In a phase two trial, a randomized trial at three centers, and this is supported by an NIH grant, a $3.2 million NIH grant to our CSO, Neil Bhowmick, to look at a biomarker that he developed for patients with prostate cancer. ENV-105 is also in a phase one trial at Cedars-Sinai Medical Center in non-small cell lung cancer. This is fully funded with non-dilutive donor funding. We have Kairos- 201, which is cleared for an IND for glioblastoma. It's an activated T-cell therapy that targets cancer stem cells in the tumor. We have a strategic relationship with Cedars-Sinai Medical Center from where the therapy was from, and this drives clinical trial efficiency in that we're investigators at Cedars and it allows us to do the trials for a fifth of the cost, and Cedars-Sinai is the largest cancer center west of the Mississippi, allows us to enroll patients rapidly.
It streamlines therapeutic innovations because the investigators are there with the clinicians. Our drugs reverse cancer drug resistance, and they're very de-risked by extensive safety studies in over 600 patients that demonstrated the safety profile of the drug. A biomarker was identified that identifies the most responsive patients to our drug, de-risking a phase three trial and success from that. We have an extensive pipeline of drugs to reverse immune suppression. Our IP portfolio goes through 2040. Our target technologies are in large markets of cancer, an $11.3 billion anti-androgen therapy market, a $14 billion lung cancer market for EGFR-dependent lung cancers, and a $118 billion immunotherapy market. This shows where we are with our portfolio of drugs. Again, a randomized phase two trial in prostate cancer for patients that have become resistant to enzalutamide, abiraterone, or apalutamide.
A non-small cell trial where patients have become resistant to Tagrisso, a glioblastoma trial and IND that's been passed. And then we are developing our agents for INDs. Kairos- 101 is a GITR ligand targeting small molecule that induces T-cell growth and Treg inhibition, allowing T-cells to grow rapidly and kill cancer cells. So the problem in cancers is that they become resistant to the drugs that are used to treat them. Kairos discovered a central mechanism of this resistance. And as patients are treated with our cancer drugs, they start making a molecule on the cell surface called CD105, which makes them resistant to the drug. Our solution is that we've developed an antibody that targets this cell surface protein and allows the cancer to be sensitive to these drugs again, whether they're anti-androgen drugs like enzalutamide, Abiraterone, and apalutamide, or anti-EGFR therapies like Tagrisso, Tarceva, and Iressa.
The important aspect of this central mechanism of resistance is that it appears to be relevant for all the cancer types that we've tested in breast cancer, colon cancer, and head and neck cancers, in addition to prostate cancer and lung cancer. This figure on the left shows a patient treated with enzalutamide and the tumor becoming resistant to the drug with the purple tumor cells densely cellular. After we add INV-105 to the enzalutamide, making the tumor sensitive again to enzalutamide. The important aspect of this is that pharmaceutical companies need to address the resistance that develops to their drugs. We did a previous phase two trial where patients had failed at least two anti-androgen agents, and they were on either Abiraterone or enzalutamide and had failed those drugs with the tumor recurring at that point.
At that point, we add on INV-105, and we found that 62% of those patients had a clinical benefit rate or responded to INV-105 with a radiographic response or PSA response when 0% of those patients were expected to have a response if they were continued to be treated with Abiraterone or enzalutamide when the tumor had recurred in that setting. We also found no grade three or four toxicities, and INV-105 appeared to be extremely safe. In this trial, we identified a biomarker through a three-gene PCR assay, distinguishing those patients that responded to INV-105 versus not. And this biomarker was sensitive with a P value of 0.0053. The biomarker allows an eventual phase three trial to increase in its success from 55% without a biomarker to 76% with a biomarker. We recently received a $3.2 million grant to our CSO, Neil Bhowmick, supporting a biomarker confirmation.
Tagrisso is a drug that works really well in these patients. I've seen patients with up to 50 brain tumors, and their tumors completely disappear on this drug, but unfortunately, patients become resistant within a year or two, and that's when we would treat them with INV-105. In this phase one trial in lung cancer patients, we have two arms. One arm is patients that have become resistant to Tagrisso, and the other is patients that are incomplete with Tagrisso with persistent circulating tumor DNA. The idea is to see the effective dose of INV-105 in these patients and whether they respond to it with Tagrisso. The immunotherapy market has been a boon in the last 10 years with CAR T-cells and checkpoint inhibition, and it's turned into a $115 billion market. However, only 17% of patients respond to these therapies.
That's the central problem here is that cancer is comprised of billions of cells, whereas our immune system can only mount a response with up to several tens of millions of T-cells. One of the solutions that we've developed to this problem is Kairos 101, which is a GITR ligand target, a small molecule that targets this ligand, allows it to trimerize and target a receptor, enabling the rapid growth of T-cells, of effector cells, and inhibition of Treg suppressor cells, allowing the balance of T-cells to kill tumors and allow T-cells to kill these cancer cells more effectively. Kairos 201 generates T-cells outside of the body and expands those T-cells with Kairos 101, reimplants them to allow them to kill cancer stem cells in glioblastoma.
Kairos- 401 converts pro-tumor macrophages with the inhibition of IL-13 and IL-4 receptors and turns them into cancer-killing macrophages within the tumor itself. So Kairos- 101 increases T-cells, and this could complement other checkpoint inhibition like pembrolizumab and nivolumab. Kairos- 102 uses the same mechanism but in reverse and decreases the number of T-cells. And this should be a dramatic improvement in the treatment of autoimmune diseases where a sledgehammer approach of knocking down the entire immune responses is used, whereas we can surgically pinpoint T-cells in this disorder. So Ramachandran Murali, our VP of Research and Development, identified the crystal structure of the GITR ligand in two papers in PNAS and developed this small molecule that stabilizes the GITR ligand, allowing it to target T-cells and expand them rapidly. And it should work better than the AstraZeneca and Merck molecules, which are antibodies which have significant toxicities.
Our drug works physiologically in these T-cells and allows them to expand rapidly without the off-target effects. Same with Kairos 102, which prevents the trimerization of the GITR ligand and then decreases the number of T-cells and increases Tregs to diminish T-cells that are autoreactive against Crohn's disease, multiple sclerosis, and rheumatoid arthritis. On our website, we show the mechanisms of each of our molecules and how they meet unmet medical needs. Again, this is a large market that we're targeting: $11.3 billion prostate cancer anti-androgen market, $14 billion market in EGFR therapies. Tagrisso itself was a $5.8 billion drug in 2023, and our drugs allow these drugs to work when they no longer do. The immuno-oncology market is a vast area as well, and we're targeting each of these subsets of this market.
We've really brought our company through non-dilutive NIH funding of $25 million in funding till now, as well as biotech grants. And we just did an IPO five weeks ago onto the NYSE American with a small $6.2 million IPO. We have a small $1.6 million share float and significant areas of inflection in the near future, including a safety data readout for both trials in the next couple of months, an interim data readout as well in early 2025 with a presentation at ASCO GU in February, and efficacy data over the next year in both the phase one and phase two trials. The IP is well protected from the materials as well as the methods of use. We have a small team of investigators that form this company.
Ramachandran Murali is a structural biologist who identified the crystal structure of these proteins and the small molecules that can target it. Neil Bhowmick here is our CSO who developed the mechanisms of resistance of cancer and the targets with antibodies. I'm a clinician, a neurosurgeon, and an immunologist and did the translational research to bring these to clinical trial. We're a small team, but people ask us how we can compete with large companies with hundreds of scientists. Really, the answer is that we're not competing with these large companies. We're actually complementing their drugs and allowing them to work more effectively and for a longer period of time. We feel that will be a value add rather than a detraction or a competitive situation.
Our independent directors are well-heeled in biotech and large pharma and will help in our partnering discussions, which we anticipate with our inflection points over the next year. So in summary, we're a clinical stage company with an antibody that targets a central mechanism of cancer drug resistance. We have an extensive pipeline targeting immune suppression. We're enrolling in phase one and two trials with interim efficacy data in 2025. We have a strategic relationship with Cedars-Sinai Medical Center allowing us to do these trials in a cost-efficient manner and effectively. And so we're a small company with technology that can impact large pharma therapeutics in widespread cancers. So thank you for your attention, and I'm happy to take any questions. Yes, sir.
You mentioned you did an IPO for $6.2 million. What's your cash on hand? What's your burn rate? How long do you think that's going to get you?
Yeah. So we haven't had our quarterly results for the cash on hand, but the $6.2 million netted about $5 million. Our burn rate is approximately $120,000 per month. And so we have the capacity to go out about a year and a half or so. Those were my questions too. Yeah. Okay. Yes.
Are there any competitors in the small pharma space?
Yeah. So the question is, are there any competitors in the small pharma space? We don't think there is. We don't think there are people that are, to our knowledge, attacking the mechanisms of cancer drug resistance as we are. It happened by happenstance that Neil Bhowmick was studying this molecule for other reasons and identified this mechanism of drug resistance. So it's a novel way of targeting drug resistance.
In the past, when drugs have become resistant, people have added on other drugs either to develop synergy or other drugs to work on another mechanism of a weakness of a cancer. But we're really targeting the central mechanism of resistance, which is a novel way of thinking about it. Yes, sir. Now, have you talked to or obtained any deals with the major drug makers that make the drugs that you're going to have? Yeah. So we have talked to them, and they are very interested in the results of our trials. As you know, large pharma wants basically a done deal or a completely de-risk asset. But we plan to demonstrate that with a randomized phase two trial, and furthermore, with the combination of your product with their drug, does that give them an additional patent time? Does that reproject their patents? Yeah.
The question was, will our drug, given impacting the length of efficacy of their drug, will that impact their patent? It shouldn't impact their patent, but we have a patent that protects our drug, and it's a mechanism of use, which is to make other drugs more effective for a longer period of time. And we think that'll add a lot of value to the pharmaceutical industry. Yes, sir.
How long do you think the target time of the phase 2 trial is?
I'm sorry?
How long do you think the completion time of the phase 2 trial is?
Yeah. We think the phase 2 trial will approximately take two years to complete, and the phase 1 trial will take approximately a year and a half. There are interim efficacy points throughout that are designed within the trial that we hope to report along the way.
Yes, sir.
So based on that answer, you're going to have to do a raise, or you're going to need to get some more capital injection probably midway through your? Well, so we'll look for opportunistic points for raising additional cash. As you can imagine, our burn is relatively small given the non-dilutive funding that we have for our trials. And so I don't think we'll be pressed to do a raise, but we'll certainly look out for moments where this would be advantageous for us. Well, if there are no more questions, I thank you very much for your attention.