Good. Thank you, Bill. Good morning, everyone. My name is Marc Hedrick. I'm the President and CEO of Plus Therapeutics. Please take note of our forward-looking statement. Plus Therapeutics is a clinical stage radiopharmaceutical company based in Austin. We've assembled a group of targeted radiotherapeutic technologies that are ideal for treating CNS indications by directly targeting the tumor. We have two drugs that we so call co-leads. One is for recurrent Glioblastoma, the second for Leptomeningeal metastases, that in aggregate address well over $10 billion in markets that are significant unmet medical needs. The targeted radiotherapeutic space is expected to grow significantly over the next decade. Drugs like Pluvicto, Xofigo, and Lutathera are showing the potential for targeted radiotherapeutic drugs. In other words, drugs that deliver their payload of radiation directly to the tumor, but minimize the effects to other organs or tissues, the so-called off-target effects. Specifically for Plus, we're going after mostly CNS indications and some commonalities in these, that they're typically on the rare side. They're typically unmet medical needs, but in aggregate, because they are so poorly addressed and unmet, they have significant market opportunities associated with them. Furthermore, overall survival improvements of two months or so can be significant and lead to FDA approval. From a corporate perspective, our goal is to take what are fatal diseases or death sentences when patients hear them from the physicians, and turn them into chronic or manageable diseases. It's sort of crazy to say we're going to cure them, but. Maybe we can get there one day, but just turning these from death sentences into chronic diseases will be a huge improvement for these patients who, who really have months and some cases, weeks to live. Just conceptually, how do you think about targeting radiotherapeutics in the CNS space? The first thing to know is the best killer of CNS tumor cells is radiation. That's been known for 50 years. The mainstay of treating CNS cancers is external beam radiation. The problem with that is it has to be fractionated over multiple small treatments over about four to six weeks, which means five visits to the clinic each week over several weeks. Plus, it's significantly limited in terms of how much radiation can be delivered to the patient. For example, in recurrent glioblastoma, which is our target currently for glioblastoma with our lead drug, those patients get about 35 gray in the recurrent setting. That's the max, and then they are done with radiation for that round of therapy. So external beam radiation shows that radiation's good, but it also shows the limitations in terms of dose. I'm going to show you in a minute, patients we're treating them with 10 to 20 times that amount of radiation, but in a very safe manner for the patient. That's a good way to treat the patients, but there's a better way, and that's that's targeted radiotherapeutics through the bloodstream. The problem with those is something called the Blood-brain barrier. Most drugs, maybe 98% of drugs, don't get from the blood system into the brain because of the Blood-brain barrier. That's the key thing we have to tackle in getting drugs directly to the tumor for the patient to treat the tumor specifically. We think the best approach is something called direct tumor targeting, where we put the drug right on the tumor, bypassing the Blood-brain barrier, minimizing or completely removing off-target effects and off-target toxicities. With the right isotope, like rhenium, which is what we use, we could actually determine in real time, not just how much dose we give to the patient, but how much dose we get to the tumor. In real time, every patient. It's really a powerful technology from a development perspective. When targeting the CNS, there are kind of two different kinds of tissues in the CNS. There's the fluid space, called the CSF, and there's the brain tissue or spinal cord tissue, which is called the Parenchyma. We have two different technologies to address that. For the parenchyma, and that's glioblastoma and other brain tumors, so to speak, we use something called convection-enhanced delivery. It's been around for 20 years, doctors just haven't had anything that's worked to go through it, the technology is relatively well-developed. I, I like to think about it as biologic fracking. You, you put catheters into the brain, you infuse the drug under pressure, it moves slowly through the brain in response to the pressure gradient, once you turn the pumps off or turn the pressure gradient off, the drug quits moving. It stays where it is. It delivers the entirety of its radiation directly to the tumor where you put it, once it's burned out, over time, it's, it's excreted through the kidneys. That's convection-enhanced delivery for the treatment of parenchymal or brain-specific lesions or spinal cord-specific lesions. The other is CSF, and one of the most lethal and unmet medical needs in metastatic brain cancer is something called leptomeningeal cancer. Almost all of these patients have something called an Ommaya reservoir, which is a little port that goes under the skin with a catheter that goes into the ventricle, accessing the cerebral spinal fluid space. It allows real-time, two-way access to the fluid that's in and around the brain, which is where the, where the tumor lurks. I'm going to address both of those for two different indications, which I would call our co-lead indications in the CNS targeted radiotherapeutic space. Let me give you an image that just gives you a sort of a mental idea of how this works in patients that have brain cancer. This is a patient treated recently in our phase II trial.... That's an AP image of the gamma particle that's part of our drug. The white dot here is the accumulation of the radiation exactly where the tumor is, and you can see that accumulation in three dimensions at 25-20% of the total infusion on three different views. That's the radiation accumulating right where the brain tumor is. These little hydra-looking things are actually individual catheters, and you're imaging, in this case, the gamma particle going through the catheters and then accumulating in the tumor. That's the idea. The drug goes directly into the tumor, nowhere else, stays there, burns out, and goes away. It's very precise and very quantitative, and we can tell in real time how things are going. For example, we had an example of one patient that had a tumor that kinked. We could turn that catheter off and infuse the drug into the other four catheters. A very versatile technique. Our lead drug is rhenium obisbemeda. Rhenium obisbemeda is a complex drug that's made from the chelation of rhenium-186 isotope that's made in a nuclear reactor. It's loaded into a liposome, and then those liposomes are then administered to the patient. The reason we do that is because if you encapsulate the drug in a liposome, it essentially stays there throughout the decay curve. It has a 90-hour half-life in the brain, whereas if you put rhenium alone or chelated rhenium, it goes away in a few hours. It's that formulation that allows it to stay in the brain. It allows it to be convected well through in, in a, in a targeted dispersion approach, but also it allows it to be uptaken by glial cells and tumor-associated macrophages, and it further keeps the radiation right where the tumor is. Rhenium, why do we use rhenium? Rhenium has an ideal energy profile for CNS diseases in between yttrium and lutetium. It's a dual energy emitter, meaning the beta particle is the cancer killer, the gamma particle is the imaging particle. It's, it's relatively non-toxic to the bone marrow and the thyroid, which are two important potential off-target organs for for off-target effects, and it has very rapid clearance. And then the radiation path length for 186 is 2 mm. You don't have radiation radiating out of the body. You don't have to worry about special precautions when this is administered to the patient. It's very simple, very straightforward, and it goes precisely to the tumor because of that path length. What's it, what's this like for the patient? Let me kind of divide it up into the parenchymal lesions and the central cerebrospinal fluid lesions. For the patient that's getting a treatment of a brain parenchymal lesion, such as a glioblastoma, they're MRI'd before, when they we think a recurrence has, has happened. When they think the occurrence has happened, they're taken to the operating room, and they're biopsied. If they're biopsy-proven, the catheters are placed. They stay overnight in the hospital. The drug is given the next day, and then the catheter is removed, the patient goes home. Typically, external beam radiation is about four to six weeks in an outpatient setting. This is about two nights in the hospital. They go home, and that's it. For patients that have leptomeningeal cancer, these patients almost always have an Ommaya reservoir, but if they don't, it's placed, we confirm that there's good flow in the brain, and then it's about a five-minute infusion in a clinic, and the patient goes home. Single administration. It's a very patient-friendly approach to treatment. Our pipeline includes several trials for treating malignant gliomas, including an active phase I dose escalation, an active phase II for tumors that are small to medium-sized, and then we think, soon-to-be-approved trial for pediatric brain cancer, two kinds of pediatric brain cancer. We have an actively enrolling Phase I, Part B study, we recently received FDA approval to move forward into Part B, for cohorts four and beyond, and that's a dose escalation study for leptomeningeal cancer, including a basket protocol for a variety of different types of causes for leptomeningeal metastases. Let me talk about malignant gliomas for a minute. Malignant gliomas occur in about 15,000 patients per year. They almost always recur. No matter how they're treated, they typically recur, and then once they recur, the patients have about eight months to live, in terms of their median overall survival rate. It's the most highly lethal form of primary brain cancer. There's no standard of care, so effectively, what happens when a patient recurs, the doctor says, "we push them into a clinical trial," and there are a number of clinical trials that are out there. The problem is, it's been very difficult, as I mentioned, to translate preclinical work or early clinical work into into phase III success. The goal is to treat adult and pediatric malignant gliomas with a first-in-class targeted radiotherapeutic that addresses specifically their cancer and prolongs their life. Just a busy slide, but where are we kind of visually? Today, we're, we're actively continuing to dose escalate at the urging of the FDA until we get to a dose-limiting toxicity, which we don't have, and then we're actively enrolling in a phase II for small to medium-sized tumors. This data will inform whether we can treat larger tumors, with the idea that either, after, some form of a phase III, potentially, opportunity for accelerated approval or market approval later this decade. How are we doing in terms of treating these patients? We've treated about 35 patients total. No dose-limiting toxicities. We're out now, we're into eight cohorts now. We've had no catheterization-related complications, and the majority of adverse events have been relatively low grade and unrelated to the study, study drug. Despite what we're doing, it's a remarkably safe procedure, not just the drug, but the procedure. What about efficacy? First, on the left panel is just the demographics. This is a very poor prognostic group. They have, on average, about 1.7 recurrences. It's a very highly recurrent, heavily retreated, pretreated population. I'm gonna show you just the phase I data. That's just 21 patients, and that's something that's being submitted for publication, currently. What we've escalated in, in the phase I through six cohorts, up to 22.3 millicuries in 8.8 milliliters of volume. We've had no treatment failures. We've used up to four catheters, and we found that as we increase the, the, the tumor coverage, as we go to higher dose cohorts, you put, put more dose in, you cover bigger, bigger tumors with more radiation, generally, as one would expect. This is essentially a biologic response graph. If there are kind of four things going on here. Each dot is a patient. If the patient is alive, it's green. If the patient has passed away, it's red. The bigger the dot is the longer that the patient has survived. On the Y-axis is the amount of absorbed dose from zero up to 800 gray. Remember, in the recurrent setting, these patients typically get max about 35-40 gray. We're giving a lot of radiation here, and this is the tumor coverage, the volume of the tumor that we treated. It's how well did we cover the target? Every patient is sort of plotted based on their absorbed dose and their volume treated. The thing that's obvious is that if you get better coverage of the tumor, and you get more radiation to the tumor, the patients do, do better. Furthermore, in the preclinical work, we found that there was 100 gray threshold, that in animals, that if you got over 100 gray absorbed dose to the tumor, those animals did great. The ones that didn't get 100 gray didn't do well. It kind of validated what we did preclinically. This is kind of an early finding. We, we built on this, and this is an unusual trial in the sense that we have long-term median overall survival data. This is the median overall survival data for the entire trial. That includes the patients that were treated with just 1 cc and 0.66 millicuries, all the way up to our end of our cohort six dose. The median overall survival was 41 weeks. When we bifurcated these patients into those that got greater than 100 gray and less than 100 gray, there was a highly statistically significant improvement in survival. The patients that got greater than 100 gray, their median overall survival was about 75 weeks, and less than 100 gray or approximately 22 weeks. Very highly statistically significant dose response curve based on overall survival. How do we think about that overall survival in context of the best real-world data? We've actually done two meta-analysis or real-world controls with our partner Medidata, showing that in, in patients that have been previously, have been recurrent and treated with bevacizumab, their median overall survival in a propensity match population is about eight months. In patients that have been subject to Convection-enhanced delivery in other trials, in their recurrent setting, they lived about 8.4 months. This is a meta-analysis showing median overall survival of seven months. That eight months is a pretty good hurdle rate from a median overall survival perspective. What we showed in all comers in the dose escalation trial, heavily pretreated population, is an 11-month or about a 40% median overall survival improvement, and those that got 100 gray, 17 months. Currently, in the latter cohorts of the trial and in the phase II, we're hitting this 100-gray threshold or higher in almost every patient now. We've gone further in terms of the analysis, and I'll go through this quickly because of time. We've, we've validated this dose response curve in terms of looking at it based on quartile. The quartile the doses have been plotted by quartile in terms of absorbed dose and tumor coverage. Again, a highly statistically significant correlation between dose and coverage and overall survival, and then looking at a Cox hazard ratio model, the things that really popped out as relevant in terms of overall survival, not only for the, for the means, but even the air bars, were below a hazard ratio of one, favoring survival for absorbed dose and tumor coverage. Such that we can say for each 100-gray increase in total dose distribution volume, the risk of death decreases by about 46%, and for each 10% increase in the ratio of treated to tumor volume, the risk of death decreases by about 67%. A couple of cases. This is actually a phase II case that we treated recently. It has about a 10 cc tumor. The colored images show the superimposed radiation over the tumor, and these are isodose lines showing that sort of decrease as you go away from the tumor in terms of the amount of absorbed dose. These are the CT scans with a registered superimposition of the radiation gamma emission with the anatomic structures from the CT scan. You can see the tumor in three views. At pre-op, you see the white enhancing tumor lesion. You see how it sort of evolves, dissolutes, and this is a patient at four, 4.5 months. This is a randomly selected phase II patient. This is sort of what we see, something called pseudoprogression. The tumors get a little bit bigger before they start shrinking. I'll show you that in kind of a patient that lived much longer in the phase I. Phase I, we have longer data, we have more data to show you. This is a patient for the phase I, not the longest living patient, this patient's about 800 days out with GBM. You can see their tumor preoperatively. You can see the drug distribution. This patient actually got 740 gray of radiation, we covered the tumor to 99%. This was the best coverage and the best dosage to the tumor. You can see how the tumor went from a small enhancing lesion to a much bigger lesion, then a bit more contrast enhancing, and then started to involute. This is at 26 months. This is the pattern we see. If we, if we do a good job hitting the tumor, we get radiation to it, it gets a little bit bigger, it's called pseudoprogression, and then it gets smaller, and then the patients live an inordinate amount beyond what they statistically should live. We're also going after pediatric brain cancer. Two highly radiosensitive pediatric brain cancers are pilocystoma and high-grade glioma. We're working with Lurie Children's Hospital, and we should have feedback from the FDA. We've been going back and forth with the FDA, but we think we'll have approval on this trial and be able to get going this year. Let me talk about leptomeningeal metastases. This is important for two reasons: one, it's a significant medical need. These patients do very poorly. Without treatment, these patients live four to six weeks. The incidence is growing as we do better with IO therapies or other anti-cancer therapies for primary disease like breast cancer, lung cancer, GI cancers. More and more of the cancer is popping up in the CNS CSF space. Even with treatment, these patients live a few months, and there's no standard of care. Nothing's approved. The only approved drug was DepoCyte, which was taken off the market two or three years ago. Excuse me. In terms of solid tumors, it's sort of a, a quarter, quarter, quarter. Quarter breast cancer, quarter lung cancer, quarter GI, quarter melanoma. These are the common tumors. There are also hematologic malignancies that could potentially be treated with this as well. Very significant unmet medical need. Again, like I showed you in GBM, the sort of hydra picture, this is sort of to give you a concept of what we're doing. These patients have Ommaya reservoirs. We infuse the drug after we prove that the CSF fluid system is patent. Relatively rapidly, in 15 minutes, you can see the drug beginning to go down the spinal cord. By 24 hours, of course, it's totally covered. You can see it in three dimensions in the various cisterns and fluid columns in the brain in this three, three dimensional movie. The phase I, part A trial is complete. The FDA has allowed us, because it's been remarkably safe to move forward into the part B. That means we're continuing to dose escalate from cohort four on to dose-limiting toxicities. I doubt we'll get there. We'll probably get to a max not to a maximum tolerated dose, but to a maximum feasible dose. Thus far, we can say several things I think are really important. The first thing is that as we increase the amount of radiation, same dose, same volume, 5 cc, but as we increase the radiation, we get-- getting a linear increase in radiation in the key, measured structures. Number two is that when we put the drug in, we see that it stays for at least seven days. So single administration, the drug is staying in the CSF column for up to seven days, probably longer. The drug is taken up by tumor-associated macrophages, which explains, in part, its ability to stay in the CSF space. The safety profile has been remarkable. Patients have done very well. No treatment-emergent AEs greater than grade one. This is a single administration, but we've actually treated one patient, a physician, pediatrician, that with triple-negative breast cancer. She's now well over a year of survival with her second dose. We treated her under compassionate use. The plan here is we're now in part B of the phase I. We'll dose escalate to maximum feasible dose. We'll be laying on multiple doses, and then with the plan of going into phase II. This trial is actually funded almost completely by CPRIT, which is the state of Texas, which is funding the, the trial up to about $18 million, which will fund us all the way through phase II, a potentially accelerated approval. Finally, a second drug that's earlier in development, it's not in the clinic yet, but it will be the first bioresorbable radio-embolic drug. Potentially, it could treat any solid tumor throughout the body. Anything you could drive an angiographic catheter to, you can get the drug there, deliver it. It delivers its radiation into the blood vessels, into the tumor, and then it's washed away and bioresorbed normally. That drug should be in the clinic probably in 2025. The company at the end of end of March, had $13 million in cash. That's cash well into 2025. We have two grants that are funding our two lead programs all the way through phase II, one from the NCI and one from the CPRIT, as I mentioned. In terms of, in terms of milestones, important milestone for us is this Friday, when we present the leptomeningeal cancer phase I part A data. We announced yesterday that we'll be hosting a roundtable with two physicians that have been involved in the trial, who are experts in the treatment of leptomeningeal metastases. We'll be talking about the data and the implications of the data and the plans going forward for the trial. And that will be at 8:00 A.M. live this Friday at the SNO ASCO meeting, coincident with the presentation of that data. Furthermore, at SNO, which is a meeting in November, in Vancouver, we'll be providing an update on the phase I dose escalation and the phase II trial, and present the open-label phase II data at that trial. Furthermore, we're in the process of publishing the phase I data, and we anticipate that will be accepted this year, and that will publish the entirety of that data in a single publication. Then, finally, in terms of our pediatric trial, as I said, we're interacting with the FDA right now with the idea that that trial will be open and running here this year. I think with that, I'll thank you for your time. If there are any questions, if we do have time, I'm not sure we do, I'd be happy to answer those. Thank you. Thanks a lot. Okay, thanks.