer and, you know, specifically in the resistant population. The combination of paclitaxel plus alisertib in small cell lung cancer, we would be interested in taking forward. In terms of HR-positive breast, you know, there's clearly a single agent activity there that is quite good. You know, it's 5.5 or 8 months, depending on the dosing. There's obviously the combination with fulvestrant and the combination with paclitaxel. I think monotherapy combo with fulvestrant combo with paclitaxel are all an option. In the triple negative, you know, it appears there is activity, so the combination of paclitaxel plus alisertib, and so that would be a combination we'd be looking at. Okay, great. Thank you so much. Thank you. Thank you. Our next question comes from Ed White with H.C. Wainwright. Please go ahead. Hi, Alan. Thanks for taking my questions, and congratulations on this deal. Just a couple of questions. First, what kind of infrastructure changes are you going to be needing to your R&D to move into the registration trials? You know, how should we be thinking of R&D spend next year? As you mentioned, you're focusing on remaining net income positive. Should we be thinking about you bringing, you know, the different indications and the different, you know, either monotherapy or combination trials? How should we be thinking about you bringing all that forward? Should we be thinking about you bringing forward several trials at once, or are you gonna be thinking about doing, you know, something more consecutively to hold costs down? Thanks. Thanks for the question, Ed. In terms of the infrastructure at Puma, you know, as you are well aware, we have an existing R&D and regulatory affairs infrastructure, you know, that is capable of running clinical trials and filing NDAs and things like that. I don't anticipate any change to the infrastructure. I think we would just probably take, you know, all of the employees who are currently working on neratinib, and as those trials kind of are ending, just transition them over to alisertib. The team is fantastic. They've done a great job. They have done a wonderful job executing on R&D, and I, you know, look forward to working with them on alisertib. On the commitment to net income positive, you're absolutely correct that we want to focus on that. In terms of the indications, we're gonna need to be, you know, very, you know, sensitive to that. Obviously, if you took all three indications forward at the same time, that would increase the R&D spend quite a bit. If you staggered them like what you are suggesting, that would be a way to be able to, you know, reduce the spend. There is no question that that's what we would be looking to do, which is again, that focus is on that net income line. If it means that instead of taking, you know, three forward, we, you know, stagger them one to three, or maybe we only take two of them forward and, you know, wait until one's approved to bring the other one or something like that, there's no question we would be focusing on that R&D line and not letting it ratchet up too much so that we protect the net income. Okay. Thanks, Alan. Thank you. Our next question comes from Gena Wang with Barclays. Please state your question. Thank you for taking the questions, and congratulations as well. This is Tong for Gena. Maybe first, just following on the question on the PD1 combo, is there any evidence suggests synergistic effect between the alisertib and the PD1, the pembro, in the head and neck cancers? Why don't you also pursue the similar combo in the small cell lung cancer? Yeah. Regarding the PD1 combo with alisertib, there is preclinical data suggesting, you know, an additive, if not synergistic effect of the combination, and I believe it was specifically in head and neck, so hence the reason that the investigators studying that. You know, we'll obviously wait for the data, and if it shows something interesting, you know, we can get to certain other tumors. In terms of doing it in small cell lung cancer, that would be a bit tricky because in small cell, PD1 is approved as a first-line regimen in combination with other chemos. I don't know that, you know, a big frontline study adding alisertib to a bunch of other chemos, that would be quite challenging to do, first of all. Second, given that we already have, you know, very strong data in the second line, I would rather kind of, you know, go with what has been, you know, risk reduced, if you will, and where we see a very, you know, clean risk benefits, from our perspective. I would rather go with that as the first indication, rather than try to do something more complicated, more expensive, and more challenging in the first line. Thank you. Thank you. This concludes our Q&A session. I will now turn the conference back to Maria nn for closing remarks. Thank you for your time and attention today. As a reminder, this call may be accessed via replay of the webcast at pumabiotechnology.com. Have a good evening. Thank you. This concludes today's conference. All parties may disconnect. Have a great day.