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Greetings, and welcome to the INmune Bio Second Quarter 2022 Earnings Call. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. [Operator Instructions] As a reminder, this conference 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 Chief Financial Officer of INmune Bio. David, the floor is yours.

Thank you, Doug, and good afternoon everybody. We thank you for joining us for the call for INmune Bio’s second quarter 2022 financial results. With me on the call is Dr. RJ Tesi, CEO and Co-Founder of INmune Bio, who will provide a business update on our DN-TNF platform; and Dr. Mark Lowdell, Chief Scientific Officer and Co-Founder, who will provide an update on our NK cell priming platform. Before we begin, I remind everyone that 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 Act Reform 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 the 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 of the facts and circumstances underlying these forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligations to update these forward-looking statements to reflect future information events or circumstances. Now, I’d like to turn the call over to Dr. RJ Tesi, Co-Founder and CEO of INmune Bio. RJ?

Thank you, David, and thank you everyone for joining the call. As usual, I will arrange my remarks to highlight the key takeaways for the first quarter and subsequent period, and provide updates on our platform programs. I will review development of – developments in XPro then hand the call to Mark Lowdell, INmune Bio CSO, who will speak about recent developments in INKmune before David discusses financial results, upcoming milestones and we move to Q&A. You are all aware that we received a clinical hold letter from the FDA. The clinical hold relates to manufacturing issues. The new XPro was manufactured by KBI at their Boulder facility, a different manufacturing site than the previous XPro batches. The triple challenge of the new company manufacturing a first-in-class therapy at a new manufacturing site, all contributes to the FDA’s caution. We are working with the FDA to answer their CMC questions. We are not willing yet to give a timeline to resolving this hold. At this point, we have not changed our timelines for reporting top-line results on MCI and mild AD trials. This decision is being continuously evaluated. If the hold persists for longer than anticipated, it will affect the timing of the top-line data readout. XPro for the treatment of ADi is our flagship program. The Phase 2 program in patients with mild ADi is enrolling patients in Australia. I remind you that ADi is capital A, capital B and small is a Alzheimer’s disease caused by neuroinflammation. XPro targets neuroinflammation. We use enrichment criteria to enroll patients who have neuroinflammation driving their dementia. We believe this is one of the reasons that we learn so much from our Phase 1 trial and I have confidence in the outcomes of our Phase 2 trial. This simple strategy allows us to design smaller, shorter trials and we believe in the U.S., this still allows us to have a market target of 40% of patients with mild Alzheimer’s disease. There may be more, but we believe at least 40% will meet our enrollment criteria. We will initiate the Phase 2 MCI trial once we have resolved the clinical hold. To our knowledge, we are the only company that has separated the development of therapies, development of strategies for the treatment of mild Alzheimer’s disease and MCI. Most trials treat something they called early AD, which is an artificial construct or combination of mild Alzheimer’s disease plus MCI. We believe two trials is more informative and less risky. While on the topic of how INmune Bio’s AD programs differ from others, I remind you we’re using EMACC as the primary cognitive endpoint. EMACC early Alzheimer’s disease, MCI cognitive composite is a validated scale design to detect cognitive changes in patients with mild AD or MCI. This sensitive instrument is purpose built for these patients. We are doing this call from San Diego while attending AAIC, The Alzheimer’s Association International Conference, which is the largest Alzheimer’s disease conference in the world. The world of AD drug development is changing rapidly. INmune Bio is leading the change of innovation in Alzheimer’s disease. At this meeting, we are witnessing a drift away from targeting amyloid and tau towards other therapeutic strategies. And I’m happy to say that neuroinflammation and glial dysfunction are frequent topic. The use of biomarkers such as those used in our Phase 1 trial and deployed in our innovative Phase 2 programs are gaining acceptance and seeing broader use. There is no question that the use of biomarkers will improve our ability both at INmune Bio and by the field at large to bring novel therapies to patients with Alzheimer’s disease faster and with less risk. XPro has uses beyond the treatment of AD. We will start a Phase 2 trial in patients with the treatment – with treatment resistant depression soon after the mild AD and MCI trials are underway in the U.S. We are performing IND enabling preclinical studies in ALS. All of our CNS programs have received support in the form of non-dilutive funding from the Alzheimer’s association, The National Institute of Mental Health and the ALS Foundation respectively. The common denominator of these CNS indications is destructive neuroinflammation caused by immune dysfunction. In our opinion, neuroinflammation drives the core pathology of synaptic dysfunction and nerve cell death. That is a requirement of cognitive loss. Our successful Phase 1 program showed that XPro safely decreases neuroinflammation and improves synaptic function, decreases nerve cell death and promotes remyelination. In the patients with mild AD, we saw a positive clinical response. INmune Bio believes that the synaptic connections can be stored degenerating axons can be made healthy, and remyelinate when the patient – when the brain’s immune system is normalized and controlled by XPro. The Phase 2 studies are designed to answer these questions. The clinical hold will delay the initiation of the Phase 2 trial in XPro for treatment resistant depression. The NIMH gave us a 2.9 million grant and the trial design is consistent with our CNS drug development philosophy. We will enroll patients with peripheral biomarkers of inflammation, including elevated CRP. Use functional MRI, a neuroimaging biomarker to evaluate the activity of a pathway in the brain tied to both depression and inflammation. This is a six week double blind placebo controlled study. It is unique. The primary outcome among measures are functional connectivity measured by MRI, but we will also be measuring other biomarkers and clinical outcomes. Finally, on the preclinical front with Xpro during the second quarterly we presented preclinical data demonstrating that Xpro promotes remyelination at the junction of the white and gray matter in animals with multiple sclerosis. This work was presented at the third European conference in neuroinflammation and provides mechanistic insight into the remyelination we saw in patients in our ADI trial. Finally, INKmune, as we consider INKmune our proprietary NK killing cell priming platform, a pseudokine that binds two NK cells induces many of the same effects in NK cells as others achieve with a complex cocktail of cytokines. Based on new data, this statement understates the power of INKmune to alter NK cell function in patients with cancer. INKmune transforms resting NK cells into cancer killing memory-like NK cells in the patient. To make these cancers killing memory-like NK cells with cytokine, you need a complex cytokine triplet of IL-12, 15 and 18, these cytokines complicate both manufacturing and the care of cancer patients because of cost and off target side effects, common to many cytokine treatments. In contrast, cytokine primed NK cells. INKmune only activates NK cells is well tolerated without any primed medication and in fact can be given as an outpatient. The ML, memory-like NK cells present after INKmune treatment may be better at killing cancer cells and the TME or the tumor microenvironment of solid tumors. The increased fitness of INKmune primed NK cells is due to an upregulation of mitochondrial proteins. I remind you that mitochondria, the engines of the cell are essential for NK survival and we believe this increased fitness may be the cause of the extended therapeutic persistence in INK – of memory-like NK cells and INKmune treated patients. Mark Lowdell will provide more details on the patients in a moment, but to our knowledge, INKmune priming is the only INKmune – NK therapy reporting improved functional mitochondrial function and therapeutic persistent lasting more than a hundred days. These observations combined with the data presented on the ability to – of INKmune to prime NK cells that thrive in the conditions of the tumor microenvironment, including hypoxia has driven our strategy to pivot our development program towards solid tumors. I’ve said enough for now. I’m going to turn it over to Mark Lowdell, Chief Scientific Officer of INKmune. Mark?

Thank you, RJ. Can everyone hear me? I’m calling from remotely.

Yes, you’re fine, Mark.

Great. Thank you. Well, thank you all for joining the call. I’m – as RJ said, I’m going to update the current status of our INKmune development program. For those of you who need a refresher, our initial in-human trial of INKmune are taking place at a single center in the UK. That’s enrolling patients with initially a bone marrow disease called myelodysplastic syndrome, MDS, or more recently with a more severe disease called acute myelodysplastic or AML. And at this point, as of today, we’ve treated four patients. Each patient has received three doses of INKmune, in fact, patient four received her third dose only today and we are monitoring their response and their progression. The four patients are actually very different from their disease perspectives. The first patient is an MDS patient enrolled in the trial and responded very well, remains alive and well, more than 14 months from the day of his first treatment last year. He showed no side effects to any of the three doses that he received and he showed increased NK cell activation and generation of as RJ described memory-like NK cells after both the first, second and third doses. These memory-like NK cells remained in peripheral blood for over a hundred days after his last infusion, which we found both remarkable and very encouraging. He is a 78-year-old man at the time of the treatment and he had severe MDS. In other words, all three lineages of his blood production were impaired. He had low neutrophils, he had low red cells and he had low platelets, had a very poor quality of life, regular hospital admissions to receive blood transfusions to cope with those certain inadequacies, including platelet donations. Months after completing INKmune treatment, his disease burden has reduced somewhat, but more importantly, his quality of life has improved so dramatically that he’s returned to playing badminton with his friends. He no longer needs frequent transfusions and he doesn’t require platelet transfusions at all. And his improved clinical status is reflected in a decrease in what we call as ECOG status from two, which is severely impaired to zero, which is what you and I would score. Now, second patient actually was a young lady of 20 years old with relapsed acute myeloid leukemia, which had relapsed after an allogeneic transplant from a nonrelated donor, so a very high risk young lady. Her bone marrow was completely dysfunctional and she’d been hospitalized for six months due to inadequate blood neutrophils, which the cells would prevent bacterial sepsis. She had a single dose of 300 million INKmune followed by two doses of the trial dose of 100 million. And as with the first patient, she immediately showed a presence of memory-like NK cells after each infusion and these persisted with over 60% of the NK cells in her bone marrow at 140 days being activated memory-like NK cells. Within one month of completing her treatment, so that’s a 21 day treatment course. Within one month her neutrophil count improved significantly and sufficiently for her to be discharged home for the first time in seven months, the disease burden reduced and she went from mixed donor chimerism to full donor chimerism. But to put that in simpler terms, her donor stem cell graft initially did not fully establish itself. And after the immune therapy, it did. Her disease became controllable with routine chemotherapy and seven months after completing INKmune treatment, she remained alive and with control disease and was awaiting a suitable donor for a second transplant. Sadly, a few weeks ago, I heard from her clinician that her disease relapsed rapidly, then she died no longer responsive to chemotherapy. But what we were delighted to hear from her treating physician was that “she definitely improved post INKmune use, this gave her a good quality of life as an outpatient, something we did not achieve with chemotherapy”. And I think that really does point the aim of this drug program it’s to improve quality of life to get people home and to ultimately cure their disease.

And then two weeks ago, we treated our fourth patient, another really seriously ill young lady. And I think this is the story that you will be aware of with other early stage drug development companies you end up treating really extremely ill patients until you’ve proven the efficacy of your drug. So this is another young lady with refractory acute myeloid leukemia. She’s now received all three doses of INKmune. So the third one was today. In fact, today she received it as an outpatient, the group of having been now so convinced that that the infusions are safe. And once again, she’s shown no side effects. We’re waiting the lab test results to see if she’s responded. But she is again another patient with a high level disease burden. So, we don’t expect to see curative results, but we hope to see an improvement. So during the quarter, we received national registration by the United Kingdom National Institute for Medical Research for INKmune MDS trial. And that means that it’s promoted in the UK to National Hematological Oncologists at all UK hospitals, and allows them to submit patients to be enrolled in the trial at the single trial center, which is the University Hospital in Southampton. Additionally, we are pleased to report that the company will be expanding its INKmune MDS trial into the European Union with submission underway for two trial – the trial in two hospitals in Athens with whom we’re working very closely. The company will provide an update along with data on this patient’s response to INKmune in the future. And then future corporate INKmune platform updates. In our previous call, we announced that we were about to submit an applications to the UK medicines regulator, the MHRA to open a second trial of INKmune in ovarian cancer. This was submitted, but it’s not been acted, and was approved, but was not been acted on by the hospital due to a moratorium on opening new Phase 1 trials in cancer in the UK because of the backlog of cancer treatment plus COVID lockdown. We’re fully committed to expanding the INKmune program into solid tumors and have a trial in discussion with relevant key opinion leaders; we will provide more guidance on the solid tumor initiative once we’ve completed discussions with the FDA. I’ll now pass the call back to RJ. Thank you very much.

Thank you, Mark. Our press release earlier this week regarding upcoming events, I will be attending the BTIG conference and participating in a panel of discuss the role of targeting neuroinflammation as a precursor to Alzheimer’s disease. As an aside, I have to say that members of the company involved in the Alzheimer’s program are increasingly being queried by both the Business Press and the Lay Press about the importance of this strategy for treating the Alzheimer’s disease. So not only is it gaining traction at the scientific and medical level, it’s gaining traction at the business and public level. We’re all quite pleased about that. The BTIG meeting in New York is open to shareholders. And if any, our existing or prospective shareholders are able to attend the event we can certainly plan to meet with you there. At this point, I’ll turn it over to David Moss, our CFO and Founder to review certain financial items. David?

Great, thank you, RJ. I’ll provide a brief overview of our financial results and upcoming milestones before we head to our Q&A session. Net loss attributable to common stockholders for the quarter ended June 30, 2022 was approximately $6.8 million, compared to approximately $6.7 million for the period ended in 2021. Research and development expenses totaled $4.2 million for the quarter ended June 30, 2022 compared to approximately $4.5 million for the comparable period in 2021. General and administrative expenses was approximately $2.2 million for the quarter ended June 30, 2022 compared to $2.1 million during for the comparable period in 2021. Other expenses were approximately $0.5 million for the quarter ended June 30, 2022 compared to $ 0.1 million for the comparable period in 2021. At June 30, 2022, the company had cash and cash equivalents of approximately $61.2 million. Based in our current operating plan, we believe our cash is sufficient to fund operation through 2023. As of August 3, 2022, the company had approximately 17.9 million shares of common stock outstanding. Now, I’d like to move on and list our upcoming milestones. Although our Phase 2 Xpro trial for treatment of neuroinflammation as a cause of mild Alzheimer’s disease is currently on hold pending the FDA manufacturing review, which we are working towards a resolution as quickly as possible. We expect to continue enroll patients over the coming months with attention to Australia in order to reach our enrollment target of 201. Top-line results for the six-month program remain tentatively expected in late 2023. I’ll remind investors the more we do in Australia, it’s currently cheaper due to the strength of the U.S. dollar and the R&D rebate program available in Australia. Upon resolution of the FDA inquiry, we remain on the path to initiate a three-month 60 patient Phase 2 program for mild cognitive impairment barring any additional unexpected delays we anticipate having top-line results mid to second half of 2023. Additionally, it remains our plan to initiate Phase 2 trial of XPro in patients with treatment resistant depression that is partially funded by the $2.9 million NIH grant. Later in the calendar year, again upon resolution of the FDA manufacturing review. Additional open-label Phase 1 data INKmune in high-risk MDS/AML later this year and next as Mark had indicated. And finally, we plan to launch a second INKmune study in a solid tumor Phase 1 program with a target date sometime early 2023. So although we’ve encountered, but we believe minor impediments to advance our XPro trial we’re building momentum with our trials in Australia, and we’re pleased to progress during the – we’re pleased with our progress during the second quarter, as we continue to advance our pipeline towards evaluating creating the milestones. We thank our local shareholders as always. And we reiterate, we’re always available to speak with you should you have questions, please don’t hesitate to reach out. At this point, I’d like to thank you for your time and attention, and I’d like to turn it back to Doug to pull for questions. Doug?

Thank you. [Operator Instructions] Our first question comes from the line of Tom Shrader with BTIG. Please proceed with your question.

Good afternoon. Thanks for taking my questions. As we head into this trial, RJ, and maybe CJ, if he’s on, what do we know about the ADi group? Has anyone ever done a post-hoc analysis from a big trial, either beta – a beta antibody or acetylcholinesterase, so they going to progress faster? Are they going to progress slower? Do we know what the placebo group will look like? I’m curious what information you have going in?

Yes, thank you, Tom. And I’m – CJ’s not on the call, but I will – I’ll put on my CJ hat. I mean, one of the things that CJ has worked very hard with his statistical team is evaluating this very question. And we, he and his group took data from the ADNI group, which is a well characterized group from USC, and basically extracted the patients that had the equivalent of our biomarkers. Remember we have peripheral blood biomarkers for the most part. We knew the ones that had an elevated CRP or APOE4, and determined how they progressed compared to patients that didn’t have those biomarkers. And there were really three important findings. The first is, that they do progress more rapidly. So patients with neuroinflammation have more rapidly progressive cognitive decline in patients without neuroinflammation. Secondly, is that rapid progression occurs in a way that has less variance. And what I mean by variance is mean there’s less statistical noise around that decline. And that is what gives us the third advantage. It provides us with an ability to model the response compared to the treatment group in a way that allowed us to do both the shorter trials and the smaller trials. As you know, for the mild AD patients, it’s a six-month trial based on 200 patients in a two to one randomization. Now by the standards of Phase 2 trials and Alzheimer’s disease, that’s quite small, but it’s because of the advantage you identified that the ADI group, the hot group, the neuroinflamed group is unique in that it is a rapid progressor with low variance. And we believe that we will very quickly see a difference that allows us to demonstrate the cognitive benefits. So that is – we didn’t pick that rabbit out of the hat that was based on hard work by CJ and his statistical consultants.

And then a second question on the EMACC endpoint, there are starting to – there’s starting to be an enormous amount of work on these endpoints that will change faster or earlier they tend to stress things like episodic memory. The question is, are they all very close, is EMACC quite close? And the question is, is there any fear that you’ll all be sort of uncovering new endpoints and it’ll be hard to compare? Or is there a sense that they’re close enough that an active drug really should hit all of them that they’re stressing the same things? It’s just, whatever is known, I’d be curious, because there’s – they’re starting to be a lot of these endpoints.

Well, yes, that’s a little beyond my casual conversation. Judy Jaeger, who is our consultant on this topic is really one of the world’s leading experts in neurocognitive evaluation. And I remind you that the way EMACC was built, it took data from three large data sets. Three were in the U.S., one was in Europe, combined them and evaluated them in a way to find out which of the elements from – for all practical purposes, either ADAS-COG13 or CDR were most sensitive and predictive in patients with mild to – mild ad and MCI. Remember the problem with CDR and ADAS-COGs, is there really designed or were built for patients with mild with moderate to severe disease. And the way I like to describe it is that, if you’re going to make sushi [ph] you don’t do it with an axe. You don’t do it with a blunt instrument, you do it with a super sharp Japanese knife. And in fact, the blunt instrument of ADAS-COGs and CDR is not well designed for mild AD and MCI. So it is a purpose built story. The advantage is right now that it is validated and although no one has gotten a drug approved on it, the FDA’s well aware of it, and other groups are using it. So, the field will move away from a ADAS-COGs and CDR, whether they decide on one end point, which is, we think EMACC is the best one, or others will take some time, but EMACC is a well designed, well validated tool, ideally suited for the purpose we’re putting it to use. And we’re confident that we and other companies, when we go to the FDI, they will have a very good conversation with them.

Great. Thanks for the answers.

Our next question comes from the line of Mayank Mamtani with B. Riley. Please proceed with your question.

Hi, this is William Wood on for Mayank Mamtani today. Congratulations again on the really nice quarter there. Just a couple questions from us on our end. I’m just trying to think about, the clinical hold and maybe anything positive that we may be able to tease out of this, just thinking about, is there a way, or can you front run site enrollment or site openings within the U.S., or are you able to shift capital more towards Australian sites, et cetera, anything along those lines that might not be on hold during the hold I guess.

So, yes. Good question. Yes. So remember this is, this whole business is a little spotty. It’s U.S. based. We continue to have patients enrolling in Australia. We have announced that, we when we think of this trial, it’s a North American Australia sites trial. So that includes Canada. And as you can imagine, we are exploring other places where we might be able to open sites. So by all means we are exploring and spending a significant amount of both human, of human capital on trying to, shall we say find a solution to this problem that is independent of the timing associated with the FDA. I will say that we did have an investigator meeting at the AAIC here. And I can tell you that the enthusiasm of the clinical teams for this trial are quite high for a lot of the reasons we always talk about when we showcase the trial, it is unique in design. They like the idea that it’s a separate trial for MCI and mild AD that it’s short and that it is that, that we actually provide patients with an additional 12 months of drug whether they’re in the active or placebo arm. So the clinical teams like it, they’re excited. They too are frustrated by those in the U.S. by the clinical hold, but we are not standing still ringing our hands, waiting for the FDA. We are being as innovative as we – as you can imagine, we would be. But by the same token, where we have learned not to make predictions until we have our bird in the hand. So you can be assured, we’re working hard and as things loosen up or move forward, we will let you know.

Thanks for the extra color. And for INKmune was curious if we might be able to expect say maybe an interim data readout. I know, you were discussing the four patients during today’s call. Maybe getting a little bit farther after the third dose really is allowed to take effect or, did six dose where more like in terms of what you saw, what you presented with the first dose a much more robust data or readout ahead of the full data readout.

Mark?

Thank you. Yes. It’s somewhat difficult to answer that in a straightforward way. But the patient’s, full patient’s treated I mean one of them has been treated on the clinical trial, the other three, because of the severity of their disease, didn’t meet the inclusion criteria for the trial, and so they’ve been treated compassionately and the law in the UK about compassionate use of an investigational drug means that we don’t get to sample those patients in a formal sampling program. So, we don’t have the – we won’t have the foresight of that the full 119 days follow up against a program of sampling dates. Having said that we have endeavored to get when the patients are being treated routinely, we endeavor to get additional blood samples, but we can’t require them, because they’re not part of a formal clinical trial. We are gathering data. We’ve gathered data on the first two compassionate use cases. And we are gathering data on the most recent compassionate use case who because of her age and the nature of her disease, we expect to be able to monitor much more closely because she’ll be having more routine blood tests. So, we will report those data as they come through. We are expecting to see the same effects that we’ve seen in the other three patients that we will see activation of our NK cells or a change in their nature. And hopefully we will see the generation of memory-like NK cells, but as I said, those assays will be done as the blood samples come in.

Appreciate that. And just to sort of follow up or expand on that, you might have covered this. I know you mentioned the, you’ve now have registration throughout the EU and a site opening up, I believe in, you said it was in Greece. Do you have plans to bring INKmune to the U.S., which may also expedite trial enrollment to reach that the nine patients?

So, we have no plans to bring that the MDS trial to the U.S. not least because of the competition for that patient population in terms of other trials that are ongoing. But we do have plans to bring me to the U.S. for a different indication. I don’t know whether I’m able to comment on that. I’ll leave that to RJ to decide how far we can go in terms of informing the, rest of the shareholder base. But yes, we have ongoing discussions to bring INKmune to the U.S.

Yes. Just to reinforce what Mark says. I mean, we’ve been touting for, I think since is the NK [ph] Killer Summit, which I believe was in February of the remarkable data that Mark has shown about the advantage of INKmune-primed cells in the tumor microenvironment of solid tumors. So, we, because of a combination of frustrations and competition, quite honestly of cell therapy programs and hematologic malignancies, think that one, INKmune is ideally suited for solid tumors. Two, we’re going to pivot the program to solid tumors. And our plan is pending discussions with the FDA to actually run those trials in the U.S. because we believe the U.S. is just a little less congested with the aftermath of COVID-19. That has been a problem in the UK. So our hope is that we will have more news after we’ve kind of had our discussions with the FDA of exactly what the tumor is? How we’re going to treat it? And when those trials will begin in the U.S.?

Excellent. Understood. I really appreciate that. And congratulations again, look forward to hearing your talk tomorrow at AAIC.

Great. Thank you, William.

Our next question comes from the line of Daniel Carlson with TW Research Group. Please proceed with your question.

Hey guys, thanks for take my questions. I know you’re excited about the trial in the U.S. once in terms of the clinicians excited about enrollment. So, can you talk anything about the momentum you’re seeing in Australia? Are they seeing enrollment faster than, than you’d expect over there?

So, we’re not going to give numbers, we’re pleased with the way things are going. I will say that because of what’s going on in the U.S., we are also expanding the sites that we had initially planned to open in the U.S., who’s going to be a trial driven. I think we’ve said this before driven primarily by the U.S. with an assist from Canada and in Australia. And obviously, as I said earlier, we’re, although we ultimately think most of the patients are going to come from the U.S., I’m not – we’re not resting on our hands. We’re moving to expand activities in these other regulatory venues. And so we’re pushing, we’re pushing hard and you know, so far we’re pleased.

Okay, great. And then in terms of INKmune, I was wondering if you could just provide a little more detail about what you’re doing in terms of solid tumors, especially you mentioned some preclinical data coming?

Mark, why don’t you review some of that preclinical data?

Yes. So we’ve got a paper which has just come back for further editing which is reviewing all presenting all of our data, both in liquid tumors, in solid tumors, in vitro. And we know that INKmune primed NK cells, as RJ said I’ll regulate 37 different mitochondrial membrane transport proteins, which for those of you on the call that aren’t biochemists. And I count myself as a known by chemist. Those are the proteins, which these engines of the cell require to bring in nutrients. And we know that unlike all of the side clients, we’ve looked at INKmune alone up regulates those nutrient receptors. And that means that the mitochondria fitter. And we’ve just got these data off in the last few months, showing that INKmune treated NK cells have these highly fit mitochondria, which should mean that they’ve performed better in the tumor microenvironment. So the data we’ve got to support that is we’ve now put these cells into a model of ovarian cancer, where we do the experiments at in hypoxia, the conditions that the tumor at microenvironment sits in, where there’s such, so much lower levels of oxygen that in immune cells are impaired. And what we find is that NK cells from patients, if we isolate them from the ascitic fluid of these patients with an ovarian cancer. So from the tumor microenvironment, they perform better after INKmune-primed than even NK cells from healthy donors. So the ability of INKmune to enhance the function of, and survival of an NK cell in hypoxia is I’m telling just, it’s we just don’t see it, with any of the cytokine cocktails that we’ve used. So we do believe it’s very likely that INKmune-primed NK cells in the tumor microenvironment will have a therapeutic benefit over adoptive NK cell immunotherapies made with cytokinin domain with cytokines. So those are really, hot off the press data. They’re in the paper that we’re submitting back to this [indiscernible] translational medicine very soon. We’ve also in that paper, we we’re looking at the molecular phenotype of these cells and demonstrating that they are unique compared to cytokine stimulated cells. So yes, an awful lot of preclinical work, that we are doing, to support the program whilst waiting to, for the patient enrollment to increase.

Thanks, Mark. That’s exciting stuff. Thank you. And that segues along to my last question here, when you talk about the tumor microenvironment RJ, I’m just wondering if you can talk a little bit about INB03, you had some good data there and I’m just wondering, if that data’s being recognized by potential partners because it’s I think your intention is to use it in conjunction with Herceptin at some point.

So good question. And I think that, yes, we are quite excited about the data we have with our the ability of INB03 decreased, decreased MUC4 expression, and much of that work has been focused on HER2 positive breast cancer. And as, that world has been turned on its head in the last two months with the approval of trastuzumab deruxtecan, which is and HER2, that area is rapidly evolving. And so we are doing two things, Roxanne [indiscernible], who’s the primary scientist behind that work is working with what is it Daiichi and is actually testing to see that in HER2 is affected by MUC4 expression as MUC4 and HER2 is a ADC and it has topoisomerase inhibitors bound to it as the payload they’re quite powerful. And that we need to confirm that in fact, that with this powerful, targeted chemotherapy in HER2 positive breast care cancer, the story is confirmed. Now as always, we have a plan B, you have heard us talk about it and not seen a lot of data yet that the combination of INB03 with TKI dramatically prevents resistance and improves response in MUC4 expressing tumors. So many GI malignancies express MUC4, our TKI targeted tumors. So we have a planned alternative plans in GI, upper GI malignancies. And we’re working towards that. The bottom line we, although we’re working with Daiichi, I wouldn’t consider it any kind of partnering discussion at this point. It’s just a collaboration. But the fact is the, the tumor space is interesting. And we believe this resistance to immune to targeted therapy strategy will yield benefits, but I want to emphasize that our lead program is expo for ADi. We are pretty excited about that, and we think that at the end of the day, that’s going to at least near term drive the value of INmune Bio.

Okay. That’s well, thank you for that answer. And I’m excited about that too, and can’t wait for the FDA to push to forward. So thanks for taking my questions guys.

Thank you, Dan.

There are no further questions. I’d like to hand a call back to RJ Tesi for closing remarks.

So that this concludes the call. We appreciate your participation. We are continue to move forward. We are quite excited about both the quality of our science and the interest in our programs by both the clinical and the investor community. And we, you guys know how to get a hold of us. Don’t hesitate to call and we look forward to speaking and seeing you soon. Thank you.