Lantern Pharma Inc. Common Stock 2026 Q2 Earnings Call

Panna, please go ahead. Good morning, everyone, and thank you for joining us to discuss our second quarter 2026 results.

As I've said before, AI and computationally driven approaches are now becoming central to how both large and emerging biopharma companies discover and develop drugs, but also how they allocate their resources and think about staffing their scientific teams. Today, we're at an inflection point that's actually accelerating, not just for Lantern, but for how science itself will be conducted. And we are watching it happen in real trials with real patients at Lantern. The golden age of artificial intelligence in medicine isn't beginning, it's actually accelerating. And this quarter, that idea has resulted in the development of a new company, Open-Medicine AI. In August, we established Open-Medicine AI as a separate company with commercial licenses and agreements with Lantern in place to take the AI data models to the next level.

We'll spend some real time on that today because I think it's the most consequential structural decision we've made since starting Lantern. Let me first walk you through what got us here. A clinical signal that sharpened into a defined patient population, a signal that was actually validated using big data, a European regulatory clearance in a challenging recurrent cancer, an allowed patent on a patient selection method for one of our most valuable assets, LP-184, and an FDA-cleared trial in triple-negative breast cancer that's moving toward launch. All of these were backed by numerous observations in our trials, the LP-300 trial, the LP-184 trial, and even the LP-284 trial. What those observations were is that the mechanistic insights gained during our preclinical work actually have real-world parallels, and they could be the basis for meaningful activity in actual cancer patients.

The remainder of 2026 is a defining year for Lantern Pharma, especially as we launch into 2027. We've achieved clinical validation across multiple programs while establishing the foundation for our next phase of growth in both of our engines, our drug development engine and also now our AI engine. In addition, our mid-year financial results reflect highly disciplined execution with a 25% reduction in total operating expenses year-over-year, even as we advanced multiple clinical programs through key inflection points and launched an entirely new company into one of the most promising and disruptive areas of AI, medicine. Our AI-driven clinical pipeline now encompasses multiple drug candidates across solid tumors, blood cancers, and now pediatric oncology, with a combined annual market potential estimated at over $15 billion.

Let's start with our phase II program, LP-300 and the HARMONIC trial in never-smokers, non-small cell lung cancer who progress after TKI therapy. We believe there's about 400,000 to 500,000 patients diagnosed globally each year that have no specific therapy aimed at never-smokers that progress after TKI. In Asia, it's about 35% to 40%-plus of non-small cell lung cancer cases. In the U.S. and Europe, it's between 15% and 20%. In June, we reported emerging data as of the May 11th cutoff, and it showed something we didn't expect to see this clearly, but that the benefit of LP-300 deepens the longer patients stay on it. Among L858R patients who completed six cycles, median progression-free survival reached 8.9 months. That's nine patients, three of whom hadn't progressed at analysis. Across the full cohort of L858R patients, median PFS was 8.4 months.

The hazard ratio for that group was 0.37, with a confidence interval of 0.15 to 0.89. That means also more than 70% of the L858R patients saw target lesion reduction, and some of the responses sustained beyond two years. We've had a 77% clinical benefit rate, which is phenomenal for that line of therapy. I'll be direct. These are small exploratory cohorts, not powered for statistical significance yet, and a median from nine patients can move up or down. What makes us take it very seriously is that a Cox regression controlling for race, gender, TP53 status, which is very important, confirmed L858R as an independent predictor. This is not a demographic or statistical artifact, and safety was comparable between four and six cycles with no added toxicity from longer exposure.

A drug that helps more the longer you stay on it without costing you more in side effects is a drug worth extending, especially where there is no other great therapy for these patients. That is actually the science and the data behind what we did next. We had a successful Type C meeting where no objections were raised to our key proposed amendments. We have concentrated the enrollment now on the L858R patients. These patients actually tend to do worse on current therapy regimens. That is why we also think there is a great need. We have extended the treatment from now 6 to up to 8 cycles, and we have moved into a single-arm design, which should be more efficient and less costly. The trial continues enrolling in the U.S. and Taiwan, and we have used this data set and other observations, of course, about the future of the program in active partnering discussions.

Let us talk a little bit about LP-184 this quarter. We have made several advances, all of which were driven by data and AI-leveraged methodologies. First, the EMA clearance. In July, we got clearance for an investigator-initiated phase I-B/II trial in advanced bladder cancer. This is in Copenhagen at Denmark's National Referral Center for Urologic Cancers, Rigshospitalet, and this is with Professor Roehrborn and Papot. They are the coordinating investigators. This will be a 39-patient trial and very uniquely on two biomarker, a dual biomarker strategy. One on PTGR1 overexpression, and then combining that with DNA damage repair deficiency. We are hoping to enroll patients, very importantly, that our platform has predicted should respond, and more importantly, have a mechanistic basis to be helped by that drug. Second major milestone is the 184 monotherapy in relapsed or refractory triple-negative breast cancer. That will be a phase I-B/II trial.

That protocol has been FDA cleared and is now moving toward launch with a number of sites. We have also applied for grants for that trial, for that study as well, which we are pretty excited about. This drug targets tumors with DNA damage repair alterations, homologous recombination deficiency, or genomic loss of heterozygosity. We expect to enroll up to 40 patients across two dose cohorts, and we will follow by Simon two-stage efficacy read. Third, very important, is that we received a notice of allowance in July covering our three gene selection, where we use three genes, PTGR1, PTPN14, and ASPH for selection of patients most likely to respond to LP-184. We were issued a notice of allowance in four tumors, ovarian, liver, kidney, and thyroid cancer.

That is a patent on the selection logic itself, which is one of the hardest parts of this to replicate, and then map that directly to a credible therapeutic intervention where safety is known and mechanism is beginning to be more and more observable. This all built on our 63-patient trial that we did for 184, and now that we have a dose of 0.39 mgs per kg. Very importantly, what we saw in that trial is that we saw tumor reduction in patients that were carrying these DNA repair deficiency genes, CHEK2, ATM, BRCA1, STK11, KEAP1. Those alterations conferred exceptional sensitivity to the drug. Unlike conventional chemotherapies and other DNA-damaging agents that indiscriminately target dividing cells, both LP-184 and 284 exploit specific genomic vulnerabilities in cancer cells.

That precision is the thread that runs parallel through both programs and which we expect to give our programs a meaningful advantage in their development. LP-284 continues in hematologic malignancies and in adult soft tissue sarcomas, where we got orphan designation earlier this year. Starlight, briefly on the science, STAR-001, which is LP-184 in brain cancers. Our RADR platform identified that those particular brain tumors would be very sensitive if ERCC3 was removed as a protein, because that's involved in the repair mechanism. What we did is we characterized that with our group at Johns Hopkins that we collaborate with, and we're using spironolactone, which is already well-characterized, safe in pediatric and adults, and it actually does exactly that. It degrades the ERCC3 protein and shuts down the repair route. We've had great preclinical data, and now we're taking that now into the clinic.