Puma Biotechnology Inc

Good afternoon. My name is John, 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 1 on your telephone keypad. If you would like to withdraw your questions, please press star 2. If you should require operator assistance during the conference, please press star 0. As a reminder, this call is being recorded. And I would now like to turn the conference call over to Marian Ohannesson, 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 Ellen Auerbach, Chief Executive Officer, President and Chairman of the Board of PUMA Biotechnology, Maximo Noguez, 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 forward-looking statements 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, Mary Ann, 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 near-link sales, as well as royalties from our sub-licensees. Product revenue net was 42 million in the first quarter of 2026, a decline from 59.9 million reported in Q4 2025, and 43.1 million reported in Q1 2025. As a reminder to investors, PUMA's reported near-link sales includes both U.S. net sales and product supply revenues of near-links 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 of 2025. As noted in our last call, royalty revenue in 2025 And Q4 2025 was driven by the shipment to our partner in China. We reported 2,328 bottles of Neuralink 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 Allocertib in small cell lung cancer and HER2-ER-positive breast cancer, also referred to as the ELISCA Lung 1 and ELISCA Breast 1 trials. Heather Blaber and Roger Storms will add additional color on Nearlink's commercial activity. Maxima Noguez will follow with highlights of the key components of our financial statements for the fourth quarter of 2025. We now move to the Aliska Lung interim presentation. As a reminder, in clinical trials to date, Alacertib has shown single-agent activity and activity in combination with other cancer drugs in the treatment of many different types of cancers, including homoreceptor-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 Alacertib 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. From a preclinical perspective, it has been shown that aurora kinase A and CMIC upregulate each other, which suggests the existence of a positive feedback loop. CMIC upregulates the cyclin complex, which leads to cell proliferation. So by inhibiting aurora kinase A with alacertib, It also inhibits CMIC, which decreases cell proliferation. Additionally, preclinical data has shown that Alicerta inhibited growth of cells with CMIC overexpression, and in xenograft models that expressed high levels of CMIC, tumor growth was inhibited. PUMA's Phase II trial, ALISCA Lung 1, 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. Alicertib was initially dosed at 50 milligrams 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 milligram BID, and the company is now in the process of increasing the dose to 70 milligrams BID. The primary endpoints of the trial is to determine whether any biomarker correlates with allocertib 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 GCSF 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 allocertib. Slide 6 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 7 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, Val asserted that 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-milligram arm and 22% in the 60-milligram 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 a 50-milligram arm and 11.1% in the 60-milligram arm. Slide 11 compares the Grade 3 and Grade 4 AE rates seen in the ALISCO Lung 1 trial to those that were seen in the previous Phase 2 trial of allosterative monotherapy in small cell lung cancer, referred to as Study C14007. C14-007 was previously published in Lancet Oncology in 2010. As a reminder, in C14-007, GCSF prophylaxis was not mandated, while LISCA lung 1 requires mandatory prophylactic GCSF. As can be seen on the slide, the use of prophylactic GCSF appeared to reduce the rates of grade 3 or higher neutropenia compared to what was seen in the previous trial. The next move to the efficacy seen in the trial. As you can see in slide 13, in the 52 patients in a LISCA Lung 1, they were treated at 50 milligrams. 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 milligram 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 milligram arm is currently 4.2 months. Slide 14 shows the Kaplan-Meier curve for PFS between the 50 milligram and 60 milligram arm of the trial. As previously stated, the median PFS of the 60 milligram 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 CMIC-H score. CMIC-H score is a semi-quantitative immunohistochemical assessment that measures the intensity and percentage of tumor cells staining for the CMIC protein, typically ranging from 0 to 300. High CMIC-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 milligrams and 60 milligrams, patients with CMIC-H score of between 0 and 100 had a median PFS of 1.68 versus a PFS of 4.17 for the patients with a CMIC score of between 101 and 300. This would suggest that Alicertib has better activity in cancers with a higher amount of CMIC activity. Slide 17 presents the KM curve for the 50 milligram and 60 milligram dose separately for the patients according to CMIC age score. As you can see on the slide, for the 50 milligram dose, patients with age score of between 0 and 100 had a median PFS of 1.68 months versus a PFS of 2.83 months for the patients with a CMIC score of between 101 and 300, while for the 60 milligram dose, Patients with an H-score of between 0 and 100 had a median PFS of 1.41 months, while the median PFS has not yet been reached for the patients with a CMIC H-score of 101 to 300. We believe that these slides are suggesting that aliceridib has greater activity in tumors with higher CMIC H-scores and, hence, more CMIC activity, which we believe is due to the inhibition of the urokinase pathway by aliceridib. Slide 18 presents the KM curve for the patients according to percent of tumor cells that are CMIC positive. As you can see on slide 18, for the combined doses of 50 milligram and 60 milligram, for tumors having between 0 and 10 percent of the cells CMIC positive, 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 percent of the cells CMIC positive. Slide 19 presents the KM curve for the 50 milligram and 60 milligram doses separately for the patients according to the percent of tumor cells that are CMIC-positive. As you can see on the slide, for the 50 milligram dose, patients with tumors having between 0 and 10 percent of the cells CMIC-positive had a median PFS of 1.68 months versus a PFS of 2.73 months for patients with tumors having between 11 and 100 percent of the tumor cells CMIC-positive. while for the 60-milligram dose, between 0% and 10% of CMIC-positive had a median PFS that has not been reached, versus a PFS of 4.17 months for the patients with between 11% to 100% of the tumor cells CMIC-positive. We believe that these slides are suggesting that allocertib has greater activity in the tumors where a higher percentage of the cells are CMIC-positive. which we again believe is due to the inhibition of the Aurora kinase pathway by Allocertib. We believe that the initial clinical data with Allocertib in small cell lung cancer are demonstrating that Allocertib is showing better activity in patients where CMIC 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 milligram 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 milligram cohort in the second half of 2026. We believe that the data generated thus far in ALISCO Lung 1 is showing that allosterative 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 allocertib monotherapy in ALISCO Lung 1, we can achieve higher concentrations of allocertib in these biomarker-defined populations and potentially open up the opportunity for a Phase III design that tests allocertib monotherapy in a randomized trial. As investors are aware, allocertib was previously tested in a randomized Phase II trial of paclitaxel plus allocertib 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 Lung 1, PUMA will be looking to a dual approach for the development of assertive and small cell lung cancer. Therefore, in addition to the monotherapy dose escalation approach in ALISCA Lung 1, PUMA will also be looking to initiate ALISCA Lung 2 which will investigate the efficacy of allocertib given in combination with paclitaxel using mandatory GCSF prophylaxis. We are hoping to initiate this trial in the second half of 2026. We are pleased with the interim data from ALISCA Lung 1, and we believe it is showing an improved tolerability profile for allocertib monotherapy and improved efficacy with dose escalation as well as improved efficacy in a biomarker-directed population that is indicative of the aurora kinase pathway activation. We anticipate additional interim efficacy data from ALISCA Lung 1 in the second half of 2026 or the first half of 2027. I will now move to the ALISCA Breast 1 interim presentation. As a reminder and as previously stated, in clinical trials to date, L-acertif 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 aurorokinase A and CMIC upregulate each other, which suggests the existence of a positive feedback loop. Preclinical data has shown that alacertib inhibited growth of cells with CMIC overexpression, and in xenograft models that expressed higher levels of CMIC, tumor growth was inhibited. PUMA's Phase II Aliska Breast 1, also referred to as Study PUMA ALI-1201, investigates alacertib in combination with endocrine treatment consisting of either anastrozole, exomestane, letrozole, fulvestrin, 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 alacertib given at either 30 milligrams, 40 milligrams, or 50 milligrams BID. on days 1 to 3, 8 to 10, and 15 to 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 a metastatic setting that will be given in combination with alacertib in the trial. The primary endpoints include objective response rate, 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 the future clinical development of Alacertib 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, we all asserted that the treatment emergent adverse events seen were those characteristic of a cell cycle inhibitor with neutropenia being the AEs seen in the highest percentage. Slide 27 shows that 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-milligram arm, 10.2% in the 40-milligram arm, and 26.9% in the 50-milligram arm. It is important for investors to note that prophylactic GCSF was not given in the study. Slide 27 also compares the grade 3 or 4 AE rates seen in the ALISCA breast 1 trial to those that were seen in the previously published phase 2 of ALICERTID, And HER2-ER-positive breast cancer that was published in JAMA Oncology in 2020 referred to as study TBCRC41. As can be seen in the slide, the rates of grade 3 or higher neutropenia appear to be lower in the ELISCA breast 1 trials compared to what was seen in TBCRC41. 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 milligram arm, 20% in the 40 milligram arm, and 18.4% in the 50 milligram 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 milligram arm is currently 2.04 months The median PFS of the 40-milligram arm is 5.45 months, and the median PFS of the 50-milligram 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 trial according to CMIC copy number, also referred to as CMIC 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 CMIC copy number of greater than 2 had a median PFS of 7.29 months versus a median PFS of 2.0 months for the patients with a CMIC copy number equal to 2. 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 CMIC positive. As you can see on the slide, for the patients with between 0 and 10% of the cells CMIC positive, 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 CMYK positive. Slide 34 presents the KM curve for the 50 milligram and 40 milligram doses separately for the patients according to percent of tumor cells that are CMYK positive. As you can see on the slide, for the 40 milligram dose, patients with between 0% and 10% of the cells CMYK positive. 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 CMYK positive. For the 50 milligram dose for patients with between 0% and 10% of the cells CMYK positive, 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 CMYK positive. Similar to the data for molluscal lung 1, We believe that these slides are suggesting that in patients with that L-acertib has greater efficacy in a LISCA breast 1 in tumors where a higher percent of the tumor cells are CMIC positive, and hence a greater degree of CMIC activation. Preclinically, it's been shown that L-acertib inhibits CMIC positive cells, so we believe that this increased efficacy is due to the mechanism of action of L-acertib 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. So these patients have already received treatment with a selective endocrine receptor degrader or CERD. Since enrollment of this trial was done while the newer oral CERDs have either been FDA approved or in later stages of clinical development, many of the patients in the ALISCA breast 1 trial have been previously treated with the new oral SIRDS. More specifically, approximately 58% of the ESR1 mutated patients in the trial were previously treated with oral SIRDS, including camazestrant, alicestrant, giradestrant, immunolestrant, or paliazestrant. Slide 36 presents the KM curve for the 50 milligram and 40 milligram dose groups separately for patients according to ESR1 mutation status as measured by ctDNA. For patients in the 40 milligram 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 mild type as measured by ctDNA. For patients at the 50 milligram group who were 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 milligram and 60 milligram dose separately for patients who are ESR1, according to ESR1 mutation status, as measured by tissue. For the patients at the 40 milligram group who were 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 were ESR1 wild type as measured by tissue. For the patients at the 50 milligram group who were ESR1 mutated and 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 were 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 milligram and 40 milligram dose separately for patients according to PIK3CA mutation status as measured by ctDNA. For patients at the 40 milligram 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 milligram 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, and 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 three 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 milligram and 40 milligram doses separately for the patients who were PIK3CA wild type according to ESR1 mutation status and measured by ctDNA. For PIK3CA wild type patients at the 40 milligram group who were 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 PIK3C8 wild type patients at the 50 milligram group who were ESR1 mutated, the 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 milligram 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 milligram and 40 milligram 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 milligram 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 milligrams who were ESR1 mutated, the BNNPFS has not been reached versus a median PFS of 2.14 months in the patients who were ESR1 wild type as measured by tissue. Again, we are very pleased to see that the 50 milligram dose group for the patients who are PIK3 assay 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. As was shown in the earlier slides, CMIC appeared to play a role in the activity of L-acertib in HER2-negative ER-positive breast cancer. And more specifically, the analysis on slides 33 and 34 showed that Alacertib had better activity in patients with a higher percent of their cells being CMIC positive. This analysis also showed that patients with between 11% to 100% of their cells being CMIC positive showed the best activity with Alacertib. We therefore conducted an analysis to see whether or not CMIC had any correlation with the activity of Alacertib 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 percent of CMIC positive 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 CT DNAG. 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 CMYK-positive 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 who are ESR1 mutant and who are both PIK3SA wild type and ESR1 mutant have between 11% to 100% of their cells being CMYK positive, which is, again, where the best activity with aliceridib has been shown to occur. We believe this analysis is suggesting that better activity being seen with aliceridib in the patients who are PIK3SA wild type, ESR1 mutated, or both PIK3SA wild type and ESR1 mutated may be due to this increased CMYK activity as it appears to be showing that CMIC 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 alicerib's mechanism of action may be playing a role. When PUMA licensed alicerib, it had stated that the goal was to enroll a list of breast 1 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 Mellisca Breast 1, 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 PIK3SA 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 Breast 1 trial in the second half of 2026. Similar to the data from ALISCA Lung 1, we believe that the data generated thus far in ALISCA Breast 1 is showing that alicerib in combination with endocrine therapy appears to be active in the third-line setting, and more specifically in patients who are PIK3SA wild-type, ESR1 mutant, or both PIK3SA wild-type and ESR1 mutant. Similar to ALISCA Lung 1, the activity of L-assertive in the trial appears to be driven by CMIC. 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 L-assertive. As we've mentioned on prior earnings calls and in response to investor questions, Pruma 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 Pruma'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.