Good day, everyone, and welcome to BeyondSpring, Inc.'s Operational and Clinical Update Conference Call. My name is Dimitrius, and I will be the operator on today's call. Please be advised that today's call is being recorded. At this time, I would like to turn the call over to the host for today's call, Joe Rayne of Argot Partner. You may begin.

Thank you. And thank you, everyone, for joining today's call. Before turning the call over to management, I would like to introduce today's speakers and their agenda for today's call. Dr. Lan Huang, Chairman and CEO of BeyondSpring, will begin today's call and provide a review of the Phase II 106 Study data reported today, as well as a brief review of the recent Plinabulin data. Richard Daly, BeyondSpring's Chief Operating Officer, will provide a brief update on regulatory plans and timelines for the Plinabulin program and an overview of the market opportunity for the company's Plinabulin franchise. And Dr. Douglas Blayney, Global Principal Investigator for BeyondSpring's chemotherapy-induced neutropenia or CIN development program and Professor of Medicine at Stanford University Medical Center, will provide his perspective on the potential role of Plinabulin in enhancing patient outcomes in the treatment of CIN. We will then open the call for questions. Dr. Ramon Mohanlal, the company's Executive Vice President of R&D and Chief Medical Officer; and Edward Liu, Chief Financial Officer, will be available to answer questions during the Q&A portion of today's call. I would like to also advise listeners that remarks made on today's call may reflect forward-looking statements relating to such matters as: BeyondSpring's clinical and preclinical research and development activities and results; regulatory and commercial plans; industry trends; market potential; collaborative initiatives; and financial projections, among others. These statements are based on currently available information and management's current assumptions, expectations and projections about future events. While management believes that its assumptions, expectations and projections are reasonable in view of the currently available information, you are cautioned not to place undue reliance on these forward-looking statements. The company's actual results may differ materially from those discussed during this call for a variety of reasons, including those described in the Forward-Looking Statements and Risk Factors section of the company's 20-F and other filings with the SEC, which are available from the Investors section of BeyondSpring's website. A slide deck will be referenced on the call and is available on the IR section of the company's website. It is now my pleasure to turn the call over to Dr. Lan Huang, Co-Founder, Chairman and CEO of BeyondSpring. Lan?

Thank you, Joe, and thank you, everyone, for joining us today. The past few months has been extremely productive from a clinical execution and the data rollout perspective, with multiple data results and presentations at pivot meetings and new emerging clinical data from our lead asset, Plinabulin, which further reinforce what we believe to be a potentially game-changing product profile for Plinabulin. We have learned how to use our lead asset first-in-class agent, Plinabulin, in our CIN clinical studies. Please look at slide Page 1. For the intermediate risk chemotherapy patient, where no therapy is the current standard of care, monotherapy of Plinabulin will be developed as shown in Study 105 design. Plinabulin potentially will have a superior overall profile than Neulasta in similar efficacy and significant better safety in bone pain, prevention of thrombocytopenia and positive impact of immune system. All this positive data were presented at the recent ASCO, IASLC, ESMO meetings. For high-risk chemotherapy patient, as shown in Study 106 design, Plinabulin, combined with Neulasta, has shown superior efficacy and safety profile, which I will detail in the call today. Today, we unveiled for the first time exciting and potentially paradigm-shifting new data from Study 106, our Phase II study of Plinabulin and Neulasta in the prevention of CIN in high-risk chemotherapy patients. This data are extremely compelling, and the potential clinical implications of this data cannot be ignored. Dr. Blayney graciously agreed to join us today to discuss this data and their potentially far-reaching indications to treating CIN. Importantly, this data suggests a new approach to optimizing chemotherapy by minimizing CIN and bone pain, providing a roadmap for how Plinabulin can be used in combination with Neulasta to improve patient care. Let me briefly review the data from the trial. This study is evaluating the combination…

Thank you very much, Lan. Good morning, everyone. In my view, the significance of the data that Lan highlighted cannot be overstated. I joined BeyondSpring just a few months ago, convinced that the data and the market opportunity that BeyondSpring has the potential blockbuster and a late stage development, which has the power to transform this company and, more importantly, [ given these ] data improved outcomes for patients in need of prophylaxis for CIN. 4 million cycles of monotherapy G-CSF are used worldwide each year to prevent CIN. And as Lan noted, there is an opportunity to improve on the current standard of care and improve the outcome for patients. Despite the current standard of prophylactic care in CIN with monotherapy G-CSF, although effective to treat mild neutropenia still, far too many patients develop grade 3 and 4 neutropenia. When neutropenia develops [ questions ] , following the NCCN guidelines are faced with 4 choices that have been referred to as the 4 Ds: number one, decrease the dose of chemotherapy; number two, delay the next chemotherapy cycle; number three, downgrade the chemo regimen; or number four, discontinue the chemotherapy. All of these choices can result in significantly worse outcomes for patients. As you can see, successfully improving preventative neutropenia matters to the oncologists and their patients. In our view, improving the prevention of neutropenia may be one of the most overlooked areas for the improvement of cancer treatment today. Prior to the release of the 106 top line data, we reported a number of key differentiating factors for Plinabulin. These include: first, a favorable adverse event profile with reduction in bone pain, a significant side effect of G-CSF therapy; second, convenience, first-day dosing and infusion 30 minutes after chemotherapy; third, clinical data that suggests anticancer activity; fourth, a…

Great. Thank you, Rich, and thanks a lot for allowing me to participate in this call today. I'm a medical oncologist. I've been active in the chemotherapy in this neutropenia space for approximately 25 years. And this is the first of what I think is exciting development in the field since the launch of Neulasta probably 20 years ago. So the Phase II data from our 106 Study was announced today. I was pleasantly surprised to see these results when I saw them. Remember that the 106 Study is looking at chemotherapy with more than a 20% risk of febrile neutropenia. As you've heard today, Neulasta, given prophylactically with the first cycle of chemotherapy, is the standard of care. Nonetheless, in spite of our use of Neulasta in this space, a significant number of patients either have to decrease or delay chemotherapy, and many of them just abandon Neulasta, TAC or high-dose chemo -- high-risk chemotherapy treatment and move on to something else. And I don't think this is a good thing for patients. Similarly, as you've heard, the combination of Plinabulin and a standard dose of Neulasta has shown not only a diminution in the stage -- grade 3 and 4 neutropenia, also shown a diminution in the grade 4 neutropenia. And surprisingly to me, and I'm very pleasantly surprised, it looks like the combination ameliorates the bone pain that patients have with Neulasta after chemotherapy. Our study showed that Neulasta alone, almost all patients have some sort of bone pain. This is underappreciated by physicians. In my experience, when I treat patients, they typically minimize it because they are afraid I'm going to say no, let's change chemotherapy or do something else. That's often underreported [ to ] patients [ that our nurses here evaluate a lot ].…

Thank you so much, Dr. Blayney, for the overview. In the past 18 months since our IPO last March, we have had significant development and growth at BeyondSpring. So we have successfully executed our clinical strategy and have built a world-class leadership team to support our transition to a commercial stage company. It's such an honor and privilege to work with such a stellar [ and a ] complementary team and with world-class KOLs, especially Dr. Blayney, to bring transforming medicine to treat unmet medical need. For Plinabulin, we have enrolled over 550 patient globally in the last 18 months in our registrational trials. Multiple data sets have highlighted Plinabulin's compelling efficacy and safety profile in CIN compared to standard of care Neulasta, a $6 billion drug. This data collectively highlights how Plinabulin could truly drive a paradigm shift in the treatment of cancer. We look forward to building on this momentum in the near term and to move our robust pipeline forward in development. We are now looking ahead to our Study 105 Phase III interim data this quarter, followed by our Study 103 Phase III topline interim data for non-small cell lung cancer early next year, which, assuming positive results, we expect to follow with NDA filings in China and the U.S. for CIN in the next 6 to 12 months and for non-small cell lung cancer in the next 12 to 18 months. We are very excited about opportunity for Plinabulin and our company, BeyondSpring. And we look forward to providing updates on our progress in the coming months. Operator, we are now ready to begin the Q&A portion of our call.

[Operator Instructions] And our first question comes from Joe Pantginis with H.C. Wainwright.

3 questions, if you don't mind. First, with regard to 106, very nice to see the data. I was wondering if you could share any information regarding the other arms on the study. Obviously, there's relatively small amount of patients in each arm because you really are looking to ask a lot of questions here. So are you seeing any trends in the arms with the lower dosages of Neulasta?

Dr. Blayney, yes, please.

So thanks, good question. And so the answer is yes. The top line answer is yes. There seems to be a dose response in Neulasta, which is not a surprise given history of development of the G-CSFs. And in our study, particularly the lower doses were not -- by lower doses, I mean 1.5 and 3.0 milligrams fixed dose. They were not as effective as the 6-milligram dose. So the answer to your question is that, yes, there seems to be a dose response in Neulasta. And this gives me personally confidence that our -- the Phase III data is likely to be -- confirmed what we found in this smaller Phase II study.

That's helpful. Maybe a question for Richard. With regard to the upcoming CFDA filing, can you discuss what some of the -- what are keeping you guys busy right now other than waiting for the data? What are some of [ the rate-limiting steps ] , outstanding issues that could get you to the finish line?

Joe, it's good to talk you again, but I think it's probably best if Lan handles that question.

Yes, this is much towards the CFDA side. So for the CFDA filing, this is -- as you know, for last October, CFDA has a new rule saying that the efficacy [ trend ] to apply for conditional approval in life-threat -- [ diseases]indication, so Plinabulin in the CIN indication does -- [ fit ] that criteria. And so with that, the data we plan to file for CFDA, the conditional approval, is the 105 Phase III data and also the 106 Phase II data. So I think we -- so we just shared with you the 106 Phase II data, which is positive, the top line, right, for the first cycle on the efficacy. And then the 105 Phase III, we are going to share this quarter, right. So we have the data ready for that filing from a efficacy point of view. For the safety point of view, we have enrolled over 450 patients in Plinabulin arm, so that's including [ these ] over 300 cancer patient requirement for the safety database, so that already complete on the data. And thirdly, for the CMC, we have already made -- or the registration batches for the API [ and drug ] product, we're already finished writing on the CMC. And so those are the 3 packages we will have for the CFDA filing, and that we are on track for that.

That's great. And then just a quick reminder, if you don't mind. With regard to the upcoming 105 Phase III interim data, can you remind us -- and I'm sorry, I don't recall if you've disclosed this, any potential stopping rules around that should the data be compelling?

So probably we should let Ramon to answer this question.

Yes. The Phase III of Study 105 has built in an interim analysis which was previously disclosed at around 100 patient, means 50 patients in each arm. That would trigger the preplanned interim analysis, which is currently ongoing. The conditions around the preplanned interim analysis indeed would allow for early stopping the study if you meet primary endpoint.

And our next question comes from Jason McCarthy with Maxim Group.

So I'd like to hear a bit more about the potential benefits of the combination, especially in the context of a now biosimilar Neulasta market. Given the difference in mechanism and the additive effects, is Plinabulin likely to be used to augment Neulasta rather than having to compete in this increasingly competitive neutropenia space?

So Jason, that's a great question. So I think I'll take it, and then I'll turn it over to Dr. Blayney who can give you a clinician's perspective. So as I mentioned earlier, we look at 4 million cycles that are utilized worldwide, and then we look at the results of this clinical trial. And we see this as an opportunity to improve patient care. So Plinabulin is given 30 minutes after a chemo cycle, so a patient can get it right away. And then the physician can decide based on their judgment whether or not they want to give Neulasta. And obviously, these data point to the fact that this combination would give the patient the best opportunity to avoid a chemo-induced neutropenia. And then we can talk about the other benefits as well, the immuno oncology benefit or the immuno benefit as well, but we'll just focus on avoiding the neutropenia and completing the chemo cycle. The focus here is on completing the chemo cycle benefit from the chemotherapy. So we'd look at this -- and when we think about -- if we were to go head-to-head straight up versus a G-CSF, you'd be thinking about market share. We're not thinking that way. We're thinking patient share because we see this as a polypharmacy approach because that's what benefit the patients the most. You reduce the bone pain. You reduce the febrile or the neutropenia and you have an opportunity to truly improve care. So we're agnostic to the G-CSF use here. We think it's best for the patient. And so we see this as a potential opportunity to really layer on top of really become foundation. We are used first and then they add the G-CSF after. I hope that's helpful.

Yes, Dr. Blayney.

Yes, this is Doug Blayney. I think that's a nice way to frame it. Jason, as you pointed out, the mechanisms of action that the 2 drugs seem to be quite different. I think of it as pegfilgrastim and Neulasta provides protection maybe in the first week after chemotherapy and Plinabulin in the second week after chemotherapy. So you have sort of this overlapping mechanism. And sure enough, that's what showed up in our Phase II data. Again, the decision -- I think it is going to be a marketing challenge because many docs will think just like you did, gee, should I pick one or the other? I think the stance is that this is -- the combination has a lot of benefits including the bone pain, the chemotherapy neutropenia protection and potentially anticancer effect and adding them, again, is best for the patient. So in the market with the high febrile neutropenia risk, it's additive would be -- the way to go, and this will build on what I think is the approach in the intermediate risk, [ that ] almost everybody will get Plinabulin or could benefit from Plinabulin. So in the physician's mind, gee, well, this is something we use for almost all of our chemotherapy, whether it's intermediate or high risk. I think that's the way to think about Plinabulin and its role with pegfilgrastim or Neulasta.

All right. And then just as a follow-up. I'd like to know -- because you saw that reduction in bone pain, I'd like to know how exactly you interpret that. Is Plinabulin itself actually reducing the bone pain? Or is it a byproduct of the reduced dose of Neulasta?

So probably, I can start and then Ramon can add and then some comment by Dr. Blayney. So as you see, Jason, bone pain actually comes from the overshoot of neutrophil of the G-CSF, right? So G-CSF sometimes makes too much of the neutrophil, and then you have too much neutrophil overshoot pushing out of bone, and then you have a bone pain. But Plinabulin is just an -- actually, what we see from the Plinabulin profile is it does eliminate -- attenuates the neutrophil overshoot [ of asset ] . So that basically gets to the less of the bone pain. So that's what I can start. Probably, Ramon, you can add to it.

Yes. What I can add to that is that the fact that Plinabulin prevents the bone pain is a clear indication that the mechanism of action resides in bone, because, otherwise, it will not give that benefit. So Plinabulin works through a different mechanism of action, and our initial data shows that that relates to a pathway that is important in the formation of neutrophils and that pathway [ relates to ] interleukin-6 in the bone marrow itself. So our hypothesis is that these 2 pathways together, they smoothen the process of the production of neutrophils. As Dr. Blayney pointed out in one of our discussions, it looks like the mechanism of Plinabulin is a stem cell protective mechanism rather than a stem cell activating or proliferating mechanism. And therefore, we believe that these 2 mechanisms together will prevent bone pain at bone marrow level.

Yes. This is Doug, if I can maybe amplify. Remember, that the bone in the human and mice too in the central part of the bone is where the bone marrow lives -- that's where the stem cells are and the pain receptors are on the surface of the bone. So anyway, when you give G-CSF 2 or 3 days later, you get this expansion of the center part of the bone. And patients tell me, doc, my skin is too small or something, my bones just ache from the inside. So I think Plinabulin is not acting on the pain receptors, but it's preventing this rapid expansion of the bone marrow or the hematopoietic compartment of the bone. And that's the reason why we don't get this bone pain, not seeing -- and that rapid expansion and the pouring out of neutrophils is what happens about day 8 after the chemotherapy. So I think the protection, as Ramon pointed out, of the hematopoietic stem cell from the [ insert ] of chemotherapy is responsible for not only the low bone pain, but also this absence of pouring out of neutrophils day 7 or 8 that we see.

All right. That was actually very helpful. So then just like as a last quick one. So when you look at the just the high dose combination versus Neulasta alone, does the reduction in duration of neutropenia widen compared to when you look through the sum of the combination data?

Yes. Perhaps, I can take that. Yes, it does. We have a dose-dependent widening -- a dose-dependent softening, sorry, with the duration of severe neutropenia, means that we have a dose-dependent benefit on duration of severe neutropenia, because this is a small trial, with relatively small sample sizes. DSN is an endpoint that is best measured in larger sample sizes. So we see the trend already in this data set, dose-dependent benefit on DSN, and with Phase III, the goal is to confirm that.

This is Doug. I'll just add that the curve -- as you look, we haven't plotted the curves, but it's in the previous study, 105. If you look at the deep neutrophil curve, it's broad at the nadir. It's not as deep with Plinabulin. It's broader, but the protection from the neutropenia comes over more days with Plinabulin, and it's a completely different kinetic or time recovery curve than you see with the pegfilgrastim alone or with Plinabulin alone. The combination seems to be the best of both of the curves. Hopefully, we'll show that later or when we have more data, as Ramon says.

Yes. So in summary, we see a dose-dependent benefit on the duration of neutropenia, which becomes shorter with the higher doses. But also we see that the depth, the nadir of the neutropenia also dose dependently is improved. So the data is consistent in terms of the duration, but also the intensity of the neutropenia with the benefit of the higher dose combination.

[Operator Instructions] And our next question comes from Matthew Cross with JonesTrading.

Congrats on the good mix of data here from both Study 105 and 106. I wanted to focus primarily on Study 106 results here. And I was hoping you could comment on your plans for a broad label for CIN. Obviously, you've established monotherapy benefit for Plinabulin that's [ noninferior ] to Neulasta in the docetaxel setting. But do you feel you need to establish this as well for TAC chemotherapy and another chemotherapy modalities outside of TAC and microtubule disruption to kind of test those protective effect on neutrophils and claim that broader label?

Well, probably I can start, and then, Ramon, you can add to this. So for the high-risk chemo indications, currently, while using the TAC, it is an example of the high-risk chemo. So I think with this showing good benefit and also with additional preclinical studies, we have shown Plinabulin in reducing the neutropenia of many different other chemotherapies which has different mechanism from docetaxel such as gemcitabine, Irinotecan and then other agents. So we think with these 4 cluster of data, potentially, we could get a broad label of the -- in the combo against the high-risk chemotherapy. So Ramon, probably you can add.

Yes. So as Lan pointed out, the development strategy is to test Plinabulin against a number of different chemotherapies, which each has a different chemotherapeutic mechanism of action. And the goal of that is to demonstrate that the benefit of Plinabulin for neutropenia is universal. So that's the way the program is set up. Those studies are ongoing, and we expect that we see the benefit throughout all the different studies, which will be the basis for approval for this broad indication.

Got it. I appreciate that clarity. And just to confirm then, there is no reason to believe you'd need to test Plinabulin by itself in this more aggressive chemotherapy in order to kind of contrast the benefits that you're seeing of the combination versus Plinabulin alone and what the contribution is there?

The effect of Plinabulin can be demonstrated in different types of study designs. It's not always necessary to test that separately. It's typically an arm that we include in the overall design with what we convey in this call is that the overall development strategy of Plinabulin will be as combination product in combination with G-CSF. The data collectively suggests that each of these 2 drugs, they have a different mechanism of action. And each of these 2 drugs, they have efficacy against CIN, but they do it in a different way, through different mechanism and also in a different time point in the cycle. Plinabulin primarily is protective in the first week and G-CSF in the second week. And together, we believe we can also protect it throughout the entire cycle. The benefit of monotherapy Plinabulin has already been demonstrated. We will further continue to study that. However, from a product development perspective, our opinion is that we should go for a combination to therefore create a superior product.

I appreciate you clarifying that for me. And then last one was just looking at the efficacy data that's presented from 106. Can you kind of comment on the openness of both the Chinese and U.S. FDAs to the use of incidences of severe neutropenia rather than DSN as an approvable endpoint? I just wanted to clarify that the reduction in DSN you saw at the stage for the combo versus Neulasta alone was clearly an improvement and clinically meaningful compared to Neulasta monotherapy, but not statistically significant. Is that correct? And then I also wanted to ask what -- the way the DSN was calculated in this study, that there's been a couple of different ways used?

Yes. Perhaps I can start. So DSN indeed was numerically improved, [ better ] combination, and the improvement was larger with higher G-CSF dose. If you look at the 2 arms, Neulasta alone versus Neulasta plus Plinabulin, we see a clear reduction in DSN. Because the data is not in the public domain, I probably don't have a lot of liberty to give you the exact numbers. The data is not only clinically significantly improved with the given -- with the right sample size, we will also be able to show that it is a statistical improvement, if this data will hold in Phase III. The other -- all other neutropenia-related endpoints, they improve consistently in same direction. So therefore, we have a high confidence that we are looking at total effect here.

And our next question comes from Graham Tanaka with Tanaka Capital Management.

Dr. Blayney, good to hear you again. And it was in winter we met and you mentioned that the medical community might be not reluctant, but slow to embrace new therapy. But based on the new data, do you believe now? It sounds like you believe that the community might actually be more willing to accept this theory -- this therapy as maybe mainline?

Yes, thanks, Graham. Appreciate your question. So the short answer is yes. I think that there's a lot of benefits to Plinabulin, this data, and also the anticancer data that is going to show. So as we talked about earlier, this data are driving a strategy, gee, whiz if we're going to use intermediate risk chemotherapy, which is what we use a lot, why not if we're going to add Plinabulin through the neutropenia protection we will [ know ] -- the licensed docs will know how to use it. And then when we do use in the high-risk settings for palliative chemotherapy, in other words, not the dose-dense, Adriamycin, Cytoxan and the dose-dense AC, but when we use it in other high-risk chemotherapy, we know how to use G-CSF, now we know how to use Plinabulin. We're very comfortable with using Plinabulin. So I think this data that you're seeing now, as well as the -- what I hope is an anticancer effect will ease the acceptance path by physicians and other clinicians to accept Plinabulin. There will be a lot of benefits to using it much more broadly. I hope that's responsive. But again, yes.

Graham, it's Rich. Good to talk to you again. So I want to add to Dr. Blayney's comments. I think that when you probably spoke, the thinking was probably along the lines of displacing the market leader by going pretty much head-to-head. And if you're thinking about this in general terms, I'm not speaking about Plinabulin versus Neulasta. In my experience, just in general terms, if you're trying to displace a market leader, it's really difficult if you're going in, you have sort of some differentiation, right. This is probably -- of the 10 products that I've launched previous to this, this is probably the most differentiated product that I've seen. And having worked in diabetes, cardiovascular, GI and all that, those are really tough spaces. The really interesting play here is that we're not trying to displace anybody. By adding on now -- if you look at the way the organization is moving and the way the therapeutics are moving, we're adding significant clinical benefit. Based on these data, we will be adding significant clinical benefit. And so we're not trying to displace anybody. The challenge becomes how to change habit. And we have a 100 -- a 360-degree program planned around professional, patient and payer. And prior to market -- prior to coming to market, we can do things around medical education. We have many awareness tools for the company around medical education, publications, abstracts, outcomes, patient surveys, et cetera, that we can make available, so that we begin to set the field, if you will. And we're trying to make, along with our partners, and when I say partners, I mean partners in general in the G-CSF space, improve therapy. So the opportunity becomes, how do we work with the G-CSF players out there and the physicians to improve therapy for patients. So by adding Plinabulin in, and the Plinabulin is the base now because we're first, we really are creating a better opportunity. And I think there's going to be less resistance to that because you're not going head-to-head and trying to displace somebody. You're really trying to improve patient care.

Now from a clinical point of view and a patient point of view, what -- this appears to be much better [ head-to-head ] profile and patients will be less likely to go off their chemo. What expansion of the potential total market do you see now if the community and the patient population embraces this as a better bone pain free, et cetera, solution, so that more people beyond chemo, and therefore, the market might actually be better? Could you mention numbers?

Sure. So let me take that and then I think Dr. Blayney can give you his clinical perspective. So we mentioned there 4 million cycles worldwide, so let me give you a little perspective. There's 4 million cycles that out there that are going on, and 60% of them are in the 2 major markets. We talked about the U.S. and China. Globally, 14 million patients were diagnosed roughly 2016, 2017 with cancer. 14 million patients diagnosed. 4 million of those patients received chemotherapy. Now these numbers are really tough to get, so it's taken us quite a bit of time to get these numbers. So 4 million patients received chemotherapy. So if you think, on average patient is on about 3, 4 cycles, so about 25% of patients are, roughly, I'm just saying roughly, are getting a G-CSF for the neutropenia. We talked before about patients are getting delayed cycles and all that or they're dropping off. So about 20 -- what's that?

I'm just saying correct, yes.

So about 25% of patients experience a delay of 7 days or more because of neutropenia and about 35% of patients have their dose reduced. And that's not including what Dr. Blayney talked about. He talked about docetaxel. 100% of patients get their dose reduced, right. He said the dose that the company tested was 100 milligrams per meter squared, and their starting dose in the clinic is 75, but you've talked about in general, 35% of patients get their dose reduced by 15% or more. So that's a very complex world we're looking at. So some patients are getting stopped. So we think that there's an opportunity to grow this market. And I think that's one the misnomers or misunderstandings about this market. People see this as a sleepy market. That's why I said in my comments. This is one of the overlooked areas of improving chemotherapy. Treating neutropenia is interesting, but that's not the goal. The goal is to improve chemotherapy and the outcomes for chemotherapy and to get the patient the best care possible. And so we really believe that this is a potential growth market. And if we're not duking it out with the G-CSFs and we're working to improve patient care, we can layer on top of it and [ now ] the CIN market becomes a growth opportunity. And we think that there's a lot of opportunity here. 4 million patients on chemotherapy and only 25% of them are getting a G-CSF right now. If we can improve the side effect profile and reduce neutropenia, it becomes easier for a clinician to use the product together. Dr. Blayney?

Yes. I think that's well said. I think I can draw the analogy too that 5-HD3, the antiemetics that were developed 20, 30 years ago. At that time also we had patients abandoning or stopping chemotherapy because of nausea. Doc, I can't take this anymore. I have been throwing up for 3 days. When 5-HD3s came along, a remarkable change, much safer to administer chemotherapy, much better adherence. So the 5-HD3s, dolasetron and granisetron, et cetera, and now palonosetron, are used ubiquitously in -- as antinausea agents. So we don't have nausea and vomiting as a side effect of chemotherapy and hardly ever anymore. We have to stop it, stop chemotherapy because of nausea and vomiting. I see Plinabulin as a analogous compound in neutropenia and dose reduction and dose delays, et cetera, as we talked about earlier. So the 5-HD3 is the analogy that I think really expanded our ability to deliver chemotherapy because of -- because they do away with a major side effect.

This is Ramon. If I can add one point to that. So this add-on strategy of Plinabulin in addition to G-CSF is also consistent with medical practice because Plinabulin is given on the same day of the chemo, after the chemo and Plinabulin infusion lasts about 30 minutes. So also from how to incorporate this strategy into the clinical practice, this is very doable.

Ladies and gentlemen, that now concludes the Q&A portion of our call. I would now like to return the call back over to Lan Huang for closing remarks.

Thank you all for joining us for today's operational and clinical update call, with a special thank you to Dr. Blayney for his participation today, as well as for his leadership in our clinical development program for CIN. BeyondSpring has the potential to change the face of CIN and cancer treatment, and I couldn't be more proud of our achievements to-date. Today, we are on the cusp of seeing the fruits of our hard work with multiple critical readouts over the next few months, which, if positive, will enable near-term NDA submissions with hopefully commercial launches plan thereafter or tremendous achievements as we begin to transition toward a global, commercial stage biopharmaceutical company. Thank you.

Ladies and gentlemen, thank you for attending today's conference. This does conclude the program, and you may all disconnect. Everyone, have a great day.

Thanks, all.