INmune Bio Inc. (INMB) Earnings Call Transcript & Summary

Thank you, Jason. I'm RJ Tesi. I'm the CEO of INmune Bio, and we are a company, an immunology company that's harnessing the innate immune system for treating diseases. And on the next slide as a public company, you can see the safe harbor. And we have a lot of programs underway. And today, I'm going to talk about our COVID-19 program exclusively. So the drug that Gilead has, remdesivir aside, really, the only therapies we currently have for the treatment of this difficult disease are mitigation. That is, buy time for the patient's own immune system to clear the virus and get the patient better. Initially, we were all worried about the lungs. They are still a big problem, but now a month later or after the thing began, we're now worried about not having enough dialysis machines. And then the problem -- new problem that's rising its head is coagulopathy. So this is a very tricky virus. It is devious as all get out. And as a clinician, I say, okay, what's the common denominator here? What the heck is going on with these comorbidities? You have age, cardiovascular disease, hypertension, obesity, diabetes and race are all significant risk factors. And in fact, it's all about inflammation. The face of this inflammation is the cytokine storm. So targeting the cytokine storm makes a lot of sense. And we do it with our DN-TNF platform drug. We call it Quellor for this application. All patients who are admitted have a cytokine storm and the cytokine storm is a triplet of inflammatory cytokines, including soluble TNF, IL-1 and IL-6. And they come from activated immune cells, and they cause problems in the brain, in the lung, in the liver, in the gut, in the kidneys and actually in the blood vessels, endothelial activation, I think, is a very underestimated pathology with this disease. In theory, you should be able to target any of these cytokines and I'm going to argue that targeting soluble TNF is the most -- the smartest way to do it because soluble TNF is the master cytokine. You stimulate soluble TNF stimulates IL-6 and IL-1 production. As a triplet, they work as a sum of parts. But if you neutralize or eliminate the soluble TNF from the triplet, you, in fact, have an outsized effect of eliminating the pathology. And finally, only IL-1 and TNF actually activate endothelial cells, and I've already hinted that those are important. So targeting soluble TNF may be the best anti-inflammatory approach. And there are really 4 reasons to do this. First of all, the obvious, when it cools off activated immune cells, we've known that for 20 years. We've had anti-TNF therapies. But those are not the ones you want to use, and I'll explain that in a minute. A less obvious reason to target soluble TNF is everybody forgets the immune cells have to get from the blood vessel to the tissue. And it's called, actually migration of the immune cells through the sub vessel wall to the tissues where they do their damage. Soluble TNF actually, by activating endothelial cell, up-regulates 2 proteins called the ICAM and VCAM. They're kind of like the traffic cop that is telling the immune cells, exit here, and they cause their damage. A more obscure reason to target soluble TNF is because it actually causes the up-regulation of tissue factor on endothelial cells. Tissue factor is the trigger for the coagulopathy that is becoming an increasingly recognized problem with this disease. And the final reason is Quellor or the DN-TNF platform is not immunosuppressive. It is nuts to take someone who is immunosuppressed or who has a life threatening viral disease and immunosuppress them. I have first-hand experience in this. I was a transplant surgeon in my previous life, and we spent a lot of time dealing with immunosuppressed patients with viral infection. And the last thing you want to do with an immunosuppressed with a patient with a viral infection is immunosuppress them more. The WHO realizes this. They've recommended against the use of corticosteroids. Corticosteroids are great anti-inflammatory drugs, but they are also immunosuppressive. The -- one of the IL-6 inhibitors has failed in clinical trials. We don't know why, but I will point out that IL-6 inhibitors are both immunosuppressive and they do not target endothelial cells. Quellor is a very potent anti-inflammatory without immunosuppression in models of bacterial infection, listeria, beta strep and tuberculosis. It actually improves the immune response and models of the parasitic infection malaria. It improves the immune response. And we worked with NIAID last year working on EEE, Eastern Equine Encephalitis virus and coxsackie B3 in animal models, and we do not affect the immune response in those. We don't make it better, we don't make it worse. So it's a safe drug to use in the setting of COVID-19. So in conclusion, we believe that our DM-TNF program is ideal, the pathophysiology of the symptomatic disease that is, is an inflammatory disease. We are not an antiviral, we are targeting the inflammatory complications of the disease. We believe targeting soluble TNF makes the most sense, and Quellor is the best drug for this because it is not immunosuppressive. Thanks.