ALX Oncology Holdings Inc.

Greetings and welcome to the ALX Oncology First Quarter 2026 Financial Results Conference and Webcast. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. Please note this conference is being recorded. I will now turn the conference over to your host, Jason Letman, CEO. Please go ahead, sir.

Thanks, everyone, and welcome to our Q1 2026 results. Really appreciate you all spending time with us this morning and are looking forward to sharing these updates with you. On slide two, and before we start our presentation as housekeeping, here are our forward-looking statements for your review. On slide three, here's the agenda and plan for today. We're going to be providing an update on our key accomplishments in the first quarter of 2026. Most notably, we are very excited to share with you the data set that was presented yesterday in Munich at ESMO Breast 2026 from the analysis of our trial evaluating Evorpercept and Xanidatamab, which clearly showed, again, that CD47 expression is a key predictive biomarker for increasing durable clinical response in heavily pretreated HER2-positive patients. This further validates the results we saw with EVO and HER2-positive gastric cancer from our Aspen-6 trial. We are also very excited today to be joined by Dr. Sarah Hurwitz from the Fred Hutch Cancer Center at the University of Washington, who is a well-recognized expert in metastatic breast cancer. She will be presenting the ESMO breast data in detail and also share her views on avorbicept's significant potential within the current treatment paradigm for HER2-positive metastatic breast cancer. Our CMO, Barb Quincy, will then recap our findings to date with EVO and HER2-positive cancers across now two different independent trials and indications, showing that patients with high CD47 expression derived the greatest benefit across all key efficacy markers, including overall response rates duration of response, and PFS versus those with low expression. These results support our targeted oncology approach with EVO, notably our ongoing Aspen 9 breast cancer phase 2 trial. Barb will then provide an update from our ongoing phase 1 trial with our novel EGFR-targeted ADC. AOX 2004, which also continues to track the plan, and we are enthusiastic about its potential to also change care in EGFR expressing cancers. So on slide four, we continue to advance both our programs, EVO and AOX 2004, and are pleased with the progress on both fronts over the course of Q1, and remain well-positioned to report on significant data readouts from these programs in the coming 12 to 18 months. On the EVO front, CD47, as you know, is incredibly important in oncology and has been a very difficult target to crack, yet it plays a fundamental role in tumor evasion and resistance. We've been happy to see EVO's differentiated approach to this target further validated in the clinic over now five different data sets, including randomized data. Further, the new data from this week's ESMO meeting and over the last year support CD47 as a strong and predictive biomarker, These new findings further support the drug is working as designed and also enables a targeted strategy, which allows us to focus on the patients who will benefit most. On ALX 2004, as you know, it is a highly differentiated EGFR targeted ADC, which was developed in-house by ALX and has the potential to be a first-in-class EGFR targeted ADC. EGFR has also been a difficult target for ADCs historically, and AOX 2004 was designed to address this with a novel epitope and linker payload construct. We have been pleased to see the strong preclinical data to date translate to the clinic and with the continued strong progress in dose escalation where we have been able to further increase dose. Overall, both programs remain on track and well positioned. Now, on slide four, Q1 was a quarter of continued good execution and additional positive data. as well as completion of key hires and a strong financing. As you'll hear more about shortly, this week's data validate again the power of CD47 in a late stage patient population. Here we observed that all patients who were confirmed HER2 positive and CD47 high achieved a response, including one complete response. We also yet again saw the durability that one hopes to see with an IO mechanism with a median duration of response of 20 months and a median PFS of 22 months, which is clearly far improved over the benchmarks. While the focus for today will be on this new data set with Evo, ALX 2004 is also progressing through dose escalation very well and remains on track for initial safety readout in the second half of this year. We remain as excited here about its potential as we do with Evo. Further, the financing from February, which was anchored by very strong investors, further strengthens the balance sheet and enables us to execute through these important data milestones. And last but certainly not least, we added Jeff Knight, who is now our Chief Development and Chief Operating Officer, which really further strengthens our leadership team. Jeff, as you may know, is one of the best operators in biotech in terms of building companies at our stage through the next phase, including commercialization. On slide six, briefly, this just highlights the execution, clinical development progress, and timelines, which remain on track for both programs. Our Evorpercept phase two breast trial continues to progress well with strong enrollment globally and increasing site enthusiasm. Overall, clinical timelines remain on track, as we're expected to read out 80 patients mid-next year. AOX 2004, as I mentioned, is also progressing well with enrollment and dose escalation ramping and are on track there for an initial safety readout in the second half of this year. Our goal and vision for both of these programs also remains unchanged as we aim to have both programs ready for registrational studies by end of next year. On slide seven and my last slide, here's also a snapshot of our clinical pipeline. As you know, we're advancing two novel cancer treatments with key near-term catalysts. And again, Aspen Breast is on track, and we continue to also be encouraged by our ongoing study with our partner Sanofi, testing EVO and multiple myeloma. Our two studies in HER2-positive cancers have now been completed, as we'll focus on today, and ALX 2004 also remains on track. I'd like to now turn the call to Barb, who will provide a quick reminder of our MOA, which is very important as we're clearly seeing it translate to the clinic. And we'll then turn the call over to Dr. Hurwitz to review the new data. Barb?

Thank you, Jason. These next few slides describe a Vorpiceps mechanism of action. What's so compelling to me is that the mechanism of action is entirely consistent with what we see in the clinical trials. So let me just go through this. Cancer cells commonly upregulate CD47 expression to evade immune detection. Avorpacept blocks the CD47 signaling, but it does so without an active FC domain. So Avorpacept by itself does not engage the phagocytic activity of a macrophage. We need to combine Avorpacept with an anti-cancer antibody. And then the combination together strongly augments the ADCP activity of the antibody. And that's likely what results in the efficacy that we see in the studies that we'll talk about today. Essentially, the antibody stimulates the eat me signal and the avorpicep inhibits the don't eat me signal. Therefore, the combinations of avorpicep with an antibody are selectively enhancing or augmenting macrophage phagocytosis of cells that express HER2, for example, in the case of a HER2-targeted antibody, while also blocking the don't eat me signal. On the next slide, we see how this mechanism of action translates into safety. Our clinical safety database is now more than 800 avorpicep-treated patients. And it also, the clinical safety data is also entirely consistent with this mechanism of action that we show here. Evorposub was designed, again, without an active FC domain. That's shown on the right side of the slide. So when we block the don't eat me signal on normal healthy cells, such as red blood cells, there is no macrophage activation, and we avoid on-target toxicities. This is really fundamentally different than what's been tried in the past by conventional CD47 inhibitors, which have essentially failed in the clinic. They attempted to use CD47 as a tumor-associated antigen with both an active FC domain to activate macrophage at the same time of blocking CD47. That ended up being an indiscriminate approach because CD47 is so widely expressed on healthy cells, especially hematologic cells in particular, and that led to the potential for significant on-target toxicity. So with that description of Avorapacept, its mechanism of action and its differentiation, let me now turn the conversation over to Dr. Sarah Hurwitz. On slide 12, you can see her background here. She is a steering committee member for our Aspen 09 Phase II study of Avorapacept in HER2-positive breast cancer patients. She was an investigator on the Avorpicep and Zanidatinib trial that we'll discuss today. And she's a senior vice president, a professor of clinical research, and the director of the clinical research division at the Fred Hutch Cancer Center at the University of Washington in Seattle, where she's also the head of the Division of Hematology and Oncology and the Smith Family Endowed Chair of Women's Health. She's an expert in the management of breast cancer and in the development of novel targeted therapies for breast cancer. Sarah?