Unlocking the Immune System: Dr. Levisetti on Cue Biopharma’s New Biologics

Matteo Levisetti, M.D is chief medical officer of CUE Biopharma which is a clinical-stage biopharmaceutical company, engineered a new class of injectable biologics that selectively activate the patient’s immune system directly in the patient’s body, without the need for ex vivo manipulation. During the interview Dr. Matteo Levisetti will talk about Cue Biopharma, about their recent studies and not only.

Matteo Levisetti is the Chief Medical Officer at Cue Biopharma. Previously he served as the Senior Vice President of Cue Biopharma. He was also the Chief Medical Officer at DNAtrix. He also served as the Chief Medical Officer at Dauntless Pharmaceuticals, Incorporated.

Dr. Roupen Odabashian is an accomplished Internal Medicine Physician and Hematology/Oncology Fellow with a profound commitment to advancing healthcare through clinical practice, research, and technology. Currently based at the prestigious Karmanos Cancer Institute, Dr. Odabashian is actively involved in pioneering cancer treatments and conducting clinical research.

In addition to his clinical work, Dr. Odabashian is a multifaceted healthcare professional. He hosts podcast at OncoDaily, engaging with leading experts in oncology to share valuable insights with the medical community. Dr. Odabashian also contributes his expertise as an advisor at Spiraldot Health and Mesh AI, supporting innovative ventures in healthcare technology and collaborative scheduling to combat clinician burnout. With his diverse roles and unwavering dedication, Dr. Odabashian exemplifies a commitment to driving positive change in healthcare.

00:00 Introduction
1:23 About CUE Biopharma
10:26 Side effects of immunotherapy
16:30 Why CUE decided to target this pathway?
23:48 About markers
25:35 Dr. Levisetti’s personal journey
33:25 Academia to Pharma

Roupen Odabashian: Hello everyone and welcome to a new episode. I’m very excited today. I have a special guest and I can’t wait to ask him questions and learn more about him and Cue.

So Dr. Levisetti, he’s a seasoned leader in the global clinical development. He’s currently the chief medical officer at Q Biopharma, but he also held like prominent roles in various pharma companies including Genetrix, Dauntless Pharmaceuticals, Mirati Therapeutics, and he directed clinical and immuno-oncology programs there.

Dr. Levisetti’s extensive background include leadership positions at Roche, Pfizer, and academic appointment at Washington University School of Medicine. He holds an M.D. from the University of Chicago School of Medicine and he completed advanced training in endocrinology and immunology. Dr. LeviSetti, welcome to the show.

Matteo Levisetti: Well thank you Roupen, that’s a very generous introduction. I’m very happy to have the opportunity to speak with you today about our work at Cue Biopharma and also you know my journey and background in this field.

Roupen Odabashian: I love it. So why we don’t start and maybe you can tell me a bit about Cue Biopharma and then we can drift and talk about the recent trials and the results.

Matteo Levisetti: Sure, so Cue Biopharma is a clinical stage biotech company. We’re made up of approximately 50 employees. The company is based in Boston and as I mentioned, we have two potential drugs in the clinic.

We have a very unique platform which really are T-cell engagers. So it’s a T-cell engager that selectively delivers the cytokine IL-2 tumor-specific T-cells. And so I think you know we’ve really learned over the past decade, you know, with regards to the immunotherapy of cancer with the approval of checkpoint inhibitors like pembrolizumab and nivolumab, that the patients with cancer harbor T-cells that are capable of recognizing cancer cells and eradicating them.

And so patients now, quite a few, we’re striving to have that number of patients become many more. But you know about 10% of patients treated with checkpoint inhibitors and most indications have very durable responses and so really even complete responses or really significant control of their cancer for several years, for you know even three, four, five years.

And so what our company has done is developed a protein therapeutic platform that selectively engages those T-cells that mediate that immune response against the cancer and gets them to become active, to expand.

And we’ve dialed in a specificity in the platform where the immunostate is what we call the drug, only selectively engages with tumor-specific T-cells. So you know we harbor an enormous T-cell repertoire of specificities, okay, of which only a tiny fraction is capable of responding to a tumor cell and killing it.

So it’s probably less than 99.99% of T-cells are specific for the cancer in a patient. And all approaches to date have just non-selectively delivered a cytokine like IL-2 or you know a checkpoint blockade blocking the PD-1, PD-L1 pathway to all T-cells.

And this leads to you know I think some efficacy which has been in advance but it’s limited if you will. And it also comes along with a lot of toxicity particularly if you look at activating cytokines like wild type IL-2 proleucin which has been approved for a couple decades where basically the toxicity is so great that it’s actually used very little.

So you have you know 80 to 90% of patients having you know grade 3 or greater you know really serious life-threatening toxicity and a response rate less than 10%. So we thought well what if you could selectively only activate those T-cells that you want active and that’s exactly what the immunostats do. The first one we took in to the clinic is an HPV positive head and neck cancer.

And the immunostate expands T-cells that are specific for the E7 peptide which is continuously expressed in HPV positive epithelial cancers and it’s presented on the surface of cancer cells. And so the 101 immunostate we give to the patient IV every three weeks expands T-cells that are HPV specific and then those T-cells go and attack and destroy the cancer. And so the data that that we presented recently at ASCO in an oral presentation was an up-to-date overview of our findings and so we’ve treated 80 patients to date.

And we started treating patients in the second line setting and beyond and so these are patients that had progressed on prior chemotherapy and checkpoint inhibitor. So those could be given in the current era together in the frontline treatment of head and neck cancer or in either sequence you know over the last five years.

So before the checkpoints became approved patients would get platinum-based chemo and now more recently with the approval of pembrolizumab in the first line setting there’s also patients that can get upfront immunotherapy followed by chemotherapy and immunotherapy followed by chemotherapy.

And so the patients we enrolled greater than 90 percent of them had received and progressed on prior treatment with both chemo and checkpoint. And what we have observed now is really a remarkable prolongation of survival. So totally unanticipated median overall survival of over 20 months.

And these are patients treated in the third line setting, second line and beyond. And if you look to the second line pivotal trials with PEMBRO and NEBO median overall survival was approximately eight months. So one line earlier, eight months.

And so this is a single arm data set. We treated 20 patients at this recommended phase two dose of four mg per kg. And we actually had to amend the protocol to extend our follow-up for patients because when we put the protocol we did not anticipate that any patients would live beyond two years.

And every year at ASCO I would speak to our investigators and say well what would be interesting? You know there’s a single arm study but what do you think? And they said well each year that you know if you have a median OS of a year of 12 months in this population that would be notable and now we’re beyond 20 months.

So we still have five of the patients alive in follow-up. The other part of this trial was treating patients in the front line setting. Okay so these are treatment naive, recurrent metastatic HPV positive head and neck cancer.

And now we’re treating patients in combination with Pembrolizumab which is approved in the first line setting. And here we’ve observed an objective response rate of 46%. And if you compare that to the historical response rate with Pembrolizumab monotherapy it was 19% in the pivotal keynote 48 trials.

So we see more than a doubling of response rate. These responses are very durable. The median duration of response has not been met but several I think five of our patients are out beyond two years.

The PFS in this population is approximately six months so it’s twice that which was observed with keynote 48 with Pembrolizumab monotherapy. And then we have a 12 month overall survival rate of 96%. And again this is maturing data but that compares very favorably to the historical rate of just over 50%.

So really encouraging differentiated data in the front line setting when we treat with the immunostate Q101 in combination with Pembrolizumab. And very importantly this combination is very well tolerated. So we don’t see any synergistic toxicity.

The tolerability profile looks like Pembrolizumab monotherapy as it’s defined in the label. And Q101 which we’ve defined now in over 100 patients which of note we don’t see any capillary leak syndrome which was associated with wild type IL-2 therapy. We’ve only seen one adverse event of CRS which was grade one.

So one patient with a fever out of 80 treated some of them for up to two years.

Roupen Odabashian: So like what other side effects like were there like any other side effects that came like nausea, vomiting, diarrhea, anything one of those common things that happened?

Matteo Levisetti: Yeah so again it looks very much like you know the the disease you know in an advanced cancer population. So fatigue, anemia, decreased appetite. We did see about 20 to 20% of patients had mild infusion reactions generally with their first infusion.

And then no patients discontinued because of an infusion reaction. And they were very easily managed. So we didn’t pre-medicate up front but if a patient had an infusion reaction we would then pre-medicate on subsequent cycles.

So we actually still have five patients on treatment a combination of 101 with Pembrolizumab and of the 25 we treated at the recommended combo dose 20 of those patients remain alive in follow-up. So it really the survival data really looks very favorable you know as it matures. And so it’s really great for these patients and our investigators are really enthusiastic you know about this as a potential you know option.

Roupen Odabashian: Yeah it’s very exciting.

Matteo Levisetti: Yeah it’s very exciting. The combination you know in the front front line setting with a Pembrolizumab with chemotherapy you know that data if you look at the four-year follow-up from Kina 48 you know it looks very strong. So their median overall survival was 14 months.

So it’s longer than the Pembromono. But again if you look at what the patients go through you know that’s a chemo regimen that had you know 70-80 percent you know frequency of treatment related grade three or graded greater adverse events you know which are well known with chemotherapy. But again it’s quite a different experience for a patient in the front line setting to not have a lot of those toxicities.

For sure.

Roupen Odabashian: And this is very interesting like the I think like when you see like this a huge response also like you worry about the toxicities but it sounds like the toxicities are not that but are not limiting for the treatment at this point. And I was wondering like going from here are you guys trying to like launch more advanced like phase three trials or maybe expanding the indications and trying it in other types of cancers like there are tons of cancers but usually happens by HPV.

Matteo Levisetti: Yeah no it’s a great question. So we’re planning a randomized phase two trial with two doses of 101 in combination with Pembrolizumab compared to Pembrolizumab monotherapy. So we had a very productive interaction with the FDA earlier this year and this is really what was now aligned with the expectation and recommendation.

I’m sure you’re familiar with what really is a mandate by the FDA called Project Optimist to optimize the selection of dose in combination immunotherapy regimens.

This also gives us an opportunity to again confirm that which we observed you know in a randomized controlled trial before you know investing and going into a large pivotal phase three and some of that again you know is it’s moving forward it needs to be funded and we’re we’re a small biotech and the scope and cost of a randomized phase two with less than 100 patients compared to a pivotal phase three with 600 patients is vastly different.

So that’s our plan. Regarding your question it’s a fantastic question and I you know I just wish we had more resource to do more because as you allude to and I’m sure know very well that that there’s a whole other you know set of HPV driven cancers where there’s really a huge unmet need and that includes cervical cancer

Probably it’s the next circle and then some genital urinal you know which are just terrible you know vaginal penile vulvar cancels which are really nasty you know malignancies and so based on what we’re observing particularly in combination with the checkpoint inhibitor

I think there’s a very strong rationale to consider going into for example cervical right the front line of care is a checkpoint inhibitor plus chemotherapy so to consider you know a combination up front you know particularly in patients with you know advanced disease that diagnosis makes a lot of sense so it’s just a matter of resource and being able to do that but again it should really have

I mean it should work in a way that’s very much analogous because you know we the HPV you know genome that there’s a component of it so there’s different parts of it that have different peptides that are expressed and in the E7 it seems to be really ubiquitously expressed in all of these HPV driven cancers so if you have an HPV16 cervical cancer it’s an absolutely rational and good target to go after.

Roupen Odabashian: So that brings me to a question now I thought about it like this is very innovative and the results are very exciting and I hope like in the next year or so it will be available in one of the centers that I work in too to try it but like going back to the early days of Cue how and why they chose to target this pathway and like what was the thinking process of creating this drug and if you don’t know that’s completely fine but it’s interesting question for people who are trying to innovate there and find a similar targets or pathways to treat like how did this idea came about?

Matteo Levisetti: Yeah so it’s an outstanding you know question and I’ve been with Cue now three and a half years. I’m actually was very familiar with the company all the way back I as a consultant worked with the company to prepare the IND on the first drug with the about five years ago and so you know the premise here the concept was you know in Cue basically refers to you know sort of taking the nature’s cues okay to modulate the immune system so in cancer to turn on anti-tumor adaptive immunity and T cells

And we also have a pre-clinical autoimmune pipeline which does the converse but so the thought was well what would be a good specificity okay and tumor to go after and so you know the first choice that ultimately was to go with a virally driven okay tumor right and so viral is not self okay

And so I think scientists and the company reasoned that it was it would make sense to choose a foreign antigen you know a cancer with a foreign antigen target that was consistently expressed and that the immune response against this would naturally be stronger than an immune response against a self-protein okay because there’s no tolerance right against this because it’s a viral protein it’s an you know it’s an infectious agent

The second drug that we brought in the clinic is called Q102 and it’s the identical platform construct but instead of the E7 HPV peptide now this has a peptide of Wilms tumor 1 and so Wilms tumor 1 is a tumor antigen

Okay so it’s an onco fetal protein it’s expressed during embryogenesis and then goes away except for a couple tiny traces and a couple tissues and so this is expressed at very high levels okay in a whole set of liquid tumors and solid tumors so in AML it’s expressed in almost 100 percent of cells at a high level WT1 it’s overexpressed

And then if you go and look in other cancers so we’ve treated now 40 patients in in a dose escalation and expansion with colon cancer pancreatic cancer gastric cancer and ovarian cancer and so that’s where we started in the clinic is that basket of indications but but there’s a very strong interest in taking our 102 immunostat into patients with leukemia AML we have a leading investigator in glioblastoma who wants to take it into glioblastoma

So it’s been a target that’s been investigated with cancer vaccines but none terribly successfully unfortunately so what we’re seeing to date is really encouraging so we see expansion of tumor reactive WT1 reactive T cells in these patients we see reductions in tumor burden in advanced patient with ovarian advanced patient with gastric cancer this is just during dose escalation

And then a quite a fair bit of just disease stabilization and so as i’m sure you know well right in your experience in overseeing and doing phase one trials in oncology right that that incredibly you know these are late lines of treatment so colon cancer patients have gotten at least five or six lines before they see a q102 but in pancreatic cancer for example you know we have two or three patients that that again being treated in the second or third line so they receive front line therapy then a second line therapy

And then as you know well unfortunately not many of these patients are around for many more lines of therapy but you know we have three patients now with that that have experienced disease stabilization you know so without you know absence of resist defined progression for six months one up to eight months and so that’s you know piqued the interest of some of our investigators and then again ultimately

Well i think it will our plan is to look for the next rational combination of q102 in patients with a wt1 overexpressing tumor where again we would hope to see what we saw with 101 in hep in HPV driven cancer that when you add another again another agent here which is a checkpoint blockade agent that you somehow enhance

You know the ability of the immunostate to expand relevant anti-tumor t-cells to have durable responses to have you know a response rate that that’s close to 50 percent all right and that that’s a very different picture right if you can tell your patient but you know for example patients with low pdl1 expression or cps scores less than 20 in head neck cancer for example have a a response rate that’s actually less than 19 percent it’s 14 percent yeah and it’s very sad

Roupen Odabashian: yeah like those patients like you don’t put them on this drug it’s is it going to work or it’s not but they don’t have any options right like it’s very dissatisfying and and so what we’ve observed is a response rate um across levels of pdl1 expression

Matteo Levisetti: That’s 50 percent there’s no difference um and so something about this combination overcomes or whatever it is I mean it gets complicated trying to interpret what that that means um uh you know with regard to whether the  pdl1 you know expression the pdl1 cps expression uh is just telling you about a hot or cold tumor or how immunologically active a tumor is but in the case when you come in with a combination it overcomes whatever is sort of more immunologically cold or inactive but that that’s just kind of hypothesized you know do you think that maybe the target that

Roupen Odabashian: You are looking for like the pdl1 here maybe it’s not the right marker to look for to guide us to maybe this is the right treatment or not

Matteo Levisetti: Well you know it’s a great question it’s the it’s the best thing that’s come up to date um in terms of checkpoint therapy checkpoint inhibitor therapy but it’s not a great one no and so again you know we always build in sort of exploratory biomarker assays

And you know it’s too early now there’s too small numbers of patients but in the combination with an immunostate is there something that we can use as a biomarker to identify those patients that really that respond okay and because the pd the cps like you know expression level the pdl1 expression level just gives you kind of a trend you know if you’re greater than 20 you’re more likely to respond if you’re less than 20 you’re less likely

Roupen Odabashian: Exactly and it’s not like it’s not causality it’s an association and some Patients like even with low pdl1 might respond and do great

Matteo Levisetti: Exactly and that that’s precisely what you know i’ve gotten to know through working with really a great set of 15 investigators on a trial in the u.s and um you know and when it when it really comes to practice there’s much more than a consideration you know in making decisions and you know and so again having something that that’s more predictive of course would be fantastic if we can get there again

Roupen Odabashian: Gotcha i want to switch gears toward another topic and i want to talk more about you and so Dr Levy said i went through your background and you have an impressive background through from academia to pharma industry so we talked earlier about your work with Pfizer with DNA tricks with dauntless can you take me to the early days and tell me how your career shaped after you left medical school what happened how did you end up here well yeah it’s been a long

Matteo Levisetti: Seems like a long circuitous route all right so um i i initially um matched into a general surgery program oh wow on the stett Hopkins and so i matched as a Halstead resident at Hopkins in 96 when i graduated from medical school and very quickly realized that i’d made a mistake

So I spent one year so i did an internship in general surgery oh okay you realize that i that this was just too much for me i mean i i just to be honest about it i mean i thought i could do everything when i was in medical school but it was physically emotionally exhausting other parts that i really enjoyed talking to patients some of the more academic work you know I missed

And so i went back to Chicago actually and did research for a year with an immunologist and an endocrinologist that i knew as a medical student um and then decided that internal medicine would be a better fit and so i did a residency in internal medicine um and and then one of my mentors at the time ken blonsky who is a an endocrinologist

And i was going to do my fellowship with him in in Chicago and with Jeff Lusto in immunology because i was fascinated by autoimmune endocrine disease and so he ended up moving to Washington in St louis and invited me to check it out

So i ended up going to Washington university in St louis for a clinical fellowship in endocrinology and a postdoc in immunology in a lab of a famous immunologist Emily Nanoway

And i ended up staying there for nine years and so i completed my clinical fellowship and then spent three months a year attending at barns hospital in general internal medicine and doing you know endocrine consult service and a half day a week of outpatient clinic and endocrinology and i had my own lab you know so i had a sort of the you know the academic medicine setup which was a lot of fun you know for a while

And then at a certain point I must say I stopped having fun and I found it to be really pretty highly competitive very onerous in terms of the amount of work for the reward that one could anticipate trying to get grants and funding constantly is just a pain and perhaps most importantly I it became evident to me that you know I never was going to make any great stride or discovery or cure type 1 diabetes you know

I mean I wasn’t you know I wasn’t some you know brilliant you know Nobel prize winning scientist who was gonna you know I just that was clear to me that that i limited what I what I thought I could achieve and also what was focused on this very narrow question of you know what are the molecular levels you know at the t-cell receptor the MHC peptide complex in type 1 diabetes that results in the loss of tolerance to self

And I was really focused on autoimmune diabetes and so then after nine years there I this about 15 years ago I had a friend who had gone into pharma and said Mateo you should come check this out I think you might like this and so i went on a couple interviews with a couple of big pharmas and then i and then i i took a job offer at merck research labs in raway and and so I started in at merck as an associate director where I was a medical monitor on a huge global trial in in endocrinology and bone metabolism

And I spent two years at merck which was a fantastic entree into industry so just a really incredibly good group of super high quality clinical researchers but then I just kind of missed some of the earlier science you know and translational parts of medicine like taking things into patients for the first time and being you know really at the sort of cutting edge of taking something novel for the first time into patients

And then I got contacted and about an opportunity at Pfizer in la jolla California working in early clinical development and and so i took that and i spent four years at Pfizer in early clinical development and that’s where i really branched out from  endocrinology metabolism in more immunology development in oncology

So you know I had rotated through you know oncology services as a resident you know but yes and at ufc that was great but i was not an oncologist but but by the time I completed you know four years at Pfizer i was 60 percent of my effort was running early phase one oncology trials so I took gosh five of the adcs that Pfizer was developing in 2014

You know into the clinic different cancer indications and so you know over several years really learned quite a bit about certain areas of oncology and most importantly just drug development so the principles of drug development go across therapeutic area but i was really motivated as i am today you know and then i did a little bit of a sidewinder where where i was recruited to to go to roche in basel Switzerland for a year to build immunology inflammation group

That must that must be a really nice trip Switzerland it was well i thought it would be But it was tough at the time i have two daughters that were little and my wife we were living in la jolla i don’t know

We live in i live in southern California yeah so the weather made a huge difference for you right yeah just like the culture and the climate and things so the job was great and I got a lot done but I was working like crazy and then my family was not happy and they wanted to come back

And so that’s how I ended up coming back to San Diego and working at maradi therapeutics which was a lot of a lot of fun and the CEO of maradi was my boss at Pfizer before and so he had asked if I would come oversee and set up their immunotherapy combinations with their small molecule tkis that they were doing in in lung cancer which are immunomodulatory with checkpoint inhibitors in in renal and lung cancer

And so I spent two years there and I kind of move on once I kind of learn all that I can learn from a certain experience

Roupen Odabashian: Yeah I can see this trend which is very interesting because like you’re always looking into a new challenge and you’re looking new opportunity and I think many physicians right now are like they are trying to find a way through pharma and innovation and that brings me like i want to go back a bit

So you made the transition from academia to pharma and then you were able to once you were in pharma you were able to like branch to other pharma companies so what do you think helped you to make that transition from academia like if someone right now an academic physician listening to this what advice would you give them that help you to make that transition from academia to pharma should they do like postdocs should they focus on research like what’s the secret sauce

Matteo Levisetti: That’s a good question so at least for me you know what i would say is one of the most important things is to be very open-minded  to learning um about all sorts of different areas that you probably will have had zero exposure to okay I love that I agree yeah zero okay

And I never thought you know it was my whole academic career one of my first programs at Merck that i was assigned to was um so this is a group that developed fosamax for osteoporosis right so before that osteoporosis wasn’t recognized as a disease okay

So you know this ended up being an enormously important um advance in in medicine you know and so um fosamax which is a lendronate you know it was a blockbuster drug for Merck for over a decade

You know well over a billion in sales for over 10 years and one of my i was assigned to the program where i was working with a team based on the Merck partner shugai in was it shubai yeah in Japan to try to make a capsule or a tablet of fosamax and vitamin d in combination right which became a branded product for Merck

That was small enough okay for Japanese women to swallow okay and i thought like whatever this is what you know we got a team of 20 people that are going to work on this you know and so um apparently okay and so there’s really clear market research and that in the culture and in Japan pills above a certain size are not marketable and in this case it’s women that need to take it because it’s for osteoporosis okay

So that was a blockade to having a successful product even though all the clinical data was there the clinical trials were done that that was done okay and so then it really came down to like formulation science okay and so I for two years had this incredible you know learning in this world of formulation science

Okay and this has been the hardcore chemistry properties of the drugs of the excipients of spray drawing them how you formulate little emulsions and droplets and you know I found that to be fascinating okay and then you know they wanted my input from or my team you know

I mean at the time i was very junior you know on the clinical aspects of this or that or you know what will this do to the bioavailability and what you know so this was a whole realm of something that i would have never thought about in my whole career but i had a lot of fun i learned a lot and we ultimately failed in making a tablet or capsule

And so we ended up doing a sachet which is it’s a little like a little sugar yeah yeah and then you just sprinkle it on you know yogurt or applesauce but that’s just one example all right

And so you know I got very involved with with the whole question of reimbursement market access target a product profile for a program that I championed at Pfizer for type 1 diabetes so the trained endocrinologist immunologist it was a natural fit and i ran the trials that took us through phase two and an anti-l7 receptor antibody um that looked very promising but then you know had to interact with the business unit at Pfizer to really create a value proposition that would support further development okay

And so that that gets into really learning about you know what determines market access um what’s reimbursed why and how do you overcome barriers because the payers just said well we have insulin you know that’s good enough but as any physician or endocrinologist knows

You know any a little bit of endogenous function you have you have better health for the rest of your life so that that was shown in the dcct trials so um you know if you imprint you know even two more years of endogenous non-diabetes glucose control those patients will live longer and they’ll have less morbidity

And so it’s very cool that in the last year and a half that a drug was approved to delay the onset of diabetes by two years but just working through and getting to kind of understand all the forces all the things that have to come together to develop a medicine okay that’s going to be successful ultimately get approved get the patients and have provide benefit and so back to your question i mean it certainly one is to be open about learning you know in all these different areas where you may be uncomfortable

Because you don’t know you don’t know them but welcome those opportunities welcome opportunities to work across therapeutic areas that you you’re not the subject matter expert in and then the other thing which I’ve only recognized more so in the last five years is in pharma and biotech I’m constantly in a position where i have to make decisions okay with limited data okay

But my job is to make the right decisions right and to make good decisions but you have to get to a point um where you have to feel comfortable in that space and that’s not consistent with the academic medicine mindset okay yeah I agree so I recruited this fancy md Phd from Dana-Farber you know who was on the faculty at Harvard for over 10 years you know

And he’s my senior director now a medical monitor brilliant guy um but in the over three years that i’ve sort of you know had him work with me the greatest challenge has been to get him to that point you see to feel comfortable making decisions providing the input that’s asked of us with incomplete information and you’re never going to have the level of scholarship that you did in your area in academics right

Because you’re going to be pulled into another indication you’re going to be pulled into areas that that you just you know had a few weeks to learn about but you know you still can develop a skill set and you have to um because you do have with the medical background and that that you know what what’s being asked for it’s just a question of being comfortable with delivering it with a certain degree of confidence

And it takes a little while but you know some folks who don’t make the transition so well I think they don’t um they don’t change they’re fundamentally okay and how they approach uh you know their work in and you you have it uh have a flexibility that that uh it’s certainly not taught or groomed in in academic medicine I’ll tell you that

Roupen Odabashian: Gotcha great thank you so much I appreciate that that brings us to the end of the episode that was very helpful and insightful

Matteo Levisetti: Well thank you so much this has been a pleasure