That first button before movies and television is podcasts. Traffic is staggering, right? Then you've just seen Hulu and Disney enter, right? Now you saw, in shocking fashion, HBO Max just went into the Howard Stern world. Listen. Everybody is now coming in. They're renting it. They're either going to come in as strategic partners or they're going to start buying up everything. My guess is they're going to start buying networks. You're going to have to get over $100 million for the big, big to try to get seven times revenues. But those 3.7 times revenues are there. What I said on the last conference call and what I wrote publicly in our last press release is that based on the inbound calls, we have retained bankers to, A, to protect our shareholders.
Because as a fiduciary, we have to, no matter where the bids come in, you have no choice. You have to look at it from what's fair for shareholders, right? When I built iWon.com, the bids came in at $200 million, then it was $400 million, then it was $600 million, and Barry Diller just keep bidding it up and we sold it for $860 million. I wasn't looking to sell and I'm not looking to sell now, but if the right price comes along, you have no choice. We're in that world. The second thing we said is we'll consider all options to increase shareholder value. We spun out PodcastOne to be the only podcast network traded publicly in the world, and I do think there is a real place for that. But it's not where it's trading at $1.70. There's no value to it, right?
You can't do the roll-up strategy. We are looking at that, and as we buy up stock indirectly, we're buying more and more. The businesses really are all together. They're just two separate companies. It's really almost a tracking stock. Even though there's separate management, all of our podcasts are across our LiveOne business as well. When we do a deal with a retailer or AT&T, when you get a LiveOne app, you're getting just like Spotify, you're getting everything that's in it, including audio, podcasting, pay-per-view, live streaming, all our events.
Do you also relicense those podcasts that you guys are creating out to other distributors?
Well, we don't relicense them. We just put them on their platform. We have partnerships with Spotify, Apple. Where most of the traffic is, I keep all the revenues up. It's a trade. What's going to happen next is they're going to start paying for it.
Think of ESPN and all the fights with ESPN and cable and satellite, right? Now the consolidation's happening, and it's going to come down to maybe there's cable and satellite and television. Maybe there's seven this time. There may be seven partners, and they're going to be competing with content. That's where Howard Stern just got paid. Someone may call me tomorrow and offer Adam Carolla $5 million a year to put him on their platform. It's shocking to me because I know the traffic numbers. It's great, but they're coming, and they're coming fast.
Thank you so much. Any other questions can be taken outside.
Thank you so much for being with us today. It is my pleasure to introduce you to John Yu, Chairman and CEO of Kairos Pharma.
Thank you for joining us this afternoon. Here are forward-looking statements, too small to read. Our mission at Kairos Pharma is to advance therapies that overcome critical challenges in cancer drug resistance and immune suppression. The problem is that resistance develops to even blockbuster drugs like antiandrogen therapies in prostate cancer and TAGRISSO in non-small cell lung cancer. The solution is that CD105 is elevated as the cancer cells become resistant, and our antibody, ENV-105, reverses this resistance. These are large opportunities in prostate cancer, non-small cell lung cancer, and other tumor types. We have three clinical programs in progress. Our lead drug, ENV-105, in Phase II trial, is treating prostate cancer with NIH grant funding. ENV-105 is also in a Phase I trial treating non-small cell lung cancer with non-dilutive donor funding.
We have an experienced team at Cedars-Sinai to drive enrollment and grant funding to create non-dilutive value. Our prostate trial is a Phase II trial that is randomized between 80 patients. Our lung cancer trial is a 60-patient trial, and the glioblastoma trial is getting underway and funded by a donor. We have solid tumors that will be treated with KROS-101 with grant funding. Resistance develops to many different types of therapies, including tyrosine kinase inhibitors like TAGRISSO, radiation therapy, immune therapy, and hormone therapy. In our prostate trial and lung trial, tumors become resistant, and this is through a mechanism of CD105 which becomes elevated during treatment. What CD105 does is it targets a molecule called BMP4. BMP4 is involved in making a cancer more stem cell-like.
What that means is in parallel to normal stem cells in the organs that drive all of the cells of a particular organ, cancer stem cells drive the cancer cells to become more stem cell-like. What that means is the stem cells are important cells that make all of the cells of the organ. It differentiates to all of the cells. In a similar fashion, cancer stem cells drive and initiate the cancer and make all of the tumor cells of that cancer. What CD105 does is by signaling BMP4, cells become more stem cell-like, and stem cells are known to be resistant to different types of toxins in the environment.
Just like normal cells need to be resistant to radiation and to the toxins in the environment to be able to recreate all the cells of the organ, cancer stem cells are resistant to radiation and the therapeutics that are used to treat it. As BMP4 signaling is made by CD105, the cancer cells become more cancer stem cell-like and resistant to the drugs. Here you can see when you look at lung cancer patients, the expression of CD105 is directly related to their overall survival. Here you see the survival of patients with a high CD105 expression and a low CD105 expression. Survival is significantly longer in the low CD105-expressing patients. There are 45,000 patients with EGFR-driven non-small cell lung cancer, and TAGRISSO is the standard of care for these patients.
We demonstrated in an animal model that when you compare a treatment with TAGRISSO or osimertinib, there is a significant decrease in the growth of these tumors when you add ENV-105, otherwise known as carotuximab. Based on these data and other data, we went into a Phase I trial with TAGRISSO to see if our drug would make these patients go longer on TAGRISSO. This is our Phase I trial with 20 patients on TAGRISSO that are resistant and 20 patients that are incompletely treated with TAGRISSO, which we are actively accruing on. We recently reported the safety results. There were no grade three or higher toxicities in 11 patients treated to date on ENV-105. An interim efficacy readout will be reported this quarter in 2026. ENV-105 restores sensitivity to hormone therapy in this human tumor.
You can see whereas the tumor grows despite the use of enzalutamide, the first-line antiandrogen agent that is used. When you add ENV-105 to it gets rid of the tumor cells and only the blood vessels and fibroblasts are left. When you add ENV-105 to the therapies, it significantly decreases the tumor volume in these models as well. This is largely due to the tumor cell becoming more cancer stem cell-like. By virtue of doing that, it makes less of these decoy receptors, the AR-V7, which is the most common one. The decoy receptors take away the drugs that are used to treat it, like enzalutamide. When carotuximab or ENV-105 is used, then these androgen receptor decoy receptors are no longer made so that the cell becomes susceptible to treatment.
We went to a randomized Phase II trial comparing apalutamide to ENV-105 plus apalutamide. This is presently accruing at Cedars-Sinai Medical Center, the Huntsman Institute at the University of Utah, and the City of Hope, with the primary endpoint being progression-free survival. These were the first patients that were treated. The patients had either one to three different antiandrogen agents that were used. The progression-free survival expectation was between four months and six months, as was shown in a previous randomized trial in The New England Journal and The Lancet. This is what happens when you just change out the antiandrogen agent. That would be the expected survival of four to six months. In the first treatment cohort, we showed a significant decrease in PSA when ENV was added to apalutamide.
Most recently, we reported the results of the part of the randomized treatment where patients with apalutamide alone had a survival of approximately two months, and apalutamide plus ENV-105 had a survival of approximately seven months with a P value of 0.0008. Given these results, we changed our protocol. We are still able to use the safety lead in patients, but we went to an earlier time point when patients are treated with enzalutamide and failed the first treatment or enzalutamide. This allows us to treat a wider swath of patients upon their first failure of the first antiandrogen agents and will allow us to rapidly enroll in a trial given these patients are much more available. We plan to enroll these patients in a consortium that we created along with the Mayo Clinic, with other institutions including Stanford, Vanderbilt, Rutgers, and Cleveland Clinic.
This allows us to start all the trials at once and to have a regulatory oversight of each of these places, basically functioning as a CRO, but an academic CRO, keeping costs down and allowing these academic centers to collaborate together. Radiation therapy resistance is the other arm besides therapeutic resistance, where radiation when given to a tumor, the tumor becomes resistant to it in a very similar fashion with antiandrogen agents and to TAGRISSO. Largely, it's because they become more cancer stem cell-like, and they also have enhanced DNA damage repair, just like normal stem cells. This is through that inhibition of BMP4 signaling. We showed previously in an animal model that when you add ENV-105 to radiation therapy, there's a significant decrease in the tumor growth. This led us to a collaboration with Bayer and their use of Xofigo.
This is ending in t wo weeks, and I hope to report the results soon thereafter with the potential supporting of a Phase II clinical trial between Xofigo plus or minus ENV-105. Overcoming immune therapy resistance is another area that we're interested in. KROS-101 is a small molecule that targets the GITR ligand, which is an important molecule that either increases T effector cells as well as decreases Tregs or the suppressive T cells. This will be used when patients become resistant to therapeutics like PD-1 inhibitors like the Merck drug and nivolumab. This is being supported through NIH grants. NIH grant funding is a common theme among our therapeutics.
We have a $3.2 million grant that's supporting the ENV Phase II trial, a $2 million grant from the Department of Defense supporting the lung cancer trial, as well as other donor and federal grants. Our company is involved in addressing mechanisms of resistance to tyrosine kinase inhibitors, radiation therapy, immune therapy, and hormone therapy. Our patent portfolio is strong and covers composition of matter as well as methods of use. We have a small team of three investigators and our CFO, and people ask us how we can compete with large pharma companies like Pfizer, and that's really because we're collaborating with these pharma companies to make their drugs work better. Our directors are well-heeled in the pharma industry as well as in biotech, and they have made our connections with these pharma companies to enable discussions and collaborations.
Kairos Pharma is a clinical stage company with an antibody that impacts a central mechanism of cancer drug resistance. We have an extensive pipeline that targets immune suppression. We're enrolling in Phase I and II trials with completion in 2027. We have a strategic relationship with Cedars-Sinai Medical Center, giving us access to the top medical centers in the country, allowing us to drive enrollment and bring down costs. We're a small company with a technology that could impact large pharma therapeutics in widespread cancers. We have enough cash to last at least three quarters.
We've been very keen on bringing in funding in the most least dilutive way to our shareholders and plan on continuing until we can drive enrollment to the end of our Phase I and II trials, where we anticipate having further discussions with the pharma companies that are involved in the development of the therapeutics for prostate cancer and lung cancer. Thank you very much and happy to take any questions. Yes. Sure.
Is this an mRNA strategy? I missed the beginning.
It's a neutralizing antibody that targets the CD105 molecule. It inhibits that, which then inhibits the BMP4 signaling, which is involved in the cancer stem cell pathway.
How does that compare to the mRNA?
mRNA targets the genes before they get made into the protein. Neutralizing antibodies target the protein itself. I think both are valid means of targeting mechanisms of action. Neutralizing antibodies are good for targets where there's the protein on the surface of the cell, which CD105 is. By virtue of that, we can target most of these cells. The main limitation of mRNA strategies has been the ability to target all of the cancer cells. The mRNA has to actually enter the cell and be made into proteins to effect their work. The expression of the mRNA into protein has been the limitation so far, particularly in cancer, but by virtue of using an antibody that targets the protein on the surface of all these cancer cells, we believe we can target the vast majority of the cancer cells in a more efficient fashion.
It's systemic, right? The treatment is systemic in case the cells-
Yes, it's systemic and IV to get to the cancer cells.
Thank you very much.
Sure. Yes, sir.
Can I ask why you guys chose to study prostate and lung cancers specifically?
Well, our Chief Scientific Officer, Neil Bhowmick, is actually a prostate investigator, so he looked at that first, then looked at lung as another target. We have really seen this mechanism be relevant in colon cancer, breast cancer, and head and neck cancer. So we think this will be a strategy to treat many different types of cancers and many different types of drugs. The goal of the company is to target pharma companies with particular drugs that ENV-105 will work on, and to partner with them to make each individual drug work better, and that would be done in repetition with the different therapeutics that are used in different types of cancers. Our overall goal is to make cancer a chronic disease with a good quality of life. Just as when HIV first came out, patients died within weeks of getting diagnosed.
Cancer is in a very similar phase where acutely patients really die sometimes within several months or a year. What we would like to do is by using ENV-105 and making drugs work for a longer period of time and work more effectively, make cancer into a chronic disease that can be lived with for a long period of time, rather than just shuttling between different drugs and trying different strategies that all really end up toward resistance. Yes.
Patients that you're testing this on now, you talk about patients dying within months or years with the antiandrogen. What's the profile of the patients that you're testing on?
Yeah. Prostate cancer patients, these are metastatic castration-resistant patients. They are not the ones with small tumors in their prostate. Usually, they've had surgery on their prostate to take all of the prostate out, and they have metastases usually to the bone. When this happens, they're started on antiandrogen agents, and the most common one is enzalutamide which is a Pfizer drug. As the patients are treated with these drugs and become resistant, then the next line of therapy oftentimes is Pluvicto. Pluvicto has a very high toxicity rate, between 30% and 50%, depending on the trials you look at, whereas our toxicity rate is exceedingly low. We've really seen no Grade t hree or four toxicities in the patients that we've treated with lung cancer and just one Grade three toxicity in our prostate cancer trial.
The idea is that our drug is very safe and very non-toxic to patients so that it can be added to a multitude of different drugs without inducing a lot of additional toxicity. By doing so, patients can have a relatively good quality of life, and their progression-free survival can be extended significantly.
CD105 goes after cancer cells or receptors that are on the surface of cancer cells?
Yes. As a matter of fact, if you want to get into the weeds a little bit, it also targets CD105, which is made on the fibroblasts that surround the cancer cells as well, and those function to support the cancer cells. So by targeting CD105 both in the cancer cells and the microenvironment, we think we have a pathway to really inhibit the cancers as a whole. Well, thank you very much for your time.