All right, good afternoon all, and thank you for giving me the opportunity to introduce you to Aptose Biosciences. As I look around the room, I actually see a lot of familiar faces. Maybe we can catch up afterwards. Back to Aptose. Let me see if I can move on. Oh, it actually works. All right, Aptose is a clinical stage precision oncology company. We're developing our lead drug, Tuspetinib, as part of a triple drug therapy, or triplet. It is for the treatment of patients who are newly diagnosed with acute myeloid leukemia, or AML. This Tuspetinib-containing triple drug therapy is being developed as a one-of-a-kind, safe, and mutation-agnostic—and I'll explain that in a few minutes—frontline therapy for AML. To fully appreciate why such a therapy like this is needed, I'll first need to introduce you to AML. I want to highlight that AML is a very aggressive and deadly cancer of the bone marrow and blood. I believe that all of us are aware that the interior of our bones contains bone marrow. Within the bone marrow, you have stem cells. Those continually divide throughout your lifetime to replenish the normal blood cells: red cells that carry oxygen, the white cells that fight infections, and then platelets that prevent excessive bleeding. This comes at a price, because as those bone marrow stem cells divide over your lifetime, they also accrue mutations. Depending on the mutations that arise, that can lead to AML. These mutated AML cells then divide uncontrollably. These cells are nonfunctional. They do not function properly. They actually crowd out the normal functioning cells. This disease is extremely heterogeneous at the genetic level, makes it very difficult also to treat this disease. It's the most common type of acute leukemia in adults. While it can occur at any age, the majority of the patients are actually 65 years or older. Okay? Why is that important? If you look at the very bottom, if you're age 65 or over, the five-year survival is estimated at 9%. There's a lot of work to do here. Okay, how do clinicians currently treat these elderly patients once they're newly diagnosed with AML? The current standard of care therapy is a two-drug cocktail we call VEN-AZA. The two drugs are venetoclax and azacitidine, but that's a mouthful, so VEN-AZA is what we say. If you look down at the bottom, the newly diagnosed AML patients on the bottom left, they start to receive the VEN-AZA. What happens? If you look at the red box on the very bottom, one-third of the patients are what we call refractory. That means these patients do not respond. Their expected life survival is in the matter of weeks to a few months. Bad news for them. You see the black box here where it says complete remissions, CRs, that's good news. The patients are responding. Some of them can even go on to get a stem cell transplant. They are feeling pretty good. They shouldn't. Why? Because the median overall survival of those patients who have responded is just 14.7 months. Because most of them will relapse and go into this other red box, and their survival is on weeks to months. It is even worse if you have some of these adverse mutations like TP53. Your estimated survival is less than six months, even if you're going down the best-case scenario. Okay, what do we need? We need, critically, an improved frontline therapy for these patients. We need to get more patients into the complete remissions. They need to be deeper remissions. Simply, we need to keep more people in the black boxes and keep them out of the red. Because once they go into the red boxes, they're relapsed refractory, and there is very little that can be done for them. Okay. We also need therapies that are safer therapies so you can have better quality of life. What's critical is the industry does not yet have drugs that are broadly active in AML. They only hit these very specific subgroups of AML. We need a therapy that is active across all the genetic subtypes. The good news is there's a new paradigm that has emerged for AML therapy, and it's triple drug therapy. Sounds really simple. You just add a third drug onto the VEN-AZA. It's anything but simple. VEN-AZA already brings toxicities with them, and you have to be very careful when you add on a third agent. It has been done by certain other drugs, and guess what? They brought in toxicities that were just unacceptable, or they only hit a small group of patients. What we really need is a safe drug, third drug. We need a better third drug. Safe, convenient. We need it to extend the patient's survival. It needs to be of a proven drug class so that we know what to expect from the drug. Again, it needs to be broadly active across all these genotypes. This precisely describes our lead drug, Tuspetinib, that you'll see abbreviated as TUS. It's an ideal third drug to add onto the VEN-AZA backbone. Excellent safety. It is convenient. Once-a-day oral tablets. Broad activity against every class of AML, regardless of the mutations. It's derived from the most successful class of drugs for oncology in history. That's the targeted kinase inhibitor from the same group of drugs as Gleevec, Ibrutinib, and these classes of drug. If you're an investor sitting there, you're probably saying, "Yeah, yeah, yeah, but does it work?" Yes. It works. We've already combined Tuspetinib with VEN-AZA. We've administered this to newly diagnosed AML patients as part of our TUSCANY clinical trial, and I'll describe that in a moment. We've already seen a very favorable safety profile. We're seeing high response rates. We're even seeing complete remission, CRs, across every type of AML patient, even the ones that have the worst mutations. Okay? This profile has a market potential of over $1 billion annually. The National Cancer Institute came to us, selected Tuspetinib for a very prestigious MATCH program in which they are going to be combining our drug with other drugs for both AML and MDS. If you're an investor, you want to know that we have multiple clinical milestones ahead this year and next year, and we do. All right, clearly we're focused on the triplet drug therapy in newly diagnosed AML. Guess what? The FDA doesn't allow you to start there. No, no, that's too easy. The FDA requires that all new drugs in AML start in those relapsed refractory patients. Remember those patients in the red box? That's where we have to start. They have to have failed all frontline therapy, all approved therapies, investigational drugs. Their lifespan is expected to be two to five weeks. That's the patient you have to start with in AML. You also have to start with your drug as a single agent, do dose escalations. We did that. We've done thorough dose exploration. We actually identified four dose levels that give us complete remissions in patients with no DLTs. That's unheard of in AML. We have orphan drug designation and fast-track status. We then moved on and we combined our drug with venetoclax. The FDA requires that. Because it's tough to combine certain drugs with venetoclax. They interfere with pharmacokinetics. But ours is fine. We have no interference with pharmacokinetics. We demonstrated that the doublet was safe. We demonstrated complete remissions. Everything was great. We had a very successful program in relapsed refractory that took several years. We presented the data to the FDA. Now we're dosing patients with the Tuspetinib AZA triplet in these newly diagnosed patients. That's our TUSCANY trial. The purpose of this TUSCANY trial is to select the optimal dose for the pivotal studies for approval of the drug. We expect to be able to select that dose this year to move into the pivotal studies. How do you begin selecting your dose? Remember all those studies we did in relapsed refractory? Out of that, we said 80 mg is our target dose. We get all these complete remissions there. It is very safe. It did not cause any dose-limiting toxicities. Every patient that we gave achieved exposure levels that we know as active in patients. The FDA says, "Of course, though, you have to reduce the dose level because you are combining with two other drugs, and it is all based on safety." That is what we expected. Our starting dose was 40 mg. That was the initial dose. We have now completed the cohort with the 40 mg in our triplet. We also then dose-escalated to the 80 mg in triplet. As you can see on the top right, the way we administer it is the patients receive Tuspetinib once a day orally for 28 days, 28-day cycles. The venetoclax is ramped up to 400 mg and administered for one to 28 days. The azacitidine in green there is administered for seven days. The clinical trials are being conducted by all key opinion leaders, KOL, clinical investigators at 10 of the leading clinical sites in the U.S. The findings to date with the 40 mg and the 80 mg, I used the word earlier to I think I was talking to, and I said it was thrilling. It's not a professional word. Everybody says, "Oh, you use something like that. You're gratified." No. When you start watching these data and these patients, it was thrilling. No safety concerns. No DLTs. We observed complete remissions in these patients, and they're achieving what's called MRD negativity. I'll have to explain that. You want to know if there's any residual disease in the bone marrow of these patients. You want to get rid of all of it. How do you do that? We have very sensitive techniques. We collect the bone marrow. We have to do this about every four weeks from these patients. We can measure if there's any residual disease. Now the gold standard in AML, if you want to have a durable response, you need to get a CR, complete remission with MRD negativity. That's the gold standard. Okay, what are we getting? The Tuspetinib AZA triplet now has already delivered safety. It's delivered CRs. It's delivered MRD negativity. That then pertains durability over the time of years, months to years. Four patients have been placed on the initial dose, 40 milligrams. Three of those achieved a complete remission. One did not. They had a dramatic reduction in their what are called the blast leukemic cells in their bone marrow. In AML, if you do not get to a complete remission, the patients are discontinued. PRs mean nothing in AML. If you don't get a complete remission, it means nothing. That patient was discontinued. We moved up to the 80 mg. We've now put three patients on there. Even though they're very early in their treatment, all of them already achieved a complete remission. One other thing I want to point out on this slide. That term mutation-agnostic means our drug doesn't care what mutation you have. It's active. You can see IDH over here. This is a mutation that's been found in 10%-20% of AML patients. There's a drug that targets those, but only those. Our drug is active there. Under that, NPM1, menin inhibitors target those patients. It's about 30% of the patients. FLT3, there's FLT3 inhibitors. That's about 30% of the patients that are FLT3 inhibitors. Guess what? They leave behind 70% or so of the patients that are just not treated. Okay? I'll also point out one other thing. At the very top, I mentioned that TP53. That mutation is so bad, most companies will not put their drugs on the clinical trials, those patients on the trial, because it makes their drug look bad. It's that bad. We have activity there. What I'm going to do is kind of paint a picture for you. The best way to do is talk about the patient journey. I'm going to give you about four case studies of examples of patients. I'm going to show you the first three patients there that have the CRs at 40 mg. I'm going to show you one of the patients that's received 80 mg. You will see why. I'm showing you the diversity of mutations where we have activity. This first patient, 74-year-old, came in, had to have transfusion all the time. They had the IDH mutation as well as a variety of other. They received the lower dose of our drug, 40 mg, the initial dose in the triplet. Guess what? They are now, they have achieved a complete remission and MRD negativity. Doesn't get any better, and they're transfusion independent. That is an IDH mutant patient, plus all these other mutations. Here is the next one. Remember I mentioned that TP53? Again, doesn't get any worse than this. This is an 80-year-old woman, transfusion dependent, has what's called the biallelic TP53 mutation. It's the worst you can get. Complex karyotype. That means you have three or more abnormalities in your chromosomes. And other mutations. Put them on the triplet, our lowest dose. In cycle one, they achieved the first 28 days there, they achieved a complete remission. Now they also are MRD negative and transfusion independent. If you have to put a W in your WIN column, you put a W here, and then you bold it. You underline it. You highlight it in yellow because it does not get any better than this. Here is our third patient at that 40 mg, completely different mutation profile. This patient has the FLT3 ITD mutation. You might treat that with a FLT3 inhibitor. They also had the NPM1 mutation, which you might treat with a menin inhibitor. Guess what? We put them on our drug. Again, this patient also had a complete remission and MRD negativity very quickly. They are still fairly early in their cycle of treatment. All those patients at the 40 mg, they are continuing on therapy. Now I'm going to show you one more patient. One patient at the 80 mg. Why am I showing you this patient? It's another TP53 mutant patient. So out of these four patients, I've shown you two of these. Okay? Another 81-year-old female. I mean, these patients are in really poor shape. Again, had the biallelic TP53 mutation, complex karyotype, and a host of other mutations that are related to another disease also called MDS, myelodysplastic syndrome. This patient is early in cycle one, yet they've already achieved a complete remission. We'll continue to treat these patients. We'll monitor all these patients at the 80 milligram for MRD negativity. To date, we've had no dose-limiting toxicities, no safety issues. We just could not be more thrilled with the data that we're seeing. I can tell you the patients and the clinicians are too. Okay. To put it in context, we started this trial in December of last year. We initiated the TUSCANY trial, this triplet therapy. We expect to dose patients throughout the remainder of this year and into next year. Why so long? We expect these patients to survive based on the data. Beginning next year, we plan to start our pivotal trials, which means we also have to select our pivotal trial dose this year. We are on track to do that already. Okay. We said in Q1 we were to release data. We did. We issued two separate press releases showing data with the 40 mg and then 80 mg. We said we released additional data in Q2. This morning, we issued a separate press release in which we went through all the data of all the patients, a portion of which I've presented here today. We don't hide. We don't hide the data. We are very proud of this drug, and we want people to know about it. One month from now, we present the vast majority of our data, all the clinical data, pharmacokinetics, everything at the European Hematology Association meeting. That's in Milan one month from now in June. At that point, we'll also be meeting with all the big pharmas while we're there because they're looking for a drug like this. Why do we wait until then? You have to go to them. You have to show them data. You have to show them CRs. You have to show them safety and MRD negativity. Because what they want to know is durability of your therapy. What correlates with that? CRs and MRD negativity. Okay, we're going to be showing those data. Toward the end of the year, we'll also present additional durability data at the ASH, American Society of Hematology meeting. That's in Orlando. As I said, plan to next year go into our pivotal trials toward the approval. Lots to do there. I want to say I'm very proud of our company. We have 15 full-time employees. Very small company doing all this. A point at the bottom left, that's our Chief Medical Officer. He also is a KOL and key opinion leader in AML and MDS. You look at our scientific advisory board, it's populated by icons of clinical drug therapy. I'll highlight just Dr. Brian Druker at the very top. You've probably heard the name, may not recall. He was responsible for developing Gleevec. Okay? So that's our clinical advisory board. We also work closely, excuse me, our scientific advisory board. We also work closely with clinical advisors. These are considered to be the greatest athletes now, though. These are the physicians that are treating all the AML patients around the world. They're the elite clinicians. I'll mention Dr. Naval Daver on the top here. He's at MD Anderson. He is the world's leading authority on triplet drug therapy in AML. He's also the global principal investigator on our trials. Okay? Last slide. I'll wrap it up here, and hopefully I didn't take too long trying to get through it for you. This triplet concept now, it is proven. I mentioned certain other drugs that have been used for the third drug. There's one, it's a FLT3 inhibitor. They put out data on this. They combined their FLT3 inhibitor with VEN-AZA. They reported essentially a 100% CR rate, response rate. That was amazing. What's the problem? I told you, VEN-AZA also already has toxicities. That drug brought on a lot of toxicities. At their target dose, a lot of toxicities. They really could not continue treating patients properly. It only targets, when they say 100% of the patients, it is only 30% of the patients. Left 70% of the patients behind. That is kind of, but that is the proof that it works. We have a better solution. Our Tuspetinib AZA, it is also HMA, hypomethylating agent, Tuspetinib AZA, HMA. It is an improved triplet. It is very safe. It has an excellent safety profile. It is the only triplet out there that is being developed as a mutation-agnostic. I can tell you big pharmas are looking at that. They're impressed with the data, as are the patients, the physicians, the NCI, the KOLs. We're all thrilled with what we're seeing in the patients, but we have a lot of work to do ahead. In terms of some of the milestones, accomplishments, last year we raised $37 million. We reported all the response and safety data. Remember I said in the relapsed refractory patients, the single agent, and then the combination with venetoclax. We reported all those data last year. We initiated our triplet trial in newly diagnosed patients. The NCI then selected our drug for this prestigious MALOMATCH program. The first half of this year, we told you already, we've reported data on 40 mg, 80 mg. We put out additional press release today so that you can read about these quite remarkable data. We'll be presenting at the European Hematology Association, as I said, one month from now. That's a really important meeting for us to get the data out. Finally, at the end of the year, American Society of Hematology. These are big meetings for us, presenting a great deal of data. Also around that same time, we plan to designate our pivotal study selected dose to move forward into for the pivotal studies later this year. We have a lot ahead of us. The last thing I'll just remind you is I did make certain forward-looking statements today. As a public company, you have to always say this. Oh yeah, and we are publicly traded. We're on the TSX under the ticker symbol ABS. With that, I'm going to close. Thank you for your attention and answer any questions.