TRANSCRIPT
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Rakesh Dixit:
My name is Rakesh Dixit, and I would like to welcome you all to the Chain Protein Engineering Podcast. And today's episode is very meaningful to me. And because I get to introduce someone who had a significant impact on my own career, my previous boss, Dr. Bahija Julal. She has been my mentor for nearly 20 years. So this is a really great privilege to me. So very quickly about Bahija, I will let her talk about her career and what inspired her to get into RD. But currently she's the CEO of Immunocore, a biologic company, rising biologist company, I will say. And before that, until 2019, she was president of MedImmune, a company of AstraZeneca, where she led development and approval of a large number of biologics. And also about some leadership and leadership principle about putting people first. So now I am excited to flip the script and ask her to share her story with all of you. So let's just jump in, Bahija. So welcome to the podcast. And what I would suggest that maybe you can introduce very quickly about yourself before we go to the questions.
Bahija Jallal:
And uh the pleasure was mutual to work with you and uh uh your role in everything uh in drug development in general and all the the medicines that are on the market. So I really appreciate uh your kindness here. Uh yeah, um as you said, I'm uh right now a CEO of uh Immunocore, I'm a UK US based uh company and in the TCR field, and we can talk a little bit more about that.
Rakesh Dixit:
Yeah, so so let me get uh get on to it. Um so Bahija, what first inspired you to uh pursue a career in science and then also then following biopharmacy RD? And you have more than 30 years of journey in this field, and including your current company. So it'll be good to hear that story uh uh from your humble beginning, where you grew up, uh, and then to France and Germany, and then United States, and then achieving almost everything that you wanted to achieve. Yeah, almost.
Bahija Jallal:
Yeah, no, thank you for that question, and it's actually has a lot of meaning for me this week. It started, you know, I just was really one of this annoying uh child that kept on always asking the question why, why? I needed to understand. But I think the origin of really um wanting to to to be in science and seeing that science really satisfied a lot of of things that I was longing for started with a little bit of a tragedy, if you will. My father died when I was nine years old, and it was um with the uh a medical error. And I say this this week is very meaningful because on Monday it was you know 55 years that he died at that time. So um, you know, it turned that into wanting to understand why, you know, and science really provides that because you don't understand everything, but you have the opportunity and the privilege of going and actually, you know, me making meaningful um or meanings out of this these questions. And um and you never stop because science, you never say I arrived. You still you constantly um learn. So that that longing for learning is really what got me into science.
Bahija Jallal:
So that's the science in general, and I think you know, the um, you know, from that I as as we we talked about, I did my PhD in Paris, went to um uh Germany because uh wanted to do the postdoc, and and there I was lucky again, just really learning how signal transduction and what's happening inside the cell. And then it's in California that I fell in love with the drug discovery, if you will, because and it's a cliche a little bit, is hearing a patient coming to say thank you to scientists for um that she participated in phase one. And I remember vividly that moment, you know, coming out from that uh, you know, that that center and thinking, it's amazing, this is exactly what I want to do. And I never turned back and I never had any regrets because I felt like taking the science that we do and making it even more meaningful for patients. And that is, I feel it's not a job, it's a real privilege.
Rakesh Dixit:
Great, fantastic. Um, tell me something about your journey from California to Maryland to the MedImmune, where you both almost joined at the same time. I was your first hire. And uh your experience at your MedImmune AstraZeneca as well as uh currently at the next uh at the Immunocore.
Bahija Jallal:
Yeah, so um I was I actually I I when I look at my career, I feel like I was so lucky because I was always at the right uh uh right place at the right time. So in in California, I was working the the first time on targeted therapy, and that was a really novel, you know. Uh Suzanne uh with um uh Jossi Schlessinger and Ulrich, who are you know the fathers of the whole kinases, I had to the privilege of learning there what targeted therapy and small molecules. And then when I was recruited to come to Maryland with uh by MedImmune, it was also the first, you know, the the first the era of monoclonal antibodies and biologics. And so that was the absolute uh luck and and privilege to be in a new area that made a huge difference in cancer again. Um and like you said, I was um the first thing I had to do is to put some order into the uh the talks and and PK group, and and that was uh I was uh privilege of hiring you. You were my first hire, uh, and and the right hire, I would, I would say. Um we we had a lot of um uh we did a lot of great things together.
Bahija Jallal:
So MedImmune was was uh uh really wonderful. We had in the biologic space five therapeutic areas, and we had, if you remember, a goal, uh a vision, a strategy to to bring um one BLA from out of nothing, the you know um the pipeline was empty, as if you remember. We together we killed multiple, almost every every project in uh in oncology and started over again. And we promised AstraZeneca to bring a BLA by 2016. We actually did it in 2015, um, and then you know, multiple, multiple medicines in different therapeutic areas that are on the market today. So we're very proud. Uh we had the fantastic team, you know, there's nothing you can do without a fantastic team. We had a lot of um a lot of fun, I would say, science-based and and and a lot of medicines uh to patients. And I think after achieving that that vision, it was time again to to get into um um another um challenge, if you will. And and again, I was I would say I was really lucky here because when Immunocore recruited me, um I saw something in the data that they had. Uh it was a new modality, again, uh the T cell engager, a new modality in cancer. And it's really seeing something that was that could be that had the potential to be transformative. That's how I I went into Immunocore. And yeah, the rest we can we can talk about it, but uh uh yeah, it was quite it was quite an experience, I have to say. But uh was uh it's it's great, and I'm still living it today.
Rakesh Dixit:
Yeah, so that that's fantastic. Um so from your career, what you will say that that you had the most rewarding project? I mean, it's very difficult because all projects are rewarding, but if you have to, if you have to put your finger and saying, aha, this was the most rewarding project to me because it is helping so many patients, uh, or something like that, or or or something where you thought that you made a meaningful difference. Yeah.
Bahija Jallal:
Yeah, I think the you know, look, I I can't, I was I really had the privilege of of you know, together with with my team, always to bring some meaningful, you know, medicines to patients that made you know huge difference. But I have I have to say it's it has to be what I'm doing right now, which is the T T cell receptor. It's it's uh um it there are two contexts here why this is important. You know, from the scientific context, this is novel. This is a new modality. You know, again, I I was lucky to be associated with the new modality here. Um, you know, using the T cell receptor uh to really um uh attract uh, if you will, the T cells to kill the tumors and things like that. But what was really uh amazing is, and that's how I made the jump to to Immunocore, is when I saw the first scans, that it had um an impact in the liver, which we know uh uh checkpoints inhibitors and and others don't work, you know, when um the liver is is touched. So that told me we have something really transformative. We know that checkpoints inhibitors made a huge difference in the treatment of cancer, and yet, you know, they work a lot better in what we call the hot tumors. And you know, I always wondered, you know, but how can we get these T cells into the tumor? And it seemed with this technology you can actually really get even the cold tumors to be hot again, if you will, and attract this those T cells. So that's from the scientific context that we I thought we had something different than what existed already.
Bahija Jallal:
But when you look at the actual, you know, uh patients we are helping, these are patients who have uh what we call the UV melanoma. So it's a tumor behind the eye. And at least 50% of these patients, once diagnosed and the first tumor is is gone, 50% of them will develop metastasis. And then after that, um once they develop metastasis, the the um prognostic was basically they live for one year a maximum, right? Nothing was working. Checkpoints inhibitors don't work, um the uh um uh chemotherapy doesn't work. So basically, when we talk to patients, we talk to them before I even start here to to PIs, there was nothing for 40 years for these patients until you know we get the product that we have now, KimTrack, in HLA2 positive, helping these patients. And and it's a real privilege um to be talking to patients who are alive today with six years, seven years later. So it it definitely making uh a huge difference, and I'm feel privileged to be part of that.
Rakesh Dixit:
Fantastic. And I think there are more to come from Immunocore, I'm pretty sure. Uh, because the technology is, in my opinion, very novel and it has a lot of potential. Um, so from from the from that experience at Immunocore, what would you say from your experience? From what what you what is the most critical project at your other roles in MedImmune, where you where you were the president of MedImmune, because we developed, we got several antibody drugs approved. Uh and I still remember the Darula map. Uh, what you would say about that molecule, uh uh, or or anything else you want to discuss from that that pipeline. Yeah.
Bahija Jallal:
Yeah, it's it's really hard to say because, you know, you know, we uh I I think where I loved about that uh era is the cutting-edge science and also taking taking um uh risks, if you will, and doing things that are completely novel. So if you think about Benuralismab and the IL-5 receptor, so that was a real, you know, uh again following the science, you know, and we're not being afraid to take risks. But if you put the science first, we had IL-5 had not succeeded in uh in trials, and we went after the IL-5 receptor. And then look today is a multi-billion dollar um um drug, I think. Uh, you know, we did the same thing for um the for lupus. Right, right. You remember how devastating lupus as uh as a disease. Um, you know, I am I'm very proud to see the CD19 making it in animal, right?
Rakesh Dixit:
So those are all molecules, it's almost like your kids, they're molecules you follow because they came from that pipeline and um, you know, and you still yeah, you're absolutely right, because I still remember that there were a lot of skeptical folks back at MEDI and AstraZeneca that whether or not any of these things will actually get to the final stage, and we made them made it happen. Uh, I still remember the ruler web was almost killed at one time because it was not that active in animal studies, but it did it did so well. And same thing with L5 receptors, you said interference, you know, uh uh receptor therapies, uh enormous, where people did not, even the CD19. I mean, remember the one where there was the very first, yeah, very first AP-cartilated molecule, and it did okay in the in the cancers, but in non-cancer diseases, making uh doing miracles actually, unbelievable. So that's what the beauty of the science is. So continuing on that theme, Bahija, so how do you balance the scientific excitement uh with the, of course, as a scientist, we also have ethical responsibility for developing the drugs that could save people or in some cases could harm as well, because it's a balance between these two. Uh, how do you how do we balance those? Because of course I'm going to ask questions because my training is in toxicology, so I have to ask that question: how do we manage both safety and efficacy and and and make sure that we we do the right thing for patients? Yeah.
Bahija Jallal:
Well, I I learned that uh you know, having your head of safety, an excellent head of safety is always really important, right? Uh Rakesh? Yeah, absolutely.
Rakesh Dixit:
Yeah.
Bahija Jallal:
You know, I think it comes into the decision making is knowing, you know, what you stand for. We are here for patients. We have to make decisions that are always, I always say when you hear me here in the company and you heard me in in MedImmune, is always the patients, the science, and profit will follow. And it's never, you never reverse that. You have to do, you have to make to make the decisions that are that you know it's it's gonna be important for patients. So uh we absolutely, absolutely put safety at the top. You know, if there is any any any doubt, um, you know, we we don't experiment on people. If we have any doubt, if we don't have strong belief, we don't go to the clinic. But if we go to the clinic, as you know, I am a very, very big um um uh advocate for translational medicine, because if you go to phase one, uh you should be able to do everything to say if you have a go-no-go decision, basically, and and you know, if the drug is not doing what it's supposed to do, and if we if we see any toxicity or an acceptable toxicity and so on, we should not continue. We should not expose more people to to that. So I think you have to put the right, you know, the right people, the right um, you know, decision making in a company and follow the science and put absolutely patient spurs.
Rakesh Dixit:
Absolutely. No, that's that's great advice. Um, so I know that how you're going to answer this next question, but I'm going to ask you anyway. Uh, if we had to bet on a one therapeutic modality for the next 10 years, let's just say that, what it would be.
Bahija Jallal:
Well, it has to be uh T-cell occasions, of course. I know that you're and I and I really believe it, otherwise I would not have come here. Okay, I believe it because we have, as you know, if you look at the drug development right now, um, even with other modalities, we're going after the same the same targets again and again, right? Is the HER2s, is the this and that. Yeah, we're predicting for, yeah. You know, it's limited, right? So these with T cell engagers, we have the possibility to access 90% of the proteome. You know, we're not there yet, I think. You know, but that's really the promise is we can open up more possibilities for target. What I'm also excited about is that, and we're testing it, so we'll see. Uh it is, I I call it high risk by high reward, is we're testing the platform in infectious disease and in autoimmune. And it's all, you know, not incremental. We want something transformational. So we're going into H5B to look at can we have a functional cure?
Bahija Jallal:
And the the the uh value proposition in autoimmune is you know, can we downmodulate the immune system very much organ-specific, right? Because now we have these targets that we can target with the TCR and that are very much specific for uh an organ. So for instance, we're starting with type 1 diabetes, we have pre-pro insulin that will bind to the T cell receptor, and then we have PD1 agonist there. If that works, right? So, and we are testing that in the clinic, that opens up a huge opportunity in autoimmune, in infectious disease, and of course in in oncology. So I have I am biased, but I I have I really believe that by validating that in the clinic and in the market with our first product, we're just scratching the surface.
Rakesh Dixit:
And I I totally agree with you because what I am seeing also, like you, that the the targets that we are pursuing in cancer or even autoimmune diseases, these are the same targets we have been pursuing for the last 25-30 years. Exactly. Didn't we look at something versus just getting on the bandwagon targets? And you know, I because I do a lot of consulting in now in the ADC field, there's a lot of old targets uh with some new linkers and things like this. And I said, how many CD19s you want? How many C D20, how many PD1s? Okay, come on, they got to something more than that, you know. Exactly. That's not innovation, just uh maybe step improvement here and there. But you know, so what you said that is is highly meaningful uh in terms of uh therapeutic modality, that we need to work on modalities where there is still a lot of people are pretty skeptical that how well these things are going to work in autoimmune and infectious disease, and not to mention the safety risk, you know, because once you activate T cells, they bring their own things, you know. And and and and related to bicep, biospecific T cell engagers, uh, which we also worked very early in our career at medicine. Exactly. Yeah. So the compared to biospecific T cell engager therapies and your TCR therapies, could you could you give me potential advantage over you know the traditional bispecific T cell engager versus versus the TCR therapy, but that you have to there really is.
Bahija Jallal:
I think the the you know the TCR biospecific gives you the opportunity to to have access to 90% of the proteome. Like I said, every protein will go through the proteosome and get degraded, right? And then you have eight to ten amino acids, um, you know, peptides, which one makes it to the surface is not is not yet something that you can predict. However, we do the hard work with the with the best pack. And then, you know, having them access, having the TCR uh binding to the uh HLA, you know, presented peptide, it opens up the the whole proteome, which I think is is really um uh is really amazing. So and then the other advantage is that we can actually kill a cell with five to ten copies. You compare to monoclonal antibodies, you need at least a thousand uh you know molecules on the surface.
Bahija Jallal:
So we can go very, very we we increase the affinity because TCR is is low affinity, we increase it a million times while keeping the specificity. And that's exactly why we went after the HIV, because the reservoir, you know, for these patients that are very well controlled with the antiretroviral, but the reservoir, the x no one has or you're reliably uh um uh be able to actually hit that reservoir. But because we can go with the sensitivity so low, you know, five to ten copies, at least the first experiments we've done in the clinic as um uh multiple ascending dose, we can show reliably that we hit we hit that. So that's one, these are two two things that really distinguish the TCR by specific from antibody by specific.
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Rakesh Dixit:
And there's another thing to just continue on that theme that is still uh the patient selection, finding the right patient that you advocated once since I started working for you uh in 2006, finding the right patients. You may have the best drug if you have a wrong patients and not reasonable biomarkers, then it doesn't matter how great the drug is because you're going after the right wrong patients. How do you uh what are what is your current thinking on finding the right patients uh for the therapies?
Bahija Jallal:
Well, I think, you know, so I I completely agree with you. And I think, you know, first of all, I again we owe it to patients, right? That that we we test what we test in in the right uh patient population. And I think this is the whole work that needs to be done preclinically before even going into the clinic and identifying where it's more likely to work. And and you know, if we think about where the whole field has gone, we've gone into targeted therapy, into, you know, um, I call it now what we do is is really targeted immunotherapy, uh, if you will. It's the same thing. If we don't have the expression of the target, we're not going to that indication. Or if we know, you know, now we have still a lot to learn in the TCR and how, you know, is it the expression? Is it what is it? Is there a threshold of expression? Is it something else? So we're still it's still a lot of learning, but at least the we know it has to be that the target is is expressed, that you don't go to other places where it's not expressed. And then now it's the real work, you know, is there a threshold? Is it some other thing? So we're just at the at the beginning of understanding that from the clinic.
Rakesh Dixit:
Do you think that someday a drug could be approved just based on biomarkers, which correlate well with overall you know, benefit to patients in terms of survival benefits or you know, uh, you know, disease progressions, so you know, shortened disease progression?
Bahija Jallal:
Yeah, I think they I think everything is possible, I would say, if it's backed up by science, right? I think you know, we like to say the FDA and so on, but they're all scientists as well, and you have to bring evidence, right? So in this case, for instance, for us, uh, there was something really remarkable. It's very different. Um, we are still actively looking to understand how it works, if you will. If you think about ChemTrack, and again, we took a huge risk, but by listening to investigators and to patients. So the why we took a risk because the ORR was very low, was 5% to 7%. You know, that's the the um by resist criteria, you would have actually said, well, it doesn't work. However, what we heard from from um investigators before I even took the job, basically they said, look, we have patients, they should not be alive today who are alive. You know, they're the maybe this the tumor didn't really shrink. However, they feel very, very well and they go on about their about their business and they're alive. So when we did the trial, we had um it has a ratio of 0.56, which is amazing in oncology, as you know. And basically, the ORR completely underestimated the OS. And so we had to go with all this data, obviously, to to the FDA, and you know, the overall survival is the gold standard.
Rakesh Dixit:
Absolutely.
Bahija Jallal:
But how do you you do all that? And you know, so you'll have to look at DCR like disease control and and so on. And we're we're there is a lot of great science going on right now to understand and to see how we can boost that ORR and so on, and and really understand that mechanism very well.
Rakesh Dixit:
So, why do you think for ChemTrack you got a better overall survival, which is very different from other therapies I have seen, where you know, our objective response rate to resist is a lot more important to give you more sustained response, the durability of responses, versus with your therapy, although you had a lower objective response rate, but much better survival, which is kind of unique for uh for the immunotherapy.
Bahija Jallal:
It is unique and it's not super surprising either, right? So if you look at just the you know, at the ORR and the resist criteria were really done for chemotherapy, that's how it started, right? So you you bring the volume of the of the the stuff. When you think about um, you know, the mechanism, this is attracting any T cell in the body, right? And it does that in a in a very remarkable way. So when we did the phase one, you see a huge influx of of T cells, actually, after once you you give Chemtrack, it's a huge influx of of the T cells into the tumor. So, you know, I believe that this is more sometimes a pseudoprogression. We don't have all the facts, right? So we can't, we have not done a study to just look at what's happening with these tumors because some of these patients um they want we have anecdotal um you know evidence where a tumor is there for two years, the patient is doing just fine, and the investigator said, okay, you know what, I'm gonna take it out because it's just sitting there. And when they look at we looked at some of these tumors, not again, not in a in a very systemic, systematic way, and what you see is necrosis. Now, I don't understand why you have a necrotic tumor that the volume doesn't change and it's almost like encapsulated, right?
Bahija Jallal:
We had also examples of tumors the same way, again, encapsulated, it's almost like a bacterial thing, you know. Um, and inside there were only macrophages, no tumor cells. You know, so we still have a lot to learn there. I but I do believe that that rush of T cells into the tumor is what um give sometimes this misleading that you're not having an an impact. But we see it differently. We see it, you know, we see along, really um, you know, even in phase one, you see a disease stabilization. So the way the the last point, the way we we characterize it here is you know how in phase one, when uh patients um uh basically, you know, so they they progress, you see these things going like an open umbrella. What we see is a closed umbrella, you know, so it's patients that maybe didn't Hit the four percent, but or forty percent, but they go for a long disease control hair. So we look at the DCR now, um, and that's very, very informative for us.
Rakesh Dixit:
Yeah, that's great. Uh, so just changing a little bit on that one. Um, so if you think about 10 additional, let's say next 10 years from 2025 to 2035, what do you think uh there will be changes in the way we discover and develop new drugs? We are seeing some encouragement from the FDA for reducing the use of animals in in the toxicology study, which I think is a very important one. But we also face that, you know, there are limits of uh any in vitro technology to predict what will happen in vivo. Uh so that's on the toxicology side, but also on the preclinical, non-clinical efficacy and pharmacology side, what do you think we will be making uh uh you know, uh doing the RD different differently than that we have been doing for the last 30, 40 years, you know?
Bahija Jallal:
Yeah, I think I think frankly, what's the the highest impact that's can and it's starting actually starting, and I see it for the next 10 years that can make a huge difference in everything we do is definitely AI. You know, because as you know, we are it takes 10, 20 years from the from the idea until you bring it to to patients. And I think for the first time we have an opportunity now with AI, I um you know, I think this is just the beginning, and and we need we need scientists who who speak both languages. We need the scientists to understand AI and the science. Is you know, because for me, if we can improve the there are two aspects, you know, there is the science aspect that I will talk about, but I'll start with at least just looking at the the drug development process itself. If we improve just one percent every single step, can you imagine how much we can reduce that? That will allow us to test more things, to bring things much faster, because right now it's it's just way too expensive and way too long as well that it takes us. And and you know we are not the most efficient uh people, right? In um in in the drug development, we still there is still a lot of things that are done done manually, not automated, not you know, uh we have to start over again all the time. AI can if AI can can improve on every single, you know, uh one. I I'll just give you an example.
Bahija Jallal:
If you think about, you know, sometimes we get questions from the FDA or from any any regulatory authorities, uh, and um, you know, with 200 questions or something you have to answer. If you, you know, you you sit down, usually the team sits down and try to answer every single one. Now imagine if you have an AI that can actually draft the first draft, how many hours and how many days you can you can save. And I'm uh that's why I'm talking about 1% in every single step, how we can do it better. Now, at the scientific level, how AI can help us, if you think about, you know, we go through for monoclonal antibodies, you know, we you know immune immunize mice or llamas or whatever and do this and that. But we have enough and we're doing it now in the TCR space because we have we have approximately 500 uh crystal co-crystal structures so that you actually can take all this data and make sense of it and try to see if you can predict and understand how you know a peptide because how the peptide sits on the HLA um um you know, HLA peptide, HLA plus peptide presented is very important. Can you cut that, you know, empirical, you know, uh things and going into crystal structure and everything and have model all that and and and we can then do it for for for a lot of things in toxicology, the same thing, right? So can you predict from all the the data that exists there that um a peptide will be you know uh uh the same in in in normal tissues? So there is a lot of things, but as I said, we need we need more, we need the universities to produce more scientists who speak both languages. Now it becomes almost is a must. Um as I as my last point is I always say, you know, um AI is not gonna replace scientists, but scientists who understand AI will replace scientists who don't understand AI going forward.
Rakesh Dixit:
Yeah, fully, fully agree. I mean, I think one of the advantages of AI can give us information, extract the information is way the more faster than anything else as the human mind can do it. Exactly. No matter how many reviews your articles you read and all that. So if AI can be helpful with that, that's that's a huge and I think one thing will help AI, in my opinion, more database we have, whether it's internal database from the companies or where they are willing to share some of those learnings. I agree. Because AI cannot do magic if it doesn't have place, doesn't have the resources to pick the information from, you know, if it's not really available. Yeah.
Bahija Jallal:
Well, I'm happy, as you said, that the FDA is embracing AI as well because they have access to all the data, right, that they get. Oh, yeah, oh yeah. And so that's gonna be also so we have to keep up as well.
Rakesh Dixit:
Yeah, and I I hope that they will use that information in saying, hey, here's the drug, we know a lot about these drugs, this MOA. You know, you cut down some of the animal studies, expensive $5 million studies. You know, why can't we just do some in vitro studies and try to understand mechanism-based toxicities or or or or maybe a little bit hybrid approach and to move forward? I mean, total replacement is impossible at this point, but definitely we need to make improvement. We cannot keep on doing the width we have been doing science for the last 30 years.
Bahija Jallal:
Fully agree, and that will help us bring medicines to patients faster.
Rakesh Dixit:
So, uh, what advice uh would you give to young scientists and entrepreneurs who are trying to start a new company? Because you have been there before, uh, as well as new biotech CEOs, to uh they're going into first program. You know, it's a loaded question, but you know, I'm sure, I'm sure you have some thoughts, you know, what what things to do, what things not to do, you know. Uh and sometimes what not to do is more important than what's what to do. That's what I do nowadays. I tell companies what not to do.
Bahija Jallal:
That's true. I think that's a that's a very big question. Uh I always tell people who are motivated to come to the drug development side of things, is this is definitely not for the faint of heart, right? Um it's uh it's it's it as we just talked about, it takes time, it's uh it's uh it's difficult. There are a lot more things that don't work than things that work. However, this is the most rewarding uh things that you if you love it that you're gonna you're gonna do. I I always say, you know, how many people can say I wake up in the morning to come help patients? That's really, you know, for me, it's it's as I said at the beginning, it's not a job, it's uh it's a privilege uh to be doing what we're doing. Um and for scientists who didn't decide yet what they want to do, I would say follow your heart, because if you do, if you do something you love, is there you know basic science or you know more um applied science? You have to love it. If you love it, you're gonna be great at it, you know. And I I think, you know, and and you have to be entrepreneurial because a lot of things are are are tough. But it's uh it's just wonderful because you're learning constantly, constantly. Um, and that's that's really uh a privilege.
Bahija Jallal:
I think for the CEO is I would say, um uh you know, you you have to you have to understand that we are in the business of science. You have to always be close to the science. That's really important. And have your priorities straight. And for me, the priorities are always, yeah, the patience, the science, and the profit will follow. The profit will always follow. Don't don't reverse it. Right, right. Then you're gonna make the wrong decisions. I think then you have to really understand one thing is that you're only as good as the team you have. You have to hire people who are better than you in every single you know field. Um, they are to be the best because you cannot succeed. It's not the CEO who makes things happen, it's the team who makes things happen. So you are only as good as the as the team we you have. And then uh finally, I would say um, you know, pace yourself, you know, especially when you are in a biotech and you're, you know, you get uh either you raise a lot of money or you have commercial product like we do and things like that. The temptation is then just to grow too fast, you know. You have to really pace yourself and always, you know, remember what you're you you know, you have to to have um, you know, just basically what you promise, you know, and then promise and over deliver, not the opposite, you know. So that would be my my advice.
Rakesh Dixit:
No, I think that's fantastic advice, and I think that's what I've been seeing since since I uh left AstraZeneca in 2019 now for the last six years working with lots of companies. I have seen successful companies and companies that actually folded very quickly. And where I see the difference between these two, despite the fact they wanted a good team, but they in for for reasons not totally understood, they hired too quickly. Okay. And they thought that's always we have to go through organic growth. It's not necessary when you're a small company, because those are fixed expenses for you. If you don't have, you need to go after every talent you can find, whether whether it's advisor, whether it's consultant, whether it's somebody part-time, and and because otherwise you will run out of the money. This is a marathon race, this is not a thing that okay, well, I can just run in a few days and and get it done. And I think that's one advice that you give is extremely important to form a right team of right, right people, and they all don't have to be in your company.
Bahija Jallal:
Exactly. Exactly.
Rakesh Dixit:
And and and because the talent is everywhere, you know. I still remember when, you know, in my previous role, I think at Mark, you know, people used to say, Oh, don't listen to anyone. Mark is the best. And after I came to other companies, I said, that's not true at all. There are lots of very smart people, there are lots of very smart companies, you know, and lots of very smart researchers. So I think that's this is really important to to to have a broad net to get uh you know uh as many talent you can, whether internal or combination of both internal and external. So that's a really great advice. Do you want to have some closing statement? Uh, of course, we done a lot of stuff.
Bahija Jallal:
No, I I just want to say that uh, you know, I I really I feel lucky to have done what what I've done and to have uh you know the privilege of doing of being in the in a field that's evolving all the time. But I want to take this opportunity to thank you for uh being a fantastic new hire, first new hire, my first new hire at MedImmune, and for you know the 13 fun years I think we had uh there at MedImmune and developed multiple drugs thanks to your advice. And you're still you know really experts in what you do, and uh I don't I don't uh take it for granted everything you contributed to the medicines that we have in the market today. So thank you very much for that.
Rakesh Dixit:
Thank you very much, Bahija, and I'm really excited. Um also it was a great privilege to actually talk to you. Uh and uh and thank you so much. And I know you have very busy time for giving me you know 45 minutes of yours, and maybe we'll do it again uh in in a in a year or two here. Thank you.
Bahija Jallal:
My pleasure, thank you very much.
Rakesh Dixit:
Thank you, everyone. Bye bye,