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INmune Bio, Inc. (INMB) Q4 2020 Earnings Call Transcript

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INMB earnings call for the period ending December 31, 2020.

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INmune Bio, Inc. (INMB -1.08%)
Q4 2020 Earnings Call
Mar 04, 2021, 4:30 p.m. ET


  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:


Greetings, and welcome to the INmune Bio fourth-quarter 2020 earnings conference call. [Operator instructions] As a reminder, this conference call is being recorded. A transcript will follow within 24 hours of this conference call. At this time, it is my pleasure to introduce Mr.

David Moss, co-founder and CFO of INmune Bio. David, the floor is yours.

David Moss -- Co-Founder and Chief Executive Officer

Thank you, Rob, and good afternoon, everybody. We thank you for joining us for the call for INmune Bio's fourth-quarter 2020 financial results. With me on the call is Dr. RJ Tesi, CEO and co-founder of INmune Bio, who will provide a business update.

Before we begin, I remind everybody that except for forward -- except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statements disclaimer on the company's earnings press release, as well as risk factors in the company's SEC filings, including our most recent quarterly filing with the SEC. There's no assurance of any specific outcome.

Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligation to update these forward-looking statements to reflect future information events or circumstances. With the forward-looking statements behind us, now I would like to turn the call over to Dr. RJ Tesi, co-founder and CEO of INmune Bio.


RJ Tesi -- Co-Founder and Chief Financial Officer

Thank you, David, and thank you, everyone, for joining the call. I will arrange my remarks to highlight the key takeaways for the fourth quarter year to date and provide updates on our platform programs before I pass it back to David to discuss our financial results and upcoming new milestones. Then we will move to Q&A. I'll start with our DN-TNF platform, beginning with XPro59, which we are developing for Alzheimer's disease and other CNS indications, where neuroinflammation plays an important role.

The clear highlights since our last quarterly update was data we reported on January 21 from our Phase 1 trial of XPro in patients with Alzheimer's disease. INmune Bio's data-driven hypothesis is that neuroinflammation results in synaptic loss and neurodegeneration, that is nerve cell death, in patients with Alzheimer's disease. Synaptic loss and neurodegeneration is the cause of cognitive decline in these unfortunate patients. Finally, we believe the control of neuroinflammation by XPro1595 will help repair synaptic dysfunction, decrease neurodegeneration and prevent progression of cognitive decline.

Last July, we announced interim data demonstrating that XPro1595 reduced neuroinflammation by an average of 40% in the arcuate fasciculus, a white matter tract important for learning and memory in patients with Alzheimer's disease. Neuroinflammation was assessed using MRI to measure white matter free water, a validated biomarker of neuroinflammation. The small preliminary data set included six patients, three in a low- and high-dose group treated with XPro for 12 weeks As a reminder, the Phase 1 trial is a neuroinflammation trial in patients with Alzheimer's disease. At that time, based on the quality of the data, we committed to initiating a Phase 2 clinical trial in Alzheimer's disease by the end of 2021.

We remain committed to that goal. On January 21, we provided additional data from nine patients who had completed the 12-week treatment period with XPro1595. The group included the original three patients, who received weekly subcutaneous injections of 0.3 milligram per kilogram of XPro1595 and now six patients who received 1 milligram per kilogram once a week. These are the low- and high-dose groups, respectively.

We wanted to accomplish two goals with the data release in January. First, we wanted to connect the dots between white matter free water, measured by MRI, a validated but new biomarker of neuroinflammation with traditional biomarkers of neuroinflammation, namely CSF cytokines. The second goal was to determine if the downstream consequences of decreasing neuroinflammation in this small group of intensively studied patients mirrored what was seen in the extensive animal data using XPro models of neurodegeneration. To accomplish the first goal, we used the Olink platform to measure 47 inflammatory chemokines and cytokine levels in the CSF of patients -- CSF, by the way, is cerebral spinal fluid that is obtained by lumbar puncture, but to measure those levels in the CSF of patients before and after three months of XPro1595.

The cytokines all decreased significantly. For example, CCL2 -- excuse me, CCL7, a chemokine that really narrows what happens with soluble TNF, decreased by 47% after 12 weeks of XPro therapy, and you can see this in the slide. The decrease in the white matter free water and the decrease in the inflammatory chemokines and cytokines correlated closely on the next slide, and you can see that the R squared value is greater than seven -- than 0.7, which is a highly statistically significant correlation despite a small number of patients. What this means for the future is that the MRI -- using MRI to measure white matter free water, at least when looking at neuroinflammation, may be able to replace CSF and lumbar puncture.

That's what the future holds. The results presented so far have really met the primary goal of Phase 1 study. That is to demonstrate that XPro1595 decreases neuroinflammation in patients with Alzheimer's disease. We've clearly shown this now on to the second question.

The second question is what are the downstream consequences of decreasing neuroinflammation in patients with Alzheimer's disease. We used two platforms to provide insight into the consequences of the decreasing neuroinflammation. The first was Proteome Biosciences TMTcalibrator to study the changes in the CSF proteome in the Alzheimer's patients before and after 12 weeks of XPro therapy. This is a big data analysis of the CSF proteome that revealed that decreasing neuroinflammation led to a significant change in multiple Alzheimer's disease-related pathways, including the immune inflammatory response pathway, the CNS neuronal function and injury pathway and the dendritic spine morphogenesis synaptic plasticity pathway.

Notably, the analysis found an 80% decrease in neurodegeneration markers, such as neurofilament light chain and Visinin-like protein one and significant changes in Contactin-2 and Neurogranin, both proteins associated with neuroplasticity. To get a drug approved in Alzheimer's disease, you must demonstrate that the treatment decreases the rate of cognitive decline compared to placebo. This trial does not attempt to really meet those standards as a primary endpoint. It's a small open-label dose escalation trial.

But there is important information included in the data set. The data, albeit preliminary in nine patients, showed that only one patient had progression of their disease during the three-month study. Put another way, eight of nine patients were stable or had improved cognition over the three-month period. Finally, six of the patients all in the high-dose group have been enrolled in a nine-month extension study that is they basically were allowed to continue their study for their treatment for nine months after they had finished three months on study.

These patients receive safety labs, cognitive testing, MRI scans every three months. Three patients have already had a year of therapy, and two of these have been approved for a special access program by the Australian government to allow continued treatment of their Alzheimer's disease with XPro1595. We continue to study these patients, and you will hear more about them in the future. In summary, the short trial in a small number of patients clearly shows that XPro1595 quickly decreases neuroinflammation, resulting in positive changes in the CSF proteome and in MRI scans using very sophisticated measures that you will see an example of if you go back to the KOL webinar.

All of this correlates with what we've seen in animal models. We remain committed to starting a blinded, randomized, placebo-controlled Phase 2 clinical trial in the second half of the year. We have a bit more work to do before we release the precise design of the Phase 2 trial, and we continue to enroll patients in the ongoing Phase 1 trial and continue to mine the extensive data set that we have and are generating. What we have learned and are learning from these patients will prove invaluable as we design the best possible Phase 2 trial for the development of XPro1595 in Alzheimer's disease.

A second CNS trial we plan to initiate this year is in treatment-resistant depression, or TRD. In September, we announced that we were awarded a large up to a $2.9 million grant from the SBIR -- from SBIR grant from the NIH to support a Phase 2 trial of XPro1595 in patients with treatment-resistant depression. We will conduct this trial in collaboration with two of the world's pioneers in the field, Professor Andy Miller and Associate Professor Jen Felger, both at Emory University. Dr.

Miller is the pioneer in the role of neuroinflammation and depression, having described the problem in the early days of interferon therapy for cancer. Then going on to publish the first study demonstrating that targeting TNF improves depressive symptoms in patients with elevated biomarkers of inflammation. In addition, Dr. Felger discovered that the connectivity between two measures of the brain, as measured by MRI, that are vital for feelings of pleasure and motivation are lost in depressed patients with inflammation.

Our hypothesis is once again simple, XPro1595 will decrease neuroinflammation, improve clinical symptoms and restore connectivity between these vital regions of the brain, as measured by clinical criteria and by MRI. TRD, treatment-resistant depression is a neuroinflammation program that leverages a lot of what we're learning during the Phase 1 trial in Alzheimer's disease. As with the AD trial, the TRD trial, we use biomarkers of inflammation to confirm diagnosis, enroll patients and determine response to XPro therapy. The use of biomarkers is a novel approach to psychiatric drug development.

We believe the use of biomarkers will improve the efficiency of drug development in the field, and we believe we will lead that revolution. Treatment-resistant depression remains an area of significant unmet need. In the U.S., an estimated 7 million patients with major depressive disorder are resistant to current therapies, most often defined as having failed two prior lines of treatment. Current treatment strategies require treatment-resistant patients to cycle through multiple therapies and an intent to find one that works.

We hope to introduce precision into the diagnosis and treatment selection by using biomarkers to identify patients and track their progress. These two programs highlight a key advantage of the XPro1595 platform. XPro decreases neuroinflammation. Neuroinflammation is a key pathology across a number of neurodegenerative and psychiatric diseases.

A quick review of more than 60 publications on our website will give you an idea of the breadth of the opportunity for XPro1595 in CNS. Acute -- our Alzheimer's disease and treatment-resistant depression are the first, but not the last of our programs in CNS. Turning now to Quellor, our COVID-19 program for treating cytokine storm. Last quarter, we went into some detail on how the cytokine storm lands many COVID-19 patients in the hospital and why we believe targeting soluble TNF as the master cytokine is potentially more effective approach at suppressing this regulated immune response.

In November, we announced that the first patient had been enrolled in the Phase 2 trial of Quellor for the treatment of pulmonary complications of COVID-19. The double-blind, randomized, placebo-controlled trial will enroll 366 high-risk COVID-19 patients in two equal-sized cohorts. One cohort is the placebo in the standard of care cohort. The other is standard of care plus Quellor.

They'll be given a 1 milligram per kilogram subcutaneous injection and enrollment. The second dose of Quellor may be given a week later if the patient remains hospitalized. The primary study endpoint. And I'll remind you that this trial was written with the FDA.

They really dictated the design and the endpoints of the trial. Primary endpoint is the need for mechanical ventilation during the 28 days following admission to the hospital and enrollment to the study. Secondary endpoints include things like transfer to the ICU, new onset of neurologic cardiovascular, thromboembolic or renal disease and death. The first 100 patients randomized into the study will inform a go/no-go decision by the Data Safety Monitoring Board.

If the DSMB recommends the trial continue, the remaining 266 patients will be enrolled. We hope to reach that go/no-go decision by the end of second quarter. Turning now to INKmune, our NK cell priming platform. NK cells are cells of the innate immune system that play a crucial role in cancer outcomes, given their ability to target residual disease, the cause of cancer relapse.

INKmune restores the function of the patient's own NK cells to attack their residual disease. We believe that by eliminating residual disease, INKmune should improve survival in cancer patients. This year, we plan to initiate a single center Phase 1 trial in high-risk MDS patients, that's myelodysplastic syndrome, a precursor to acute myeloid leukemia that primarily affects elderly patients. This trial is set to run in the U.K.

The U.K., like the rest of the world where we would do clinical development, has had restrictions on the start-up of new clinical studies because of the strains of the pandemic on their healthcare system. We are ready to enroll patients when the NHS, the National Health Service, which is the U.K. health system, gives us the green light. We will initiate the trial that will include at least nine patients with the opportunity to expand both the number of centers and the number of patients.

Finally, we have previously announced that INB03, our oncology program, has been delayed due to COVID-19. We hope to initiate a Phase 2 trial in MUC4-positive cancer once the pandemic has been controlled. Although this program is clinically dormant, laboratory research on the combination of INB03 with tyrosine kinase inhibitors in MUC4 expressing tumors continues. Similarly, our eliminate program for NASH will not begin a Phase 2 until the pandemic is completely controlled.

We hope to have more clarity on these programs once we have reached herd immunity in the U.S. and the danger of these viral variants is understood. I will now turn it back to David Moss, INmune Bio's CFO, to discuss the financial results and upcoming announcements. David?

David Moss -- Co-Founder and Chief Executive Officer

Thank you, RJ. I'll provide a brief overview of our financial results and upcoming milestones. Net loss attributable to common stockholders for the year ended December 31, 2020, was approximately $12.1 million, compared to approximately $7.7 million for the year ended December 31, 2019. Research and development expenses totaled approximately $5.9 million for the year ended December 31, 2020, and compared with approximately $3.3 million for the year ended December 31, 2019.

The primary reason for the increase in expenses was an increase in R&D activities related to our clinical programs and costs associated with manufacturing additional drug supply. General and administrative expense was approximately $6.3 million for the year ended December 31, 2020, compared to $6 million for the year ended December 31, 2019. At December 31, 2020, the company had cash and cash equivalents of approximately $22 million with no debt. Subsequent to the end of the quarter, we raised gross proceeds of approximately $28.4 million through our at the market or ATM facility and issued 1,439,480 shares of common stock at a price of $20.17.

Based on our current operating plan, we believe our cash is sufficient to fund our operations and achieve potentially value-creating milestones into late 2022. As of March 4, 2021, the company had approximately 14.9 million shares of common stock outstanding. Now I would like to move on and list our upcoming milestones and catalysts. This current year, we plan to initiate a Phase 2 trial of XPro1595 in treatment-resistant depression that is partially funded by a $2.9 million NIH grant.

We also plan to report additional data on our Phase 1b Alzheimer's disease program prior to the Phase 2 program initiating. We also, toward the end of the year, plan to initiate a Phase 2 program for Alzheimer's disease with XPro1595 in patients with neuroinflammation. We will provide more clarity on the design of this program, including the cost of the Phase 2 trial as we get closer to this milestone. In addition, assuming the clinical landscape has not changed, we are planning trials in our other programs once the COVID-19 pandemic has been controlled and our trial sites give us the go ahead.

These include the INKmune Phase 1 program for high-risk MDS in ovarian cancer, LIVNate Phase 2 program for the treatment of NASH, INB03 Phase 2 for the treatment of MUC4-resistant metastatic HER2-positive breast cancer. So in summary, notwithstanding the pandemic, we believe we are making good progress, particularly in our neuroinflammation franchise following the compelling expanded Alzheimer's disease data that we reported in January. At this point, I would like to thank you for your time and attention, and I would like to turn it back to the operator for Q&A. Rob, could you please poll for questions.

Questions & Answers:


Thank you. [Operator instructions] Our first question comes from Tom Shrader with BTIG. Please proceed with your question.

Tom Shrader -- BTIG -- Analyst

Good afternoon. Thanks for the update. Just the Phase 1b trial, will we see more patients? Or will this be deeper analyses and patients followed for more time?

RJ Tesi -- Co-Founder and Chief Financial Officer

Yeah. Thanks, Tom. You're gonna see both. I think I've made it clear that we are exploring additional doses, and we -- so we will have more patients, and we will also -- the patients that have been studied will have longer time.

So you're gonna get both, more doses and longer time.

Tom Shrader -- BTIG -- Analyst

OK. And then, hopefully, this isn't too big a question. But for TRD, how do we think about this? Is this a subset of patients with systemic inflammation that this all patients -- and just a little bit of a sense of is there any hint as to the time course of helping these patients? And if they have TRD from inflammation, are they reversible? Or would this be a stabilization? I know that's like 80 questions.

RJ Tesi -- Co-Founder and Chief Financial Officer

So I'm gonna give you what -- the way we think about it. We clearly think that it's a subset of patients with treatment-resistant disease. If you look at the biomarkers we used, we think about a third of those TRD patients probably have biomarkers of inflammation. That's the group we're gonna focus on initially.

Remember, we do our CNS trials kind of like an oncology trial. We look for those biomarkers. It's not to say that those other patients wouldn't benefit. But at this time, we don't have any data to support that.

So in those patients that have biomarkers of inflammation, the data we have suggests you will see a response in three months, basically, probably actually shorter. But the trials are designed to last three months because that's what the initial data shows. Now I think the more interesting million dollar question is, do these patients then remain on XPro? Or does this reset them, so they now become responsible to, let's say, an SRI or something like that? We don't know the answer to that. We do know that when patients are enrolled, we don't -- we'll not be taking them off their current therapy.

So they will be ended up on double therapy or combination therapy. And then, it will be up to their clinician to decide at the end of the study, just like we do in Alzheimer's, whether we'll be keeping them on XPro as kind of a compassionate use or actually it will be stopped. But I think that's the second question that we need to answer. The first question is, our hypothesis is clear that patients with treatment-resistant disease, who have biomarkers of inflammation, will have -- will respond to therapy if you get rid of that neuroinflammation, and that's what XPro is all about.

Tom Shrader -- BTIG -- Analyst

Got it. All right. Thank you, that's very helpful.


Our next question comes from Jonathan Aschoff with ROTH Capital Partners. Please proceed with your question.

Jonathan Aschoff -- ROTH Capital Partners -- Analyst

Thank you, guys. I was wondering if you were looking at any different neuroinflammation biomarkers for TRD versus what you're doing now for AD?

RJ Tesi -- Co-Founder and Chief Financial Officer

Yeah. Thanks. Well, you know as we mentioned, there's this very special connectivity biomarker that you can see using functional MRI in the TRD patients. So that is a unique biomarker to that patient population.

We will be measuring all of our standard MRI biomarkers. As you know, we're interested in both white and gray matter markers of both inflammation and quality, such as cortical disarray measurements. We'll be measuring them also, but those are secondary exploratory endpoints. For the most part, what's driving the TRD program will be really standard clinical measures using validated clinical scales of depression and really anhedonia, but also this very unique observation using fMRI of connectivity that's associated with symptoms in these patients.

Jonathan Aschoff -- ROTH Capital Partners -- Analyst

OK, thanks. Last question is, I was wondering to what extent have you had inbound interest from investigators wanting to use your anti-TNF or indications for which you are not planning at the moment. So we have a significant effort that is at the preclinical stage. In other words, people ask us all the time, can I get the drug to study this model of neurodegeneration with that model.

We have a very extensive and carefully curated program, but then we harvest the best of the best of these data. And I can tell you there's a number of programs that you have not heard about yet that we have not announced that are very promising. For now, on the clinical front, our focus is really on the programs we've announced. We believe that the CNS franchise is -- in neuroinflammation is making progress in Alzheimer's disease.

And we think that will bring significant value creation that will then allow us to expand into some of these other really unmet needs that we have on tap.

Thank you, RJ.


Our next question comes from Swayampakula Ramakanth with H.C. Wainwright. Please proceed with your question.

Swayampakula Ramakanth -- H.C. Wainwright -- Analyst

Thank you. This is RK from H.C. Wainwright. A couple of quick questions.

On the Alzheimer's disease program, what additional data should we expect from the Phase 1b? And also, you're talking about initiating a Phase 2 program in neuroinflammation in the AD patients. What sort of time frame are you thinking of?

RJ Tesi -- Co-Founder and Chief Financial Officer

Yeah, thanks, RK. So we are -- as I've mentioned publicly, we're exploring doses in between the current cohorts of 0.3 and 1 milligram per kilogram. We see there are -- there is a dose response between those two groups as it relates to both measuring white matter free water and also looking at the CSF proteome. So I'm not convinced we have nailed the dose, so to speak.

So we're exploring that. The reason that we are spending time, even though there's no safety signal, there's no reason that we can't use the 1 milligram per kilogram per week dose. The average Alzheimer's patients survive seven years without therapy. We expect patients who have therapy to be on -- have extended survival.

So we can see that a patient will be on drug for, let's say, 10 years. And so we wanna nail the dose because that makes a difference. And as you know, once you do a registration trial, I mean, it's very hard to change the dose. So we wanna have the right dose going into Phase 2.

So that is one of the primary things you will -- information you will get midyear when we kind of do our final download on the Phase 1 trial as it relates to how we're gonna do the Phase 2. The second issue is what I call the duration issue. I mean, currently, if you look at any of the amyloid studies, both Biogen and Lilly, they're both 18-month studies. To me, 18 months in drug development -- to do an 18-month studies, minimum of two years, probably closer to three years, man, I'm getting old fast.

I don't wanna have to wait three years to do a Phase 2 study and then another three years to do a Phase 3 study. We think that with all of the sophisticated biomarker analytics that we have in place, we can shorten the trial. In other words, we don't think it has to be 18 months. I don't know whether we can cut it in half or what yet, but that is the second question we plan to answer in the next few months before we really publicize the design of the Phase 2.

So dose duration and the third thing is design, which is just kind of fine-tuning the cognitive endpoints. So we make sure we have the right one because our goal, once we launch the Phase 2 trial, is that it's gonna be a trial that hopefully not only enrolls quickly, but is short enough so we can -- maybe we can do a nine-month trial and then a registration trial in nine months. And basically, we get to the market in the same amount of time that it takes for a more traditional amyloid 18-month trial to do their registration trial, i.e., the Lilly situation. So that's what you can expect in the next few months.

As I mentioned with Tom Shrader, not only are you gonna see data on more patients, but you're gonna see the three Ds, dose, duration and design. And when we talk to you midyear, we are gonna be very explicit about those elements and be very explicit about what the Phase 2 trial looks like. We expect to treat our first patients in the fourth quarter. I don't wanna give you a date or a time or a moment yet, but we are pretty comfortable with that plan.

Swayampakula Ramakanth -- H.C. Wainwright -- Analyst

Thank you. Thank you for taking my question.


Our next question comes from Daniel Carlson with Tailwinds Research. Please proceed with your question.

Daniel Carlson -- Tailwinds Research -- Analyst

Hi, guys, thanks for taking my questions. Two questions. First off, with regards to Quellor, we know that you reduce neuroinflammation Wondering if you think this will have any impact in long COVID?

RJ Tesi -- Co-Founder and Chief Financial Officer

Well, I've been waiting for that question, Dan. Thank you. So we have been very interested since day one when the early symptoms of losing your sense of smell and taste were identified. We've been looking for a strong signal that there is a neuroinflammatory component.

Quite frankly -- and so I'm talking about -- we've been looking at this for a year. And as you know, some of the -- other than shortness of breadth, the primary symptoms of long COVID appear to be neurologic. They are brain fog. They are fatigue.

They are depression, and there's plus or minus sleep disorders. Those look like CNS symptoms. But until literally two or three weeks ago, there was not a convincing publication that neuroinflammation played a role here. And the last thing we wanted to do was launch on a quixotic clinical trial.

So we continue to watch this very closely. You can imagine we're very interested. And I think that there will be more information coming down the pike on the role of neuroinflammation. If the -- I don't even need a consensus.

If there is a building bit of data that suggests neuroinflammation plays an important role in long COVID, you can bet we're gonna have serious conversations about this because 10% -- at least 10% of patients with COVID-19 infections end up with long COVID symptoms, and they can be quite debilitating. So 10% of the millions of patients is a very big opportunity. And if it is in our inflammation, we might have the drug that should be tested in the disease. So all I can say, Dan, is you're right, but stay tuned.

No decisions have been made yet.

Daniel Carlson -- Tailwinds Research -- Analyst

OK, that's great. Thank you. Next question. Can you tell us how many patients have passed the 12-week period at this time? And importantly, in my mind, how many of them -- and I guess, the three in the lower dose are not still on a drug, but in the higher dose, how many of those are still on the drug at this point?

RJ Tesi -- Co-Founder and Chief Financial Officer

Yeah. So yeah, the lower dose are not on the drug, and that was more a -- it took us a while to get the amendment in place for the continuation trial. They wanted to be on the trial, but we didn't have the regulatory elements in place. So of the six patients in the high-dose group, everyone enrolled for the extension trial.

So all patients are eligible for nine months additional therapy, three of those patients have reached their one-year anniversary and have -- two of those three have applied for special access, so they will continue on drug. In Australia, the way -- they have a system where you can -- the physician and the patient and the company can petition the government to allow them to stay on drug. So currently, we will have two of the three that are beyond the year that have been approved for the special access program. And the third one is in the process, we just haven't had approval yet on that.

So I guess, the way to look at it is they're quite -- I mean, the patients and their physicians think the drug is working, right? Or let me put it this way, the patients and their physicians feel that they wanna stay on the drug, and we believe that's a positive sign.

Daniel Carlson -- Tailwinds Research -- Analyst

Got it. I agree. Well, I just wanna say congrats on tapping your ATM. I think it was a great job.

You guys doing a great job to keep up the good work. Thank you.


Our next question comes from Brett Conrad with Longboard Capital. Please proceed with your question.

Brett Conrad -- Longboard Capital -- Analyst

Hello yeah, thanks. Actually, one of my questions got answered by Dan's question, but I have a second one, too, on Quellor trial. And given that kind of current rate of enrollment in that, can you give us some general dates in terms of when we expect to get a data readout? And if that's positive, how long it will take to kind of complete the whole thing with the additional, I guess, 166 patients?

RJ Tesi -- Co-Founder and Chief Financial Officer

So as I said, we -- in the presentation, we expect to reach the DSMB mark for the first 100 by the end of the second quarter. And assuming we get the green light to go forward, we would expect to complete that enrollment. I think end of year, I think, is reasonable, unless the disease just disappears with the vaccinations, but that ain't gonna happen. We're not that efficient, and there's gonna be enough people, who aren't vaccinated out there to keep the disease in the news, so to speak.

So it is a -- so our first goal is to reach the go/no-go decision by the DSMB. I wanna remind everyone that this is not really a data readout. The only thing they can do is, say, stop the trial because things aren't working or continue to enroll, which would be a sign that things are probably behaving appropriately. But we are not gonna get any kind of data report that says 50 patients did this, 22 patients did that, etc.

That's just not the nature of the data readout as the trial is currently designed.

Brett Conrad -- Longboard Capital -- Analyst

Got it. Got it. OK, no, that makes sense because the double-blind, you only actually even know and tell us all over. You guys wanna even be able to look at those interim data points, sounds like.

RJ Tesi -- Co-Founder and Chief Financial Officer

No, exactly, and as you know, I wear two hats. I'm both the CEO and the chief medical officer. So I'm the medical monitor -- the company medical monitor. There are external medical monitors also.

So I see all the reports of problems with the patients. But I can't tell anything about where they've gotten the drug or not. I can guess, but this is not -- I don't do that. I've been doing it long enough, you don't make guesses.

So it's -- the FDA is adamant, and we agree that these need to be blinded placebo-controlled trials, and that's what it is. And it's frustrating as hell, but it's the right way to get the right answer.

Brett Conrad -- Longboard Capital -- Analyst

Are you, guys, seeing any changes in the FDA in terms of the urgency lately in terms of getting treatments for COVID? Do you see that changing as these diminishes? Or do you think -- yes, just kind of what's your kind of opinion? Because I know they also come and go, the FDA does in terms of their decisions and emphasis.

RJ Tesi -- Co-Founder and Chief Financial Officer

So Janet Woodcock, who I respect, is a very experienced -- the new Director of the FDA. And you can see some changes occurring in some areas. I've not had any sense of that in COVID-19, but that's a personal one company experience. But I mean, the FDA deserves a lot of credit for the way they've handled the pandemic.

And Janet Woodcock is I couldn't -- we couldn't -- I couldn't be happier to have her leaving the agency. She does what's right for patients. And if you take the approach that we do, it's all about what happens at the bedside, I'm confident that the FDA will respond appropriately when we provide them good data.

Brett Conrad -- Longboard Capital -- Analyst

Great. Thank you.


Our next question comes from Michael Irwin with Univest Securities. Please proceed with your question.

Michael Irwin -- Univest Securities -- Analyst

Hi, Michael Irwin of Univest. I have one question. It's about Alzheimer's and depression. So there's been a recent study that indicates that depression -- patients with depression are more likely to develop Alzheimer's disease by about one and a half years, and XPro is being tested for both, Alzheimer's disease and depression.

So how do you see this affecting XPro1595?

RJ Tesi -- Co-Founder and Chief Financial Officer

Yes, thank you. That's a pretty interesting question. Actually, the way I interpret that data, it shows how neuroinflammation cuts across all of these various diseases. So the neuroinflammation contributed to both depression and Alzheimer's disease, and there are some people that get both, right? Actually, there's also a lot of patients with Alzheimer's disease actually have depression as a symptom, and it's recognized as one of the symptoms.

And I believe there's even a drug approved for treatment of depression in Alzheimer's disease. So it's -- there's no question that there's an intersection. The intersection, though, is related to a common pathology that's neuroinflammation. And that's exactly what XPro1595 is targeting, neuroinflammation.

And neuroinflammation, if you get rid of neuroinflammation, the animal data suggests good things happen in the brain, and we're beginning -- our clinical data is beginning to support that when you get rid of neuroinflammation, positive things happen in the CNS.

Michael Irwin -- Univest Securities -- Analyst

All right. Thank you.


At this time, we've reached the end of the question-and-answer session. I would now like to turn the call back over to RJ for closing comments.

RJ Tesi -- Co-Founder and Chief Financial Officer

So thank you. That concludes today's call. Thank you for joining us. We look forward to our next quarterly update.

And all I can remind everyone to please get vaccinated and wear your mask, even after you're vaccinated. And we'll speak to you again in May.


[Operator signoff]

Duration: 46 minutes

Call participants:

David Moss -- Co-Founder and Chief Executive Officer

RJ Tesi -- Co-Founder and Chief Financial Officer

Tom Shrader -- BTIG -- Analyst

Jonathan Aschoff -- ROTH Capital Partners -- Analyst

Swayampakula Ramakanth -- H.C. Wainwright -- Analyst

Daniel Carlson -- Tailwinds Research -- Analyst

Brett Conrad -- Longboard Capital -- Analyst

Michael Irwin -- Univest Securities -- Analyst

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