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 Marianne Ohannison, 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. refer to our first quarter 2026 release for a reconciliation of our gap-to-non-gap results. I will now turn the call over to

Alan. Thank you, Marianne, 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 Neuralink 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 NearLink sales includes both U.S. net sales and product supply revenues of NearLinks 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 Neerlink 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 allosertib in small cell lung cancer, and HER2-ER positive breast cancer, also referred to as the ALISCA LUNG-1 and ALISCA BREAST-1 trials. Heather Blaber and Roger Storms will add additional color on Nealink's commercial activity. Maxima Nuguez will follow with highlights of the key components of our financial statements for the fourth quarter of 2025. We now move to the ALISCA LUNG interim presentation. As a reminder, in clinical trials to date, Allacertib 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 allocertib 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 aurorokinase A and CMYC upregulate each other, which suggests the existence of a positive feedback loop. CMYC upregulates the cyclin complex, which leads to cell proliferation. So by inhibiting aurorokinase A with allicertib, it also inhibits CMYK, which decreases cell proliferation. Additionally, preclinical data has shown that allicertib inhibited growth of cells with CMYK overexpression, and in xenograft models that expressed high levels of CMYK, tumor growth was inhibited. PUMA's Phase II trial, ALISCA Lung 1, which is also referred to as study PUMA-Ali4201, 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. Allocertib was initially dosed at 50 milligrams BID on days 1 to 7 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 endpoint 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 milligrams BID and the 27 patients treated at 60 milligram BID that are included in this interim analysis. Slide 7 shows the summary of the prior treatments the patients received prior to entering the 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 Alacertib, 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 ELISCA Lung 1 trial to those that were seen in the previous Phase II trial of allocertid monotherapy in small cell lung cancer, referred to as study C-14007. C-14007 was previously published in Lancet Oncology in 2010. As a reminder, in C-14007, 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 three 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 ELISCA Lung 1, they were treated at 50 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 on 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 CMYCH score. CMYC H-score is a semi-quantitative immunohistochemical assessment that measures the intensity and percentage of tumor cells staining for the CMYC protein, typically ranging from 0 to 300. High CMYC 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 CMYKH score of between 0 and 100 had a median PFS of 1.68 versus a PFS of 4.17 for the patients with a CMYKH score of between 101 and 300. This would suggest that allicertib has better activity in cancers with a higher amount of CMYK activity. Slide 17 presents the CMYC that presents the KM curve for the 50 milligram and 60 milligram dose separately for the patients according to CMYC H score. As you can see on the slide, for the 50 milligram dose, patients with H 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 CMYC score of between 101 and 300, while for the 60 milligram dose, patients with 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 CEMIC H score of 101 to 300. We believe that these slides are suggesting that allicertib has greater activity in tumors with higher CEMIC H scores and hence more CEMIC activity, which we believe is due to the inhibition of the aurora kinase pathway by Allocertib. Slide 18 presents the KM curve for the patients according to percent of tumor cells that are CMYC positive. 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 CMYC 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% of the cells CMYK 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 CMYK positive. As you can see on the slide, for the 50 milligram dose, patients with tumors having between 0 and 10% of the cells CMYK 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% of the tumor cells CMYK positive, while for the 60 milligram dose between 0 and 10% of CMYK 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 CMYK positive. We believe that these slides are suggesting that allocertib has greater activity in the tumors where a higher percentage of the cells are CMYC positive, which we again believe is due to the inhibition of the aurorokinase 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 CMYC is playing a role in driving the tumor, which is indicative of tumors where aurorokinase 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 ELISCA Lung 1 is showing that allocertid 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 allacertib monotherapy and Aliska Lung 1, we can achieve higher concentrations of allacertib in these biomarker-defined populations and potentially open up the opportunity for a Phase III design that tests allacertib monotherapy in a randomized trial. As investors are aware, allicertib was previously tested in a randomized phase 2 trial of paclitaxel plus allicertib versus paclitaxel plus placebo, where a PFS and OS benefit was seen in patients with tumors with biomarkers that appeared to indicate that the aurorokinase A pathway was activated. Based on this data and the data from allicertib lung 1, PUMA will be looking to a dual approach for the development of allicertib in 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 allisertib 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 allocertive 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, Allocertib 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 CMYC upregulate each other, which suggests the existence of a positive feedback loop. Preclinical data has shown that allicertib inhibited growth of cells with CMYC overexpression, and in xenograft models that expressed higher levels of CMYC, tumor growth was inhibited. Puma's Phase II aliscabreast I, also referred to as study Puma-Ali-1201, investigates allicertib 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 and the recurrent or metastatic setting to be eligible for the trial. Patients were dosed with allocertib given at either 30 mg, 40 mg, or 50 mg 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 the metastatic setting that will be given in combination with allocertib 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 allocertid in combination with endocrine therapy for patients with HER2-negative, homeroceptor-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 allosertib, 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 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 ELISCA breast 1 trial to those that were seen in the previously published phase 2 of allocertid and HER2 negative ER positive breast cancer that was published in JAMA Oncology in 2020, referred to a study TBCRC 41. 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 TBCRC 41. To next move to the efficacy scene 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 the 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 CMYC 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 CMYC 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 CMYC positive.

As you can see on the slide, for the patients with between 0 and 10% of the cells, C-MIC

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, C-MIC 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 C-MIC 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 percent of the tumor cells CMYK positive. Similar to the data from ELISCA Lung 1, we believe that these slides are suggesting that in patients that with that alzertive has greater efficacy in ELISCA breast 1, in tumors where a higher percent of the tumor cells are CMYK positive, and hence a greater degree of CMYK activation. Preclinically, it's been shown that allisertib inhibits cemic-positive cells, so we believe that this increased efficacy is due to the mechanism of action of allisertib 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 people who are ESR1 wild type as measured by ctDNA. For patients of 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 ESR-1 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 myotype as measured by ctDNA. For patients at the 50 milligram 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 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 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 milligram group who are ESR1 mutated and measured by tissue, a median PFS has not yet been reached versus a PFS of 3.58 months for patients who are ESR1 wild type as measured by tissue. Slide 38 presents the KM curve for all the patients according to PIC3CA mutation status. As is seen on the slide, for patients at all three dose groups who are PIC3CA mutated as measured by ctDNA, a median PFS of 2.1 months was seen versus a PFS of 5.45 months for patients who are PIC3CA wild type as measured by ctDNA. For the patients at all three dose groups who were PIC3CA 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 PIC3CA 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 PIC3CA mutation status as measured by ctDNA. For patients at the 40 milligram group who were PIC3CA mutated as measured by ctDNA, a median PFS of 3.71 months was seen versus a PFS of 5.65 for patients who were PIC3CA wild type as measured by ctDNA. For patients at the 50 milligram group who were PIC3CA 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 PIC3CA wild type as measured by ctDNA. Based on the efficacy seen in the patients who were ESR1 mutated and PIC3CA 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 PIC3CA wild type according to ESR1 mutation status. As is seen on the slide, for patients at all three dose groups who were PIC3CA 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 PIC3CA wild-type and ESR1 wild-type as measured by ctDNA. For patients at all three dose groups who were PIC3CA 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 PIC3CA 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 PIC3CA wild-type according to ESR1 mutation status

as measured by ctDNA. For PIC3CA wild-type patients at the 40 mg 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 are ESR1 wild type as measured by ctDNA. For PIC3C8 wild type patients at the 50 milligram group 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 ctDNA. We are very pleased to see that at the 50 milligram dose group For the patients who were PIC3CA 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 PIC3CA wild type according to ESR1 mutation status as measured by tissue. For PIC3CA 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 PIC3SA wild type patients at 50 milligrams 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 tissue. Again, we are very pleased to see that the 50 milligram dose group for the patients who were PIC3SA 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, CMYC appeared to play a role in the activity of allocertib in HER2-ER positive breast cancer, and more specifically, the analysis on slides 33 and 34 showed that allocertib had better activity in patients with a higher percent of their cells being CMYC positive. This analysis also showed that patients with between 11% to 100% of their cells being CMYC positive showed the best activity with allocertib. We therefore conducted an analysis to see whether or not CMYC had any correlation with the activity of allocertib that we are seeing in the PIC3CA wild-type patients, the ESR1-mutated patients, or the patients who are both PIC3CA wild-type and ESR1-mutated. On slide 43, we present the data that shows the percent of CEMIC-positive cells for PIC3CA wild type, ESR1 mutated, and patients who were both PIC3CA 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 DNA. As you can see on the slide, patients who are PIC3CA wild type, patients who are ESR1 mutated, and patients who are both PIC3CA 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 CT DNA and in tissue. It is also seen in this analysis that a high percent of the patients who are PIC3CA wild type, who are ESR1 mutant, and who are both PIC3CA wild type and ESR1 mutant have between 11% to 100% of their cells being systemic positive, which is, again, where the best activity of allocertib has been shown to occur. We believe this analysis is suggesting that better activity being seen with allocertib in the patients who are PIK3SA wild type, ESR1 mutated, or both PIK3SA wild type and ESR1 mutated may be due to this increased CMYC activity, as it appears to be showing that CMYC is playing a role in driving the tumor in these subgroups of patients, which is suggestive of tumors where the aurorokinase A is activated, and hence where Alcertib's mechanism of action may be playing a role. When PUMA licensed Alcertib, it had stated that the goal was to enroll Aliska 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 Aliska Breast 1, the company is going to be expanding the enrollment in the trial to obtain more data on the biomarker focus cohorts with a focus in the patients who are PIC3SA 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 ELISCA breast 1 trial in the second half of 2026. Similar to the data from ELISCA lung 1, we believe that the data generated thus far in ELISCA breast 1 is showing that allicertib in combination with endocrine therapy appears to be active in the third-line setting, and more specifically in patients who are PIC3SA wild-type, ESR1 mutant, or both PIC3SA wild-type and ESR1 mutant. Similar to ELISCA lung 1, the activity of allicertib in the trial appears to be driven by CMYC. 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 Alliser. 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 require 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 Neuralink, as well as reinforcing the continued unmet need and 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 of 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 Neuralynx 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 Neuralynx continue to identify appropriate patients that could benefit from additional therapy post-adjuvant treatment, but we continue to adopt new prescribers year over year who recognize the unmet need in HER2-positive early-stage breast cancer and how Neuralynx 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 settings. 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 first quarter earnings call. Well, 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 narrow links with a main focus on patients at higher risk of recurrence. They are also dedicated to enhancing clinical education and engagement through non-person personal promotional efforts, as well as utilizing patient resources to support persistence and compliance during narrow-length 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. During the overall distribution of our business, in Q1 2026, about 58% of our business was purchased through the SB 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. Starting to slide 4, Narrowlink's net product revenue in Q1-26 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 Q1-2025. As a reminder to investors, Puma's reported Narrowlink sales include both U.S. net sales of Narrowlinks and product supply revenues of Narrowlinks 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 Narrowlinks in Q1 of 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-to-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 5 shows Q1-2026 ex-factory bottle sales and also provides both a year-over-year and quarter-over-quarter comparison. In Q1-2026, Neuralink's ex-factory bottle sales were 2,328, which represents an approximate 29% decrease quarter-over-quarter while remaining essentially flat at .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 TRX, we saw TRX 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 6 highlights the quarterly adoption of dose escalation since the launch of Neuralink. In Q1-2026, approximately 78% of patients started Neuralink at a reduced dose. This is higher compared to the 75% we reported in Q4 of 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 NarrowLynx therapy. Slide 7 highlights the strategic collaborations we formed across the globe. Most recently, in Q1, 2026, NarrowLynx 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, and while meaningful progress has been made, we know there's still important work ahead and even more we can accomplish together. I will 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 thank you, which will be filed today and includes our consolidated financial statements. For the first quarter of 2026, we reported a net loss based on gap 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-gap basis, which is adjusted to remove the impact of stock-based compensation expense, we reported a net loss of $1.9 million for four cents per share for the first quarter of 2026. Cross revenue from Netlink sales was $57.5 million in Q1 2026 and $82.9 million in Q4 2025. As Alan mentioned, net product revenue from netlink 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 netlink sales includes both U.S. net sales of netlinks and product supply revenues of netlinks 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. Therefore, U.S. net sales of Neuralink 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. Coftal sales for Q1-2026 was $10.4 million and includes $2.4 million for the amortization of intangible assets related to our Neuratinib license. Cost of sales for Q4 2025 was $23.2 million. Going forward, we will continue to recognize amortization of milestones to the license of about $2.4 million per quarter as cost of sales. For fiscal year 2026, Puma anticipates that net Neuralink's product revenue will be in the range of $202 to $206 million, higher than our prior guidance of $194 to $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 to 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 to $19 million, also higher than our prior guidance of $10 to $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, as 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. This time, we do not believe that tariff imposed or proposed to be imposed by the United States, particularly with other countries, will have a material impact on our product costs or costs or results of operations. However, shifts in the trade policies in the United States and other countries have been rapidly evolving and are difficult to predict. As a point of reference, our manufacturing product costs accounts for a mid-to-high single-digit percentage of our total cost of goods sold. We anticipate that for Q2, 2026, Narlenex product revenue will be in the range of $50 to $52 million. We expect Q2 royalties revenues will be in the range of $2 to $3 million and no license revenue. We further estimate that the gross to net adjustment in Q2 2026 will be approximately 27 to 28 percent. Buma anticipates a Q2 net income between $2 million and $4 million. SG&I expenses were $18.4 million in the first quarter of 2026 and changed from the fourth quarter of 2025. SG&I expenses include non-cash charges for stock-based compensation of $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% to 2% and R&D expenses to increase by 34% to 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, POMA reported cash earn 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 eighth quarterly principal loan payment of $11.1 million related to our obligation with Ethereum. Furthermore, after quarter end, we made our final payment to Ethereum and as a result, PUMA is now debt-free. On March 31st, 2026, we had approximately $101.5 million in cash, 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 ranged between 10 and 68 days, while our day sales outstandings are about 46 days. We estimate that as of March 31st, 2026, our distribution network maintained approximately three weeks of inventory. Overall, we continue to deploy our financial resources to focus on the commercialization of the earnings, to develop and control 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 the airline 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 Nealinks in the United States, and the first time in the history of the launch of Nealinks 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 near-link 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 at 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 1 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 2. 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 any questions. And the first question comes from the line of Salvatore Caruso with TD Cowan. Please proceed with your question.

Hi. Congrats on the data. I'm looking forward to more mature data sets. This is on behalf of Mark Fram at TD Cowan. Two quick questions. The first one, given the emerging signal in CMIC positive patients in both lung and breast that you presented today, how are you thinking about incorporating CMIC biology going forward into future trial designs? Do you see, like, for example, in your registrational strategy, it evolving into some sort of biomarker-enrich program with maybe a more narrow, you know, patient selection? And then I'll ask my second one after.

Yeah, hi, Sal. Sorry, this is Alan. So you're absolutely right. We are seeing a much better signal in the patients where there's a signal ascemic, 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. So that likely may, you know, require some form of a semic positive. Now, is that going to be like a, you know, semic positive, 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 CMYK, 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. But I think likely that would, if we went for a biomarker focused in small cell lung, it would be something that's probably going to be inclusive of a number of different categories of CMYK, you know, positivity, if you will. Now, an 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-mix-driven signal. But for whatever reason, we're seeing an enrichment of that signal in the patients who are ESR1-mutated and PIC3CA-wild or PIC3CA-wild type or both, right? So, you know, if I remember this correctly, ESR1-wild type is probably 50% to 60% of the patients. I'm sorry, PIC3CA wild type is probably 50% to 60% of the patients. ESR1 mutate is about 40% to 50%, so that's quite a big number. Now, if we look at the patients that are in the both category, which is where we're seeing, especially with the 50 milligram dose, really compelling activity with no patients having progressed, that's about 20% of the patients there. So 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. It could be a fantastic benefit. So I think for right now, it looks like in ER-positive breast, we have the benefit of just having enrichment of CMYK in, you know, categories where the disease is, you know, it's already being, 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 CT&A or both to see are you, you know, PIC3SA wild type, PIC3SA mutated, are you ESR1 mild type or ESR1 mutated. So we kind of have the benefit of that already being done for us. So I think in ER-positive breast, that's probably the path we're going down. Obviously, we've got to get more data, but I think that's kind of the initial thoughts on that.

Awesome. That helps a lot. Thank you very much. And just like a quick second question, you know, looking ahead to the next updates in both programs, can you maybe kind of help ballpark for us, what specific outcomes would give you guys confidence to advance or keep progressing these programs or advance even to the next stage of

So 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 three. 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? So I think what we're looking for is going to be, you know, more patient numbers and then more duration.

Great. Thank you.

Sure.

Thank you. This concludes our question and answer session. And I would like to turn the conference back over to Mary Ann for any closing remarks.

Thank you all for joining us today. As a reminder, this call may be accessed via 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.