Good afternoon. My name is John. 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 star 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. Thank you. You may begin your conference. Thank you, John. Good afternoon, and welcome to Puma's conference call to discuss our results for the first quarter of 2026. Joining me on the call today are Alan Auerbach, Chief Executive Officer, President and Chairman of the Board of Puma Biotechnology, Maximo Nougues, Chief Financial Officer, Heather Blaber, Senior Vice President of Marketing, and Roger Storms, Senior Vice President of Sales. After the close today, Puma issued a news release detailing results for the first quarter of 2026. That news release, the slides that Alan and Roger will refer to, and a webcast to this call are accessible via the homepage and investor sections of our website at pumabiotechnology.com. The webcast and presentation slides will be archived on our website and available for replay for the next 90 days. Today's conference call will include statements about Puma's future expectations, plans, and prospects that constitute a forward-looking statement for purposes of federal securities laws. Such statements are subject to risks and uncertainties, and actual events and results may differ from those expressed in these forward-looking statements. For a full discussion of these risks and uncertainties, please review our periodic and current reports filed with the SEC from time to time, including our annual report on Form 10-K for the year ended December 31, 2025. 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, May 7, 2026. Puma 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. During today's call, we may refer to certain non-GAAP financial measures that involve adjustments to our GAAP figures. We believe these non-GAAP metrics may be useful to investors as a supplement to, but not a substitute for, our GAAP financial measures. Please refer to our first quarter 2026 release for a reconciliation of our GAAP to non-GAAP results. I will now turn the call over to Alan. Thank you, Mariann, and thank you all for joining our call today. Today, Puma reported total revenue for the first quarter of 2026 of $44.8 million. Total revenue includes product revenue net, which consists entirely of NERLYNX sales, as well as royalties from our sub-licensees. Product revenue net was $42 million in the first quarter of 2026. It declined from $59.9 million reported in Q4 2025 and $43.1 million reported in Q1 2025. As a reminder to investors, Puma's reported NERLYNX sales includes both U.S. net sales and product supply revenues of NERLYNX to Puma's ex-U.S. partners. Product revenue for the first quarter of 2026 was impacted by approximately $7.9 million of inventory drawdown at our specialty pharmacies and specialty distributors. Royalty revenue was $2.8 million in the first quarter of 2026, compared to $15.6 million in Q4 2025 and $2.9 million in Q1 2025. As noted in our last call, royalty revenue in Q4 2025 was driven by the shipment to our partner in China. We reported 2,328 bottles of NERLYNX sold in the first quarter of 2026, compared to 3,298 bottles sold in Q4 2025. In Q1 2026, we estimate that inventory decreased by 439 bottles. In Q1 2026, new prescriptions were up approximately 25% compared to Q4 2025, and total prescriptions were down approximately 4% compared to Q4 2025. Roger will provide further details in his comments and slides. I will now present the interim data from Puma's ongoing phase II trials of alisertib in small cell lung cancer and HER2 negative ER positive breast cancer, also referred to as the ALISCA™-Lung1 and ALISCA™-Breast1 trials. Heather Blaber and Roger Storms will add additional color on NERLYNX's commercial activity. Maximo Nougues will follow with highlights of the key components of our financial statements for the fourth quarter of 2025. We now move to the ALISCA™-Lung1 interim presentation. As a reminder, 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 is a large, well-characterized clinical safety database with over 1,300 patients who were treated across 22 company-sponsored trials. From a preclinical perspective, it has been shown that Aurora kinase A and c-MYC upregulate each other, which suggests the existence of a positive feedback loop. c-MYC upregulates the cycling complex, which leads to self-proliferation. By inhibiting Aurora kinase A with alisertib, it also inhibits c-MYC, which decreases cell proliferation. Additionally, preclinical data has shown that alisertib inhibited growth of cells with c-MYC overexpression and in xenograft models that expressed high levels of c-MYC, tumor growth was inhibited. Puma's phase II trial, ALISCA™-Lung1, which is also referred to as study PUMA-ALI-4201, was designed to enroll up to 60 patients with small cell lung cancer who had received prior treatment with a platinum-based chemotherapy and immunotherapy. The trial enrolls both second-line and third-line patients. Patients must provide tissue-based biopsies so that biomarkers can be analyzed. alisertib was initially dosed at 50 mg BID on days one to seven of a 21-day cycle. As investors are aware, the trial was then amended to increase the dose to 60 mg BID, and the company is now in the process of increasing the dose to 70 mg BID. The primary endpoint of the trial is to determine whether any biomarker correlates with alisertib response with endpoints of overall response rate, duration of response, disease control rate, progression-free survival, and overall survival. The secondary endpoints include investigator-assessed efficacy and survival. Mandatory G-CSF prophylaxis is also given in the trial in an effort to reduce the neutropenia that was shown to be dose limiting in the previous clinical trials with alisertib. Slide six shows the baseline characteristics for the 52 patients treated at 50 mg BID and the 27 patients treated at 60 mg BID that are included in this interim analysis. Slide seven shows the summary of the prior treatments the patients received prior to entering the study. Of note, all of these patients were treated in either the second line or third line in this trial. To first discuss the safety in the trial. In previous clinical trials of alisertib, the treatment emergent adverse events seen were those characteristic of a cell cycle inhibitor, with neutropenia being the main AE seen in the highest percentage. In this trial, the all grade neutropenia was 19.2% in the 50 mg arm and 22% in the 60 mg arm. Slide 10 shows the rates of Grade 3 and 4 AEs seen in the trial. Of note, the Grade 3 or higher neutropenia rate was 13.5% in the 50 mg arm and 11.1% in the 60 mg arm. Slide 11 compares the Grade 3 and grade 4 AE rates seen in the ALISCA™-Lung1 trial to those that were seen in the previous phase II trial of alisertib monotherapy in small cell lung cancer, referred to as study C14007. C14007 was previously published in Lancet Oncology in 2010. As a reminder, in C14007, G-CSF prophylaxis was not mandated, while ALISCA™-Lung1 requires mandatory prophylactic G-CSF. As can be seen on the slide, the use of prophylactic G-CSF appeared to reduce the rates of Grade 3 or higher neutropenia compared to what was seen in the previous trial. The next moves to the efficacy seen in the trial. As you can see in slide 13, in the 52 patients in ALISCA-Lung1 that were treated at 50 mg, we have seen four patients or 11.5% with a best response of a partial response and 18 patients or 34.6% with stable disease. The median PFS for the 50-milligram arm was 1.7 months. In the first 15 patients in the 60 mg arm, we have seen one patient or 6.7% with a best response of a partial response and seven patients or 46.7% with stable disease. The median PFS for the 60 mg arm is currently 4.2 months. Slide 14 shows the Kaplan-Meier curve for PFS between the 50 mg and 60 mg arm of the trial. As previously stated, the median PFS for the 60 mg arm is currently 4.2 months. However, we caution it is still early and we await additional patient numbers and additional follow-up. We will now move to the biomarkers in the trial. Slide 16 presents the Kaplan-Meier curve for the patients according to c-MYC H-score. c-MYC H-score is a semi-quantitative immunohistochemical assessment that measures the intensity and percentage of tumor cells staining for the c-MYC protein, typically ranging from 0 to 300. High c-MYC H-scores are believed to be associated with poor prognosis and lower overall survival in various cancers. As you can see on slide 16, for the combined doses of 50 mg and 60 mg, patients with c-MYC H-score of between zero and 100 had a median PFS of 1.68 versus a PFS of 4.17 for the patients with a c-MYC H-score of between 101 and 300. This would suggest that alisertib has better activity in cancers with a higher amount of c-MYC activity. Slide 17 presents the KM curve for the 50 mg and 60 mg dose separately for the patients according to c-MYC H-score. As you can see on the slide, for the 50 mg dose, patients with H-score of between zero and 100 had a median PFS of 1.68 months versus a PFS of 2.83 months for the patients with a c-MYC score of between 101 and 300. For the 60 mg dose, patients with H-score of between zero and 100 had a median PFS of 1.41 months, while the median PFS has not yet been reached for the patients with c-MYC H-score of 101 - 300. We believe that these slides are suggesting that alisertib has greater activity in tumors with higher c-MYC H-scores and hence more c-MYC activity, which we believe is due to the inhibition of the Aurora kinase A pathway by alisertib. Slide 18 presents the KM curve for the patients according to% of tumor cells that are c-MYC +. As you can see on slide 18, for the combined doses of 50 mg and 60 mg, for tumors having between 0% and 10% of the cells c-MYC +, there's a median PFS of 1.68 months, versus a PFS of 2.83 months for the patients with tumors having between 11% and 100% of the cells c-MYC +. Slide 19 presents the KM curve for the 50 mg and 60 mg doses separately for the patients according to the perent of tumor cells that are c-MYC +. As you can see on the slide, for the 50 mg dose, patients with tumors having between 0% and 10% of the cells c-MYC + had a median PFS of 1.68 months versus a PFS of 2.73 months for patients with tumors having between 11% and 100% of the tumor cells c-MYC +. For the 60 mg dose, between 0% and 10% c-MYC + had a median PFS that has not been reached versus a PFS of 4.17 months for the patients with between 11% - 100% of the tumor cells c-MYC +. We believe that these slides are suggesting that alisertib has greater activity in the tumors where a higher percentage of the cells are c-MYC +, which we again believe is due to the inhibition of the Aurora kinase A pathway by alisertib. We believe that the initial clinical data with alisertib in small cell lung cancer are demonstrating that alisertib is showing better activity in patients where c-MYC is playing a role in driving the tumor, which is indicative of tumors where Aurora kinase A is activated. There are currently 32 patients enrolled in the 60 mg arm of the trial. Based on this preliminary safety seen at this dose, we are continuing to dose escalate to 70 milligrams, and we hope to begin enrollment of the 70 mg cohort in the second half of 2026. We believe that the data generated thus far in ALISCA™-Lung1 is showing that alisertib monotherapy is showing a PFS at higher doses and in certain biomarker-directed populations that is as good or slightly better than the PFS for currently approved drugs in this space. As discussed previously, we are hopeful that with increasing doses of alisertib monotherapy in ALISCA™-Lung1, we can achieve higher concentrations of alisertib in these biomarker-defined populations and potentially open up the opportunity for a phase III design that tests alisertib monotherapy in a randomized trial. As investors are aware, alisertib was previously tested in a randomized phase II trial of paclitaxel plus alisertib versus paclitaxel plus placebo, where a PFS and OS benefit was seen in patients with tumors with biomarkers that appear to indicate that the Aurora kinase A pathway was activated. Based on this data and the data from ALISCA™-Lung1, Puma will be looking to a dual approach for the development of alisertib in small cell lung cancer. In addition to the monotherapy dose escalation approach in ALISCA™-Lung1, Puma will also be looking to initiate ALISCA™-Lung2, which will investigate the efficacy of alisertib given in combination with paclitaxel using mandatory G-CSF prophylaxis. We are hoping to initiate this trial in the second half of 2026. We are pleased with the interim data from ALISCA™-Lung1, and we believe it is showing an improved tolerability profile for alisertib monotherapy and improved efficacy with dose escalation as well as improved efficacy in a biomarker-directed population that is indicative of the Aurora kinase A pathway activation. We anticipate additional interim efficacy data from ALISCA™-Lung1 in the second half of 2026 or the first half of 2027. I will now move to the ALISCA™-Breast1 interim presentation. As a reminder, and as previously stated, 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 cancer, including hormone receptor-positive breast cancer, triple-negative breast cancer, small cell lung cancer, and head and neck cancer. There's also a large, well-characterized clinical safety database with over 1,300 patients who were treated across 22 company-sponsored trials. As previously stated, from a preclinical perspective, it has been shown that Aurora kinase A and c-MYC upregulate each other, which suggests the existence of a positive feedback loop. Preclinical data has shown that alisertib inhibited growth of cells with c-MYC overexpression, and in xenograft models that expressed higher levels of c-MYC, tumor growth was inhibited. Puma's phase II ALISCA™-Breast1, also referred to as Study PUMA-ALI-1201, investigates alisertib in combination with endocrine treatment consisting of either anastrozole, exemestane, letrozole, fulvestrant, or tamoxifen in patients with HER2 negative, hormone receptor-positive, recurrent or metastatic breast cancer. Patients must be chemotherapy naive in the recurrent or metastatic setting and have had previous treatment with a CDK4/6 inhibitor and have received at least two prior lines of endocrine therapy in the recurrent or metastatic setting to be eligible for the trial. Patients were dosed with alisertib given at either 30 mg, 40 mg, or 50 mg BID on days one - three, eight- 10, and 15 - 17 on a 28-day cycle in combination with the endocrine therapy of investigator's choice. Patients must not have been previously treated with the endocrine treatment in the metastatic setting that will be given in combination with alisertib in the trial. The primary endpoints include objective response rates, duration of response, disease control, and progression-free survival. As a secondary objective, the company is evaluating each of these efficacy endpoints within biomarker subgroups in order to determine whether any biomarker subgroup correlates with better efficacy, which might give the company the potential to focus future clinical development of alisertib in combination with endocrine therapy for patients with HER2 negative, hormone receptor-positive breast cancer in these biomarker-specific populations. Slide 25 shows the baseline characteristics for the 164 patients included in this interim analysis. As the slide shows, the majority of these patients were treated in the third-line or later setting. First, discuss the safety in the trial. As previously mentioned in previous clinical trials of alisertib, the treatment-emergent adverse events seen were those characteristic of a cell cycle inhibitor, with neutropenia being the AE seen in the highest percentage. Slide 27 shows the rates of Grade 3 or 4 AEs seen in the trial. Of note, the Grade 3 or higher neutropenia rate was 8% in the 30-mg arm, 10.2% in the 40-mg arm, and 26.9% in the 50-mg arm. It is important for investors to note that prophylactic G-CSF was not given in the study. Slide 27 also compares the Grade 3 or 4 AE rates seen in the ALISCA™-Breast1 trial to those that were seen in the previously published phase II of alisertib in HER2-negative, ER-positive breast cancer that was published in JAMA Oncology in 2020, referred to as study TBCRC 041. As can be seen in the slide, the rates of Grade 3 or higher neutropenia appear to be lower in the ALISCA™-Breast1 trials compared to what we're seeing in TBCRC 041. To next move to the efficacy seen in the trial. Slide 29 shows the summary of clinical benefits for the patients with at least one post-baseline scan or who ended treatment or died before they got a scan. As you can see in the slide, the best response was 5% in the 30 mg arm, 20% in the 40 mg arm, and 18.4% in the 50 mg arm. Slide 30 shows the Kaplan-Meier curve for PFS in the trial. As is seen in the slide, the median PFS of the 30 mg arm is currently 2.04 months. The median PFS of the 40 mg arm is 5.45 months, and the median PFS of the 50 mg arm is currently 5.59 months. We will now move to the biomarkers in the trial. Slide 32 presents the KM curve for all the patients in the trial according to c-MYC copy number, also referred to as c-MYC copy number gain. As you can see on the slide, for all of the patients in the trial for which there are tissue results, patients with c-MYC copy number of greater than two had a median PFS of 7.29 months, versus a median PFS of 2.0 months for the patients with a c-MYC copy number equal to two. Slide 33 presents the KM curve for all of the patients for which there are tissue results according to percent of tumor cells that are c-MYC +. As you can see on the slide, for the patients with between 0% and 10% of the cells c-MYC +, the median PFS was 3.06 months versus a PFS of 5.62 months for the patients with between 11% and 100% of the cells c-MYC +. Slide 34 presents the KM curve for the 50 mg and 40 mg doses separately for the patients according to percent of tumor cells that are c-MYC +. As you can see on the slide, for the 40 mg dose, patients with between 0% and 10% of the cells c-MYC + had a median PFS of 3.9 months versus a PFS of 5.75 months for the patients with between 11% and 100% of the tumor cells c-MYC +. For the 50 mg dose for patients with between 0% and 10% of the cells c-MYC +, there was a median PFS of 3.58 months versus a PFS of 9.3 months for the patients with between 11% and 100% of the tumor cells c-MYC +. Similar to the data from ALISCA™-Lung1, we believe that these slides are suggesting that in patients with alisertib has greater efficacy in ALISCA™-Breast1 in tumors where a higher percent of the tumor cells are c-MYC + and hence a greater degree of c-MYC activation. Preclinically, it's been shown that alisertib inhibits c-MYC + cells. We believe that this increased efficacy is due to the mechanism of action of alisertib and the inhibition of the Aurora kinase pathway. Slide 35 presents the KM curve for all the patients according to ESR1 mutation status. As is seen on the slide, for patients at all three dose groups who are ESR1 mutated as measured by ctDNA, a median PFS of 5.62 months was seen versus a PFS of 3.58 months for the people who are ESR1 wild type as measured by ctDNA. For patients at all three dose groups who are ESR1 mutated as measured by tissue, a median PFS of 7.23 months was seen versus a PFS of 3.71 months for patients who are ESR1 wild type as measured by tissue. It is important for investors to remember that these patients are being treated in the third-line setting. These patients have already received treatment with a selective endocrine receptor degrader, or SERDs. Since enrollment of this trial was done while the newer oral SERDs have either been FDA-approved or in later stages of clinical development, many of the patients in the ALISCA™-Breast1 trial have been previously treated with the new oral SERDs. More specifically, approximately 58% of the ESR1 mutated patients in the trial were previously treated with oral SERDs, including camizestrant, elacestrant, giredestrant, imlunestrant, or palazestrant. Slide 36 presents the KM curve for the 50 mg and 40 mg dose groups separately for patients according to ESR1 mutation status as measured by ctDNA. For patients in the 40 mg group who are ESR1 mutated as measured by ctDNA, a median PFS of 3.7 months was seen, versus a PFS of 5.75 months for the patients who are ESR1 wild type as measured by ctDNA. For patients at the 50 mg group who are ESR1 mutated as measured by ctDNA, a median PFS of 9.3 months was seen, versus a PFS of 2.76 months for the patients who were ESR1 wild type as measured by ctDNA. Slide 37 presents the KM curve for the 50 mg and 60 mg dose separately for patients who are ESR1 according to ESR1 mutation status as measured by tissue. For the patients at the 40 mg group who are ESR1 mutated as measured by tissue, a median PFS of 4.86 months was seen versus a PFS of 4.04 months for the patients who are ESR1 wild type as measured by tissue. For the patients of the 50 mg group who are ESR1 mutated as measured by tissue, a median PFS has not yet been reached versus a PFS of 3.58 months for patients who were ESR1 wild type as measured by tissue. Slide 38 presents the KM curve for all the patients according to PIK3CA mutation status. As is seen on the slide, for patients at all three dose groups who are PIK3CA mutated as measured by ctDNA, a median PFS of 2.1 months was seen, versus a PFS of 5.45 months for patients who were PIK3CA wild type as measured by ctDNA. For patients at all three dose groups who were PIK3CA mutated as measured by tissue, a median PFS of 3.71 months was seen versus a PFS of 4.86 months for patients who were PIK3CA wild type as measured by tissue. Slide 39 shows the KM curve for the 50 mg and 40 mg dose separately for patients according to PIK3CA mutation status as measured by ctDNA. For patients at the 40 mg group who were PIK3CA mutated as measured by ctDNA, a median PFS of 3.71 months was seen versus a PFS of 5.65 for patients who were PIK3CA wild type as measured by ctDNA. For patients at the 50 mg group who were PIK3CA mutated as measured by ctDNA, a median PFS of 3.58 months was seen versus a PFS that has not yet been reached for patients who were PIK3CA wild type as measured by ctDNA. Based on the efficacy seen in the patients who were ESR1 mutated and PIK3CA wild type, the company conducted a subset analysis to specifically focus on these two subgroups. Slide 40 presents the KM curve for patients who were PIK3CA wild type according to ESR1 mutation status. As is seen on the slide, for patients at all three dose groups who were PIK3CA wild type and who had an ESR1 mutation as measured by ctDNA, a median PFS has not yet been reached versus a PFS of 3.48 months for patients who were PIK3CA wild type and ESR1 wild type as measured by ctDNA. For patients at all 3 dose groups who were PIK3CA wild type and who had an ESR1 mutation as measured by tissue, a median PFS has not been reached versus a PFS of 2.79 months for patients who were PIK3CA wild type and ESR1 wild type as measured by tissue. Slide 41 presents the KM curve according to 50 mg and 40 mg doses separately for the patients who were PIK3CA wild type according to ESR1 mutation status as measured by ctDNA. For PIK3CA wild type patients at the 40 mg group who are ESR1 mutated as measured by ctDNA, a median PFS of 4.86 months was seen versus a PFS of 5.75 months for the patients who were ESR1 wild type as measured by ctDNA. For PIK3CA wild type patients at the 50 mg group who were ESR1 mutated, median PFS has not been reached versus a median PFS of 2.14 months in the patients who were ESR1 wild type as measured by ctDNA. We are very pleased to see that at the 50 mg dose group for the patients who were PIK3CA wild type and ESR1 mutant, no patient has yet progressed. Although we caution these numbers here are small and further patient follow-up is needed. Slide 42 presents the KM curve for the 50 mg and 40 mg dose separately for patients who were PIK3CA wild type according to ESR1 mutation status as measured by tissue. For PIK3CA wild type patients at the 40 mg group who were ESR1 mutated as measured by tissue, a median PFS of 7.23 months was seen versus a PFS of 3.98 months for the patients who were ESR1 wild type as measured by tissue. For PIK3CA wild-type patients at 50 mg who are ESR1 mutated, the median PFS has not been reached versus a median PFS of 2.14 months in the patients who are ESR1 wild type as measured by tissue. Again, we are very pleased to see that the 50 mg dose group for the patients who are PIK3CA wild type and ESR1 mutant, no patients has yet progressed, although we caution these numbers here are small and further patient follow-up is needed. As was shown in the earlier slides, c-MYC appeared to play a role in the activity of alisertib in HER2 negative, ER-positive breast cancer. More specifically, the analysis on slides 34, 33 and 34 show that alisertib had better activity in patients with a higher% of their cells being c-MYC +. This analysis also showed that patients with between 11%-100% of their cells being c-MYC + showed the best activity with alisertib. We therefore conducted an analysis to see whether or not c-MYC had any correlation with the activity of alisertib that we are seeing in the PIK3CA wild type patients, the ESR1 mutated patients, or the patients who are both PIK3CA wild type and ESR1 mutated. On slide 43, we present the data that shows the% of c-MYC + cells for PIK3CA wild type, ESR1 mutated, and patients who are both PIK3CA wild type and ESR1 mutated. The left-hand side of the slide presents the patients whose mutation status was determined by tissue. The right-hand side of the slide shows the patients whose mutation status was by ctDNA. As you can see on the slide, patients who are PIK3CA wild type, patients who are ESR1 mutated, and patients who are both PIK3CA wild type and ESR1 mutated appear to show an increase in the median percent of c-MYC + cells. This is seen in both the patients where the mutation status is determined by ctDNA and in tissue. It is also seen in this analysis that a high percent of the patients who are PIK3CA wild type, who are ESR1 mutant, and who are both PIK3CA wild type and ESR1 mutant have between 11% to 100% of their cells being c-MYC +, which is again where the best activity of alisertib has been shown to occur. We believe this analysis is suggesting that better activity being seen with alisertib in the patients who are PIK3CA wild type, ESR1 mutated or both PIK3CA wild type and ESR1 mutated may be due to this increased c-MYC activity, and it appears to be showing that c-MYC is playing a role in driving the tumor in these subgroups of patients, which is suggestive of tumors where the Aurora kinase A is activated and hence where alisertib's mechanism of action may be playing a role. When Puma licensed alisertib, it had stated that the goal was to enroll ALISCA™-Breast1 in order to perform a biomarker analysis to better understand which biomarker subgroups had the best activity and then amend the trial to focus on a more biomarker-focused population. Based on the interim data from ALISCA™-Breast1, the company is going to be expanding the enrollment in the trial to obtain more data on the biomarker-focused cohorts with a focus in the patients who are PIK3CA wild type, ESR1 mutant, or both. The company anticipates this will occur in the second half of 2026. The company also plans to present updated data on the ALISCA™-Breast1 trial in the second half of 2026. Similar to the data from ALISCA™-Lung1, we believe that the data generated thus far in ALISCA™-Breast1 is showing that alisertib in combination with endocrine therapy appears to be active in the third-line setting and more specifically in patients who are PIK3CA wild type, ESR1 mutant, or both PIK3CA wild type and ESR1 mutant. Similar to ALISCA™-Lung1, the activity of alisertib in the trial appears to be driven by c-MYC. To our knowledge, we are not aware of any drugs that have shown this level of activity in these subgroups of patients in the third line, which we believe differentiates the drug from others in development. We believe that this activity is attributable to biomarkers that are indicative of aurora kinase pathway activation, which we believe is in line with the mechanism of action of alisertib. As we've mentioned on prior earnings calls and in response to investor questions, Puma continues to evaluate several commercial-stage and development-stage drugs to potentially in-license and acquire that would allow the company to diversify itself and leverage Puma's existing R&D, regulatory or commercial infrastructure. The company will keep investors updated on this as it progresses. I will now turn the call over to Heather Blaber for an update on our marketing initiatives. Roger Storms will follow with a review of our commercial performance during the quarter. Thanks, Alan. I appreciate the opportunity to share some additional insights into our marketing strategy. The marketing team is focused on continued awareness of both clinical data for NERLYNX, as well as reinforcing the continued unmet need in HER2-positive early-stage breast cancer after adjuvant therapy. We continue to invest in market research to help us understand and validate the most effective ways to communicate our data with healthcare professionals through both personal and non-personal promotion. Our strategy is focused on increasing awareness of our dual indication in HER2-positive breast cancer. We believe NERLYNX plays an important role in the early stage by reducing the risk of recurrence and in the metastatic setting by helping protect against progression. Not only do physicians who have experience with NERLYNX continue to identify appropriate patients that could benefit from additional therapy post-adjuvant treatment. We continue to adopt new prescribers year-over-year who recognize the unmet need in HER2-positive early-stage breast cancer and how NERLYNX can help their patients. In summary, we are excited and committed about the potential to engage with more oncologists and support their patients diagnosed with HER2-positive breast cancer in both the early and metastatic setting. I will now turn the call over to Roger Storms to provide an overview on the commercial performance for the first quarter. Thank you, Heather, and thanks to everyone for joining our 1st quarter earnings call. Before I move into the commercial review, just a reminder that I'll be making forward-looking statements. The sales team remains focused on expanding overall HCP reach and frequency with a strong emphasis on driving engagement when treatment decisions are being made. Q1 2026 call activity increased 44% year-over-year and 14% quarter-over-quarter. The year-over-year and quarter-over-quarter increases are a direct result of continued emphasis put on executional excellence and increased field accountability. The commercial team continues to prioritize increasing use of NERLYNX with a main focus on patients at higher risk of recurrence. They're also dedicated to enhancing clinical education and engagement through non-personal promotional efforts, as well as utilizing patient resources to support persistence and compliance during NERLYNX therapy. Let me now transition to some of the commercial slides, where I'll provide some additional specifics around performance. Slide three is an illustration of our distribution model, which is broken out into the specialty pharmacy channel and the specialty distributor or in-office dispensing channel. Regarding the overall distribution of our business, in Q1 2026, about 58% of our business was purchased through the SP channel and the remaining 42% was purchased through the SD channel. We continue to see stronger growth in the SD channel, driven mainly by increased sales in the group purchasing organizations or GPO segment. Turning to slide four. NERLYNX net product revenue in Q1 2026 was $42 million, which represents a decrease of $17.9 million from the $59.9 million we reported in Q4 2025, and a decrease of $1.1 million from the $43.1 million we reported in Q1 of 2025. As a reminder to investors, Puma's reported NERLYNX sales include both U.S. net sales of NERLYNX and product supply revenues of NERLYNX to Puma's ex-U.S. partners. Please note that in Q1 of 2025, we reported product supply revenue to our international partners of approximately $400,000 versus the $150,000 in Q1 of 2026. Therefore, U.S. net sales of NERLYNX in Q1 2026 were $41.8 million versus the $42.7 million in Q1 of 2025. I'll provide some more details around inventory changes and Maximo will provide some additional specifics around gross and net expenses during his update. In Q1 2026, we estimate that inventory decreased by about $7.9 million. As a comparator, we estimate that inventory increased by about $5.7 million in Q4 of 2025. Slide five shows Q1 2026 ex-factory bottle sales and also provides both a year-over-year and quarter-over-quarter comparison. In Q1 2026, NERLYNX ex-factory bottle sales were 2,328, which represents an approximate 29% decrease quarter-over-quarter, while remaining essentially flat at 0.4 year-over-year. Let me specifically call out the inventory changes from a bottle perspective. In Q1 2026, we estimate that inventory decreased by about 439 bottles. As a comparator, we estimate that inventory increased by 343 bottles in Q4 of 2025 and decreased by 251 bottles in Q1 of 2025. Let me take a moment to provide some additional metrics regarding our first quarter performance. In Q1 2026, we saw enrollments increase by about 10% quarter-over-quarter and about 1% year-over-year. Commercial new patient starts, or NRXs, were even stronger, increasing by about 25% quarter-over-quarter and about 11% year-over-year. Turning to total prescriptions, or TRXs, we saw TRXs decline about 4% quarter-over-quarter and about 1% year-over-year. Finally, let me share some specifics around commercial demand overall. In Q1 2026, we saw demand decrease by about 6% quarter-over-quarter, but increase by about 7% year-over-year. As mentioned, these dynamics are strongly influenced by SD patterns. In Q1 2026, we saw SD demand decrease by about 9% quarter-over-quarter due to Q4 buy-ins, while continuing to show strong growth year-over-year at about 28%. Slide six highlights the quarterly adoption of dose escalation since the launch of NERLYNX. In Q1 2026, approximately 78% of patients started NERLYNX at a reduced dose. This is higher compared to the 75% we reported in Q4 2025. Continued messaging and adoption of dose escalation remains an important commercial priority. We believe dose escalation coupled with patient education resources will give patients better support throughout their NERLYNX therapy and ultimately help them reduce the risk of recurrence. Slide seven highlights the strategic collaborations we formed across the globe. Most recently, in Q1 2026, NERLYNX was launched in Thailand, also in the extended adjuvant setting. We really appreciate the excellent work being done by our partners around the world and look forward to supporting their continued success moving forward. I'll close by sharing my sincere appreciation for the entire Puma team and their steadfast commitment to supporting patients and families affected by breast cancer. This disease is truly devastating. While meaningful progress has been made, we know there's still important work ahead and even more we can accomplish together. I'll now turn the call over to Maximo for review of our financial results. Thanks, Roger. I will begin with a brief summary of our financial results for the first quarter of 2026. Please note that I will make comparisons to Q4 2025, which we believe is a better indication of our progress as a commercial company than year-over-year comparisons. For more information, I recommend that you refer to our first quarter 2026 10-Q, which will be filed today and includes our consolidated financial statements. For the first quarter of 2026, we reported a net loss based on GAAP of $3.8 million or $0.07 per share. This compares to net income in Q4 2025 of $13.4 million or $0.27 per basic share and $0.26 per diluted share. The fourth quarter of 2025 included a net change in valuation allowance that unfavorably impacted net income by $3.2 million. On a non-GAAP basis, which is adjusted to remove the impact of stock-based compensation expense, we reported a net loss of $1.9 million for $0.04 per share for the first quarter of 2026. Gross revenue from NERLYNX sales was $57.5 million in Q1 2026 and $82.9 million in Q4 2025. As Alan mentioned, net product revenue from NERLYNX sales was $42 million, an increase from the $59.9 million reported in Q4 2025 and the $43.1 million reported in Q1 2025. A reminder to investors, Puma-reported NERLYNX sales includes both U.S. net sales of NERLYNX and product supply revenues of NERLYNX to Puma ex-U.S. partners. Please note that in Q1 2026, we reported product supply revenue to our international partners of about $0.1 million. U.S. net sales of NERLYNX in Q1 2026 were $41.9 million versus $55.2 million in Q4 2025. The decrease in Q1 2026 versus Q4 2025 was driven by lower demand, inventory reduction in Q1 of about $7.9 million, versus inventory increase of $5.7 million in Q4 2025. Royalty revenue totaled $2.8 million in the first quarter of 2026, compared to $15.6 million in Q4 2025. The decline in royalty revenue reflects a large Q4 2025 shipment to our partner in China. Our gross to net adjustment in Q1 2026 was about 27% and 27.8% in Q4 2025. The lower gross to net adjustment was driven mostly by lower government chargebacks. Cost of sales for Q1 2026 was $10.4 million and includes $2.4 million for the amortization of intangible assets related to our neratinib license. Cost of sales for Q4 2025 was $23.2 million. Going forward, we will continue to recognize amortization of milestones to the licensor of about $2.4 million per quarter as cost of sales. For fiscal year 2026, Puma anticipates that net NERLYNX product revenue will be in the range of $202 million-$206 million, higher than our prior guidance of $194 million-$198 million. We also anticipate that our gross to net adjustment for the full year 2026 will be between 26.5% and 27.5%, significantly higher than 2025, as we expect higher government chargebacks and Medicare and Medicaid share to maintain the levels we saw in the last two quarters of 2025. In addition, for fiscal year 2025, we anticipate receiving royalties from our partners around the world in the range of $20 million-$23 million. We don't expect any license revenue in 2025. We also expect that net income for the full year will be in the range of $16 million-$19 million, also higher than our prior guidance of $10 million-$13 million. Current guidance does not include any potential release of any additional tax asset valuation allowance in our net income estimate. The company is reviewing its deferred tax assets as part of its ongoing tax valuation analysis, has not yet determined whether any adjustments will be required, if so, the potential timing or size of such an adjustment. We will continue to keep investors updated on this as it progresses. At this time, we do not believe that tariffs imposed or proposed to be imposed by the U.S., particularly with other countries, will have a material impact on our product costs or results of operations. However, shifts in the trade policies in the U.S. and other countries have been rapidly evolving and are difficult to predict. As a point of reference, our manufacturing product cost accounts for a mid-to-high single-digit percentage of our total cost of goods sold. We anticipate that for Q2 2026, NERLYNX product revenue will be in the range of $50 million-$52 million. We expect Q2 royalties revenues will be in the range of $2 million-$3 million and no license revenue. We further estimate that the gross to net adjustment in Q2 2026 will be approximately 27%-28%. Puma anticipates a Q2 net income between $2 million and $4 million. SG&A expenses were $18.4 million in the first quarter of 2026, unchanged from the fourth quarter of 2025. SG&A expenses include non-cash charges for stock-based compensation, $1.1 million for Q1 2026 and $1 million in Q4 2025. Research and development expenses were $19.8 million in the first quarter of 2026 and $16.8 million in Q4 2025. R&D expenses included non-cash charges for stock-based compensation of $0.8 million in Q1 2026 and $0.7 million in Q4 2025. On the expense side, Puma anticipates higher total operating expenses in 2026 compared to 2025. More specifically, we anticipate SG&A expenses to increase by 1%-2% and R&D expenses to increase by 34%-37% year-over-year. The higher R&D expense, the higher increase in R&D expense is driven by the progress of our clinical trials. In the first quarter of 2026, Puma reported cash earned of approximately $4 million. This compares to cash earned of approximately $3.1 million in Q4. Please note that during Q1 2026, we made our eight quarterly principal loan payment of $11.1 million related to our obligation with Athyrium. Furthermore, after quarter end, we made our final payment to Athyrium, and as a result, Puma is now debt-free. On March 31, 2026, we had approximately $101.5 million in cash equivalents and marketable securities versus about $97.5 million at year-end 2025. Our accounts receivable balance was $26.3 million. Our accounts receivables terms range between 10 and 68 days, while our day sales outstandings are about 46 days. We estimate that as of March 31, 2026, our distribution network maintained approximately three weeks of inventory. Overall, we continue to deploy our financial resources to focus on the commercial of alisertib and controlling our expenses. Thanks, Maximo. On past earnings calls, we have stressed that Puma senior management, in cooperation with the board of directors, continues to remain focused on NERLYNX sales trends and recognizes its fiscal responsibility to shareholders to continue to maintain positive net income. We believe that this focus has contributed to our commercial execution in a positive way, as according to our current projections, 2026 will mark the second year-over-year demand increase for NERLYNX in the United States and the first time in the history of the launch of NERLYNX in the U.S. that we have seen two positive consecutive year-over-year increases in demand. We are pleased to report this demand-driven growth in NERLYNX sales in the first quarter of 2026, which has been driven by better than expected enrollments and better than expected new patient starts, as well as strong increases in sales to our specialty distributors. In addition, we believe that the positive net income that the company is guiding to for full year 2026 has resulted from the continued financial discipline across the company over the last few years. The company remains committed to continuing to achieve this positive net income and will continue to reduce expenses if needed in order to achieve this. We look forward to updating investors on this in the future. There continues to remain a significant unmet need for patients battling breast cancer, lung cancer and other solid tumors. We at Puma are committed and passionate about finding more effective ways in helping these patients during their journey, and we will continue to strive to achieve that goal. 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 that 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 poll for any questions. The first question comes from the line of Salvatore Caruso with TD Cowen. Please proceed with your question. Hi, congrats on the data and looking forward to more mature datasets. This is on behalf of Marc Frahm at TD Cowen. Two quick questions. The first one, given the emerging signal in c-MYC + patients in both lung and breast that you presented today, how are you thinking about incorporating c-MYC biology going forward into future trial designs? Do you see For example, in your registrational strategy that it evolving into some sort of biomarker-enriched program with maybe a more narrow, you know, patient selection. Then I'll ask my second one after. Yeah. Hi, Sal. Sorry, this is Alan. You're absolutely right. We are seeing a much better signal in the patients where there's a signal of c-MYC in, you know, positivity, if you will, using that in a broad sense. In small cell lung, you know, you don't have the benefit of a lot of the kind of predetermined disease-driven, you know, categories like you do in ER-positive breast. That likely may, you know, require some form of a c-MYC +. Now, is that gonna be like a, you know, c-MYC +, which includes copy number or percent of cells? I think we need a little more data to say that. I think we're hopeful, you know, that as we increase dose we may get in the overall population. You know, we may continue to see that signal in c-MYC, but in the overall population, we may see it as well, so we may be able to go for something a little more, you know, general. I think likely that would if we went for a biomarker focused in small cell lung, it would be something that's probably gonna be inclusive of a number of different categories of c-MYC, you know, positivity, if you will. Now, in ER-positive breast, HER2 negative, ER-positive breast, you know, we've got a very interesting situation because you're absolutely right, it is a c-MYC-driven signal. For whatever reason, we're seeing an enrichment of that signal in the patients who are ESR1 mutated and PIK3CA wild type or both, right? You know, if I remember this correctly, ESR1 wild type is probably 50%-60% of the patients. I'm sorry. PIK3CA wild type is probably 50%-60% of the patients. ESR1 mutated is about 40%-50%, so it's quite a big number. Now if we look at the patients that are in the both category, which is where we're seeing, you know, especially at the 50 mg dose, really compelling activity with no patients having progressed, you know, that's about 20% of the patients there. You know, it's a 40,000 patient population. If that 8,000 patient population is the one that we focus on, I'm totally okay with that, as it could be a fantastic benefit. I think for right now it looks like in ER-positive breast, we have the benefit of just having enrichment of c-MYC in, you know, categories where the disease is, you know, the biomarker, if you will, is already being determined. You know, they already know post CDK4/6 standard of care is, you know, to do either tissue-based or ctDNA or both to see are you know, PIK3CA wild type, PIK3CA mutated, are you ESR1 wild type or ESR1 mutated. We kinda have the benefit of that already being done for us. I think in ER-positive breast, that's probably the path we're going down. Obviously, we gotta get more data, but I think that's kind of the initial thoughts on that. Awesome. That helps a lot. Thank you very much. Just a, like a quick second question. You know, looking ahead to the next updates in both programs, can you kinda help ballpark for us what specific outcomes would give you the confidence to advance or, keep progressing these programs or advancing into the next stage of development? In terms of advancing the next stage of development, we're all systems go on both. You know, at this juncture, I don't see any data that would tell us we're not continuing this into, you know, phase III. I think the question is just, what's the design and, you know, as you referenced in your earlier question, you know, what's the exact patient population to focus on. I think what we're looking for is gonna be, you know, more patient numbers and then more duration. Okay, great. Thank you. Sure. Thank you. This concludes our question and answer session, and I would like to turn the conference back over to Mariann Ohanesian for any closing remarks. Thank you all for joining us today. As a reminder, this call may be accessed by a replay of the webcast at pumabiotechnology.com beginning later today. Have a good evening. Thank you, ladies and gentlemen. Thank you for participating in today's conference call. This concludes our program. Everyone have a great day, and you may now disconnect.