Transcript, Dr. Jay Lalezari interview November 14th
Thanks to urocksme at Stockwits for posting. It was in 20 parts, so I might have made mistakes in cutting and pasting. But this is surely most of it:
Karen Jagoda:… welcome you to the show. I appreciate you taking a few minutes to be with us.
Jay Lalezari: Thank you, Karen. It's a pleasure to join you.
Karen Jagoda: Thank you. We wanted to talk today about triple-negative breast cancer. So tell us why the company has decided to focus on that condition.
Jay Lalezari: When I became CEO back in November of 2023, my first order of business was to figure out where CytoDyn should go with this intriguing monoclonal antibody called leronlimab that targets CCR5. And we looked at a number of indications, and by far and away, the data that we found in solid tumor oncology is clearly the place CytoDyn will go to create the most benefit for our shareholders. We recently presented some data in triple- negative breast cancer that is truly remarkable and potentially paradigm-shifting in the world of solid tumor oncology.
Karen Jagoda: So, say more about what you mean by paradigm shifting, because solid tumors have been attacked fairly successfully, but you're taking it to the next level.
Jay Lalezari: Yeah. There are a number of solid tumors, triple negative breast cancer among them, where we still struggle to find effective therapies, in part because, by virtue of being triple negative, there aren't a lot of good targets on the cancer. And some years ago, CytoDyn launched three clinical studies in oncology focusing on women with triple-negative breast cancer. And those studies ran for a couple of years, they were then shut down, and there was a period of time where patients were lost to follow-up.
We have now been able to follow up on the 28 women who were enrolled in that study and have found that five of them are alive today, about five plus years later, three of whom have no evidence of disease. And these are women who were fourth-line median, fourth-line treatment median of two previous lines of treatment in the metastatic setting. 60% had organ metastasis, 30% had brain metastasis. The median survival of a population like that is generally measured in weeks or months. And the fact that we have five out of 28 who are alive and doing well in what appears to be a sustained remission five years later is absolutely remarkable. It is retrospective, but it is remarkable nonetheless.
Karen Jagoda: Tell us a little bit about the CCR5 receptor, which is part of this story, and why has that been an unexplored target in the past?
Jay Lalezari: Well, CCR5 emerged in the context of HIV, where it was found to be a secondary co-receptor for HIV entry. And for years, the development of leronlimab was focused on its potential role in the treatment of HIV. And indeed, leronlimab works as an antiviral. And over the years, leronlimab, I would add, has been given to almost 1600 patients, and we do not see a dominant safety signal or concern, which is just not something you can say about another cancer candidate therapeutic.
Jay Lalezari: Over the years, it became clear that CCR5 was not just for the virus to get inside the cell, but was playing a key role in setting up the tumor microenvironment in a variety of solid tumors that were CCR5 positive. That included typically triple- negative breast cancer, colon cancer, prostate cancer, pancreatic cancer, sarcoma, glioblastoma, and the urothelial cancers in particular.
So CCR5 helps the cancer set up a tumor microenvironment that helps it both build blood vessels to provide nourishment for the cancer and attract suppressor cells that keep the host immune system at bay.
Jay Lalezari: And by blocking that signaling through CCR5 with our antibody with leronlimab, we are breaking down that protective, suppressed immune environment and allowing the host immune system to now go after the virus. And what we found as the common denominator in these five women who received leronlimab was that they then had an induction of something called PDL-1 on their circulating tumor cells, which is an indication that the tumor has gone from cold to hot or from suppressed to inflamed.
And then these five women were the ones who just happened to get an immune class of drugs called immune checkpoint inhibitors, PDL-1 or PDL-1 blockers, commonly known as Keytruda. So that was the magic formula that seemed to now correlate with their long-term sustained remission - that they received leronlimab, they induced PDL-1, they got a checkpoint inhibitor, and now they're alive today despite the long odds given their situation five years ago.
Karen Jagoda: And it's really significant that what happens is that you turn the tumor from cold to hot. So, say a little bit more about the nature of cold tumors and how they're able to evade the immune system
Jay Lalezari: Yes, that is absolutely correct, and it's the center of this. When a cancerous solid tumor sets out to grow, it has to do two things. It has to build blood vessels that specifically provide nourishment so that it can grow beyond a certain size. And then the tumor is a foreign antigen that the normally the immune system would attack and eliminate. Cancers have a variety of strategies for keeping the immune system at bay. It's just that some solid tumors use the CCR5 receptor on suppressor cells in tissue macrophages to recruit those cells to do the cancerous business for it. And so that cold tumor environment has blood vessels that feed the cancer, but has a collection of suppressor cells, both cells called regulatory T cells, for which the Nobel Prize in Medicine was just awarded a couple of weeks ago, and other suppressor cells to create a cold tumor environment that the immune system doesn't penetrate very well, if at all
Jay Lalezari: And so that keeps the tumor from being recognized and destroyed. And so that's called a cold tumor microenvironment. And when you can break down that microenvironment and allow the cytotoxic T cells to enter the microenvironment and generate all these inflammatory cytokines, that's when tumor environment becomes hot. And one thing a cancer can do in response to an invading immune system is to generate this protein called PDL-1.
Jay Lalezari: What PDL does is bind to an off switch on these attacking immune cells called BD-1, and by flipping that off switch, the tumor is able to downregulate or turn down or push back on the invading immune system. And so that's where the checkpoint inhibitor, Keytruda, comes in. And that is that the women who received leronlimab apparently had a breakdown in the tumor microenvironment, then secreted PDL-1 in an effort to repel the immune system.
The women who just happened to get a checkpoint inhibitor to block the action of that protein, PDL-1, they're the ones who survived.
Karen Jagoda: And the PDL-1 would not have worked otherwise, in terms of the immunotherapies. I mean, those people would be in the category where the immunotherapy just didn't work. Would that be fair to say?
Jay Lalezari: That's exactly right. And so immunotherapy has been very successful, particularly in the last decade, but it's been successful in patients with solid tumors who express PDL-1. And unfortunately, it's the majority of solid tumors that don't. So the majority of solid tumors are cold. So for the patients whose cancers are PDL-1 positive, immunotherapy is hugely successful. GSK just got a breakthrough designation for their PDL-1 inhibitor, where their response rate was 100% in patients with rectal cancer who had hot tumors
Jay Lalezari: So if we can cause cold tumors to go hot, we have a treatment that is highly successful. The trick is getting those cold tumors to turn hot. And that's where the excitement with leronlimab is that we saw that patients who got one of the two higher doses, both of which were well tolerated, 88% of those women had their tumors go from cold to hot over a period of one to two months.
Karen Jagoda: That's really significant. And would this also be effective for colorectal cancer?
Jay Lalezari: Yes, indeed. We started, we didn't know the full PDL-1 story, so we were working with the FDA and their requirements for how CytoDyn should move forward. And so the first study we designed was in colorectal cancer, looking at two doses, but it was all before we knew about the PDL-1 and checkpoint inhibitor story.
Jay Lalezari: Over the last six to eight months, CytoDyn has gathered all the information on the patients that I've mentioned, the 28 patients with TNBC, and about 13 other patients as well. We've put it together into a briefing book. We'll be meeting with the FDA in the next couple of weeks, and they'll finally have the opportunity to see the story that you and I are discussing here today. And that will give us the opportunity both to submit our proposed follow-up study in triple negative breast cancer, submit a compassionate use program in triple negative breast cancer, as well as do some redesign of our colorectal cancer, updating it with the information we have about PDL-1 and the role of using checkpoint inhibitors in this case in patients with colorectal cancer who started with cold cancers, hopefully received leromlimab, and then their tumors turn hot, at which point they become eligible for a checkpoint inhibitor.
Karen Jagoda: Would this be a frontline approach to other cold tumors, would you say, in the future, once the trials are completed? Is that the general direction you might be going in?
Jay Lalezari: That's a great question. I think that first of all, the safety profile of leronlimab is so unusual that it is worth talking about a cancer therapeutic that doesn't have toxicity or side effects. It's administered once a week under the skin like insulin. And again, there's no dominant safety signal that suggests it should probably be used earlier. We also have studies showing both in triple-negative breast cancer and in colorectal cancer, and animal studies that leronlimab is very effective at preventing the spread of cancer or the establishment of metastasis.
Jay Lalezari: And that's crucially important because it's generally not the primary tumor that kills patients, but rather the spread of that tumor into distant metastasis. And by blocking CCR5 with leronlimab, we're actually blocking the GPS system that the cancer uses to spread. So that's a second argument in favor of potentially using leronlimab as an earlier line of therapy. And as we said earlier, most patients are not eligible for immunotherapy precisely because they have cold tumors. But if we can turn cold tumors hot with a benign drug like leronlimab, and now have the majority of patients with solid tumors become eligible for a checkpoint inhibitor, that would obviously be much preferable to rounds of chemotherapy.
Karen Jagoda: And are the checkpoint inhibitor drug developers also looking at this path, or is that not their lane?
Jay Lalezari: The companies, the big companies, Merck, BMS, GSK, and others about, I think more than a dozen have checkpoint inhibitors are all aware of how important it would be to shift a cold tumor to hot and how that would open up a pathway to provide treatment to the majority of patients with solid tumors who are currently not eligible. So that is very much on their minds. And we're actually presenting an abstract to the meeting at the American Association for Cancer Research that's having a session specifically on turning cold tumors hot. So it's very much dead center in the research oncology. And once the awareness is raised about how important this particular status is, I imagine lots of people are starting to think more creatively about how to work in this new environment.
Karen Jagoda: So would you say this would be a therapy that would be seen as something that would be a maintenance therapy after a certain point?
Jay Lalezari: Well, we do not know a lot about the timelines. The one patient who's a long- term survivor and has been on leronlimab and a checkpoint inhibitor called atezolizumab for five years, the other four were on leronlimab for a period of time, then on a checkpoint inhibitor for a period of time. So we don't know what the timelines are of how long either drug would be required, and that's going to require the clinical studies to show us whether long-term maintenance is required or not.
Karen Jagoda: Would you say that this is just the beginning of this process of understanding how your platform can really blossom?
Jay Lalezari: Absolutely. The first order of business is for us to prospectively confirm what we've seen retrospectively. When we do that, it's a game-changer for CytoDyn. I think it's a game-changer for patients with CCR5-positive solid tumors. And at that point, we've spoken to quite a number of the pharmaceutical entities that have checkpoint assets, and they're really just waiting to see us confirm this signal prospectively before diving in, because it gives them an opportunity, not only will patients benefit, but it'll give the companies an opportunity to vastly expand their markets.
Karen Jagoda: Yes, I've always wondered about the drug manufacturers who are designing these drugs that don't work for a small portion of the population. So I'm just guessing this would open up a much broader range of patients that they could help. So that's also part of the mission here, right?
It's not to reinvent the wheel, but to make what's already out there just more effective for more people.
Lalezari: Absolutely. As I said, checkpoint inhibitors are very effective in patients who are candidates for them. The problem is, as you said, most patients are not candidates, and pharma has been working for years trying to figure out how to convert these cold tumor environments to hot. So what CytoDyn has stumbled into is that's why I use the word paradigm shift. It really is a game-changer, potentially in solid tumor oncology.
Karen Jagoda: Before we run out of time today, say more about your background and your experience.
Jay Lalezari: So I'm an internist. I started a clinical virology research program in San Francisco on June 20th, 1986. And I continue to run it today, 36 years later. And most of the HIV drugs came through the clinical trial unit that I run here. And I started working with leronlimab back in 2005. So I've had 20 years with this drug and helped with the HIV development program, even as it became clear that the true value of leronlimab is probably in solid tumor oncology. But I'm very excited about what we're seeing here. And even at Quest, we continue to do studies in oncology. So I have frequent contact with patients with solid tumors. So I never forget for a day how urgent this is to prospectively show our signal, bring a partner on board, and launch the kind of studies that'll bring an FDA approval as quickly as possible/\.
Karen Jagoda: Also, it's required to be patient. You've been at this for 20 years, and you really understand this drug. So, have you been surprised at how long it's taken to better understand the effect, or have you been pleasantly surprised that things have grown as quickly as they have?
Jay Lalezari: That's a whole other interview for another day. What I would say is that, as an immunotherapy, leronlimab blocking CCR5 is complicated. And that I think if anyone had begun 20 years ago, it could have taken some time to sort out at various points. CytoDyn was looking at fatty liver oncology, COVID, long COVID, and HIV graft versus host disease. CCR five shows up all over the textbook of medicine now. And so identifying which indication would be the shortest distance between now and an approval would've been a tricky task, no matter who was driving the company.
But I think yes, as you said, it's been a long haul. But what's really gratifying is I think we have a clear sight now to where this company needs to go and how to get this drug approved for patients.
KJ: Thanks to my guest today, Dr. Jay Lalezari, CEO of CytoDyn, cytodyn.com. I'm Karen Jagoda, Host of the Empowered Patient Podcast. Thanks for listening, and we'll see you next time. The Empowered Patient Podcast can be found on the Libsyn network, Amazon Music/Audible, Apple Podcasts, Google Play Music, iHeartRadio, SpotOn, Spotify, TuneIn, radio.com/, Gaana, Deezer, JioSaavn, Audacy, PlayerFM, Samsung, and YouTube Dr. Jay Lalezari Cytodyn
Thanks to urocksme at Stockwits for posting. It was in 20 parts, so I might have made mistakes in cutting and pasting. But this is surely most of it:
Karen Jagoda:… welcome you to the show. I appreciate you taking a few minutes to be with us.
Jay Lalezari: Thank you, Karen. It's a pleasure to join you.
Karen Jagoda: Thank you. We wanted to talk today about triple-negative breast cancer. So tell us why the company has decided to focus on that condition.
Jay Lalezari: When I became CEO back in November of 2023, my first order of business was to figure out where CytoDyn should go with this intriguing monoclonal antibody called leronlimab that targets CCR5. And we looked at a number of indications, and by far and away, the data that we found in solid tumor oncology is clearly the place CytoDyn will go to create the most benefit for our shareholders. We recently presented some data in triple- negative breast cancer that is truly remarkable and potentially paradigm-shifting in the world of solid tumor oncology.
Karen Jagoda: So, say more about what you mean by paradigm shifting, because solid tumors have been attacked fairly successfully, but you're taking it to the next level.
Jay Lalezari: Yeah. There are a number of solid tumors, triple negative breast cancer among them, where we still struggle to find effective therapies, in part because, by virtue of being triple negative, there aren't a lot of good targets on the cancer. And some years ago, CytoDyn launched three clinical studies in oncology focusing on women with triple-negative breast cancer. And those studies ran for a couple of years, they were then shut down, and there was a period of time where patients were lost to follow-up.
We have now been able to follow up on the 28 women who were enrolled in that study and have found that five of them are alive today, about five plus years later, three of whom have no evidence of disease. And these are women who were fourth-line median, fourth-line treatment median of two previous lines of treatment in the metastatic setting. 60% had organ metastasis, 30% had brain metastasis. The median survival of a population like that is generally measured in weeks or months. And the fact that we have five out of 28 who are alive and doing well in what appears to be a sustained remission five years later is absolutely remarkable. It is retrospective, but it is remarkable nonetheless.
Karen Jagoda: Tell us a little bit about the CCR5 receptor, which is part of this story, and why has that been an unexplored target in the past?
Jay Lalezari: Well, CCR5 emerged in the context of HIV, where it was found to be a secondary co-receptor for HIV entry. And for years, the development of leronlimab was focused on its potential role in the treatment of HIV. And indeed, leronlimab works as an antiviral. And over the years, leronlimab, I would add, has been given to almost 1600 patients, and we do not see a dominant safety signal or concern, which is just not something you can say about another cancer candidate therapeutic.
Jay Lalezari: Over the years, it became clear that CCR5 was not just for the virus to get inside the cell, but was playing a key role in setting up the tumor microenvironment in a variety of solid tumors that were CCR5 positive. That included typically triple- negative breast cancer, colon cancer, prostate cancer, pancreatic cancer, sarcoma, glioblastoma, and the urothelial cancers in particular.
So CCR5 helps the cancer set up a tumor microenvironment that helps it both build blood vessels to provide nourishment for the cancer and attract suppressor cells that keep the host immune system at bay.
Jay Lalezari: And by blocking that signaling through CCR5 with our antibody with leronlimab, we are breaking down that protective, suppressed immune environment and allowing the host immune system to now go after the virus. And what we found as the common denominator in these five women who received leronlimab was that they then had an induction of something called PDL-1 on their circulating tumor cells, which is an indication that the tumor has gone from cold to hot or from suppressed to inflamed.
And then these five women were the ones who just happened to get an immune class of drugs called immune checkpoint inhibitors, PDL-1 or PDL-1 blockers, commonly known as Keytruda. So that was the magic formula that seemed to now correlate with their long-term sustained remission - that they received leronlimab, they induced PDL-1, they got a checkpoint inhibitor, and now they're alive today despite the long odds given their situation five years ago.
Karen Jagoda: And it's really significant that what happens is that you turn the tumor from cold to hot. So, say a little bit more about the nature of cold tumors and how they're able to evade the immune system
Jay Lalezari: Yes, that is absolutely correct, and it's the center of this. When a cancerous solid tumor sets out to grow, it has to do two things. It has to build blood vessels that specifically provide nourishment so that it can grow beyond a certain size. And then the tumor is a foreign antigen that the normally the immune system would attack and eliminate. Cancers have a variety of strategies for keeping the immune system at bay. It's just that some solid tumors use the CCR5 receptor on suppressor cells in tissue macrophages to recruit those cells to do the cancerous business for it. And so that cold tumor environment has blood vessels that feed the cancer, but has a collection of suppressor cells, both cells called regulatory T cells, for which the Nobel Prize in Medicine was just awarded a couple of weeks ago, and other suppressor cells to create a cold tumor environment that the immune system doesn't penetrate very well, if at all
Jay Lalezari: And so that keeps the tumor from being recognized and destroyed. And so that's called a cold tumor microenvironment. And when you can break down that microenvironment and allow the cytotoxic T cells to enter the microenvironment and generate all these inflammatory cytokines, that's when tumor environment becomes hot. And one thing a cancer can do in response to an invading immune system is to generate this protein called PDL-1.
Jay Lalezari: What PDL does is bind to an off switch on these attacking immune cells called BD-1, and by flipping that off switch, the tumor is able to downregulate or turn down or push back on the invading immune system. And so that's where the checkpoint inhibitor, Keytruda, comes in. And that is that the women who received leronlimab apparently had a breakdown in the tumor microenvironment, then secreted PDL-1 in an effort to repel the immune system.
The women who just happened to get a checkpoint inhibitor to block the action of that protein, PDL-1, they're the ones who survived.
Karen Jagoda: And the PDL-1 would not have worked otherwise, in terms of the immunotherapies. I mean, those people would be in the category where the immunotherapy just didn't work. Would that be fair to say?
Jay Lalezari: That's exactly right. And so immunotherapy has been very successful, particularly in the last decade, but it's been successful in patients with solid tumors who express PDL-1. And unfortunately, it's the majority of solid tumors that don't. So the majority of solid tumors are cold. So for the patients whose cancers are PDL-1 positive, immunotherapy is hugely successful. GSK just got a breakthrough designation for their PDL-1 inhibitor, where their response rate was 100% in patients with rectal cancer who had hot tumors
Jay Lalezari: So if we can cause cold tumors to go hot, we have a treatment that is highly successful. The trick is getting those cold tumors to turn hot. And that's where the excitement with leronlimab is that we saw that patients who got one of the two higher doses, both of which were well tolerated, 88% of those women had their tumors go from cold to hot over a period of one to two months.
Karen Jagoda: That's really significant. And would this also be effective for colorectal cancer?
Jay Lalezari: Yes, indeed. We started, we didn't know the full PDL-1 story, so we were working with the FDA and their requirements for how CytoDyn should move forward. And so the first study we designed was in colorectal cancer, looking at two doses, but it was all before we knew about the PDL-1 and checkpoint inhibitor story.
Jay Lalezari: Over the last six to eight months, CytoDyn has gathered all the information on the patients that I've mentioned, the 28 patients with TNBC, and about 13 other patients as well. We've put it together into a briefing book. We'll be meeting with the FDA in the next couple of weeks, and they'll finally have the opportunity to see the story that you and I are discussing here today. And that will give us the opportunity both to submit our proposed follow-up study in triple negative breast cancer, submit a compassionate use program in triple negative breast cancer, as well as do some redesign of our colorectal cancer, updating it with the information we have about PDL-1 and the role of using checkpoint inhibitors in this case in patients with colorectal cancer who started with cold cancers, hopefully received leromlimab, and then their tumors turn hot, at which point they become eligible for a checkpoint inhibitor.
Karen Jagoda: Would this be a frontline approach to other cold tumors, would you say, in the future, once the trials are completed? Is that the general direction you might be going in?
Jay Lalezari: That's a great question. I think that first of all, the safety profile of leronlimab is so unusual that it is worth talking about a cancer therapeutic that doesn't have toxicity or side effects. It's administered once a week under the skin like insulin. And again, there's no dominant safety signal that suggests it should probably be used earlier. We also have studies showing both in triple-negative breast cancer and in colorectal cancer, and animal studies that leronlimab is very effective at preventing the spread of cancer or the establishment of metastasis.
Jay Lalezari: And that's crucially important because it's generally not the primary tumor that kills patients, but rather the spread of that tumor into distant metastasis. And by blocking CCR5 with leronlimab, we're actually blocking the GPS system that the cancer uses to spread. So that's a second argument in favor of potentially using leronlimab as an earlier line of therapy. And as we said earlier, most patients are not eligible for immunotherapy precisely because they have cold tumors. But if we can turn cold tumors hot with a benign drug like leronlimab, and now have the majority of patients with solid tumors become eligible for a checkpoint inhibitor, that would obviously be much preferable to rounds of chemotherapy.
Karen Jagoda: And are the checkpoint inhibitor drug developers also looking at this path, or is that not their lane?
Jay Lalezari: The companies, the big companies, Merck, BMS, GSK, and others about, I think more than a dozen have checkpoint inhibitors are all aware of how important it would be to shift a cold tumor to hot and how that would open up a pathway to provide treatment to the majority of patients with solid tumors who are currently not eligible. So that is very much on their minds. And we're actually presenting an abstract to the meeting at the American Association for Cancer Research that's having a session specifically on turning cold tumors hot. So it's very much dead center in the research oncology. And once the awareness is raised about how important this particular status is, I imagine lots of people are starting to think more creatively about how to work in this new environment.
Karen Jagoda: So would you say this would be a therapy that would be seen as something that would be a maintenance therapy after a certain point?
Jay Lalezari: Well, we do not know a lot about the timelines. The one patient who's a long- term survivor and has been on leronlimab and a checkpoint inhibitor called atezolizumab for five years, the other four were on leronlimab for a period of time, then on a checkpoint inhibitor for a period of time. So we don't know what the timelines are of how long either drug would be required, and that's going to require the clinical studies to show us whether long-term maintenance is required or not.
Karen Jagoda: Would you say that this is just the beginning of this process of understanding how your platform can really blossom?
Jay Lalezari: Absolutely. The first order of business is for us to prospectively confirm what we've seen retrospectively. When we do that, it's a game-changer for CytoDyn. I think it's a game-changer for patients with CCR5-positive solid tumors. And at that point, we've spoken to quite a number of the pharmaceutical entities that have checkpoint assets, and they're really just waiting to see us confirm this signal prospectively before diving in, because it gives them an opportunity, not only will patients benefit, but it'll give the companies an opportunity to vastly expand their markets.
Karen Jagoda: Yes, I've always wondered about the drug manufacturers who are designing these drugs that don't work for a small portion of the population. So I'm just guessing this would open up a much broader range of patients that they could help. So that's also part of the mission here, right?
It's not to reinvent the wheel, but to make what's already out there just more effective for more people.
Lalezari: Absolutely. As I said, checkpoint inhibitors are very effective in patients who are candidates for them. The problem is, as you said, most patients are not candidates, and pharma has been working for years trying to figure out how to convert these cold tumor environments to hot. So what CytoDyn has stumbled into is that's why I use the word paradigm shift. It really is a game-changer, potentially in solid tumor oncology.
Karen Jagoda: Before we run out of time today, say more about your background and your experience.
Jay Lalezari: So I'm an internist. I started a clinical virology research program in San Francisco on June 20th, 1986. And I continue to run it today, 36 years later. And most of the HIV drugs came through the clinical trial unit that I run here. And I started working with leronlimab back in 2005. So I've had 20 years with this drug and helped with the HIV development program, even as it became clear that the true value of leronlimab is probably in solid tumor oncology. But I'm very excited about what we're seeing here. And even at Quest, we continue to do studies in oncology. So I have frequent contact with patients with solid tumors. So I never forget for a day how urgent this is to prospectively show our signal, bring a partner on board, and launch the kind of studies that'll bring an FDA approval as quickly as possible/\.
Karen Jagoda: Also, it's required to be patient. You've been at this for 20 years, and you really understand this drug. So, have you been surprised at how long it's taken to better understand the effect, or have you been pleasantly surprised that things have grown as quickly as they have?
Jay Lalezari: That's a whole other interview for another day. What I would say is that, as an immunotherapy, leronlimab blocking CCR5 is complicated. And that I think if anyone had begun 20 years ago, it could have taken some time to sort out at various points. CytoDyn was looking at fatty liver oncology, COVID, long COVID, and HIV graft versus host disease. CCR five shows up all over the textbook of medicine now. And so identifying which indication would be the shortest distance between now and an approval would've been a tricky task, no matter who was driving the company.
But I think yes, as you said, it's been a long haul. But what's really gratifying is I think we have a clear sight now to where this company needs to go and how to get this drug approved for patients.
KJ: Thanks to my guest today, Dr. Jay Lalezari, CEO of CytoDyn, cytodyn.com. I'm Karen Jagoda, Host of the Empowered Patient Podcast. Thanks for listening, and we'll see you next time. The Empowered Patient Podcast can be found on the Libsyn network, Amazon Music/Audible, Apple Podcasts, Google Play Music, iHeartRadio, SpotOn, Spotify, TuneIn, radio.com/, Gaana, Deezer, JioSaavn, Audacy, PlayerFM, Samsung, and YouTube Dr. Jay Lalezari Cytodyn
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