We’re getting close to the end of our discussion. I want to thank all of you. This has been a great discussion and very informative. We’ve covered a lot of things, which we’ve expressed our opinions on. Before we close for the evening and conclude the discussion, I wanted to get some final thoughts from each of you in terms of the topics we’ve covered. I’ll start with Gilberto. Give us some of your final thoughts in closing the program.

: We still have a lot of work to do in lung cancer. We have certainly done a lot better in the past few years than we did in the couple of decades before, but of course, there’s a lot of work to do. If we look at targeted agents, most patients eventually will progress. If we look at immunotherapy, most patients don’t benefit from it. So of course, we have to continue bringing new drugs to the market, and we need to find out what this sweet spot, the perfect balance, is between bringing innovative drugs to the market and charging for them. And I don’t know that we have that answer today. We need to continue looking for that.

:I think, as oncologists, we are all trained to take charge of helping our patients and protecting them as much as we can. I think the financial toxicity is real and is here. It isn’t going to go away unless we step in, and I don’t want to say solve the problem, but be part of the solution of this real problem for all of our patients, regardless of the disease and regardless of the treatment.

: I think that we have some agency here. I used to do more GU [genitourinary] oncology, as well as thoracic, and we saw sipuleucel-T, or Provenge, basically die on the vine. I don’t think that was because the data were so poor, but because the world wasn’t ready for a drug that cost $93,000. Now, today that would be extremely restrained, but the world wasn’t ready for it at that time. Because of that, it just didn’t get uptake. We have more modern agents, like ramucirumab has a survival benefit, but people weren’t that impressed by it. It gets intermittent use as well. Necitumumab was FDA approved, but I don’t think anyone ever used it because it didn’t seem to provide meaningful benefit relative to the cost of the drug, and arguably, the toxicity. So we do have some control where FDA approval isn’t the same as a mandate to use something clinically. I think that’s especially true when you have fungible choices, like multiple ALK inhibitors or PD-L1 inhibitors, etc. We also see that when we have the enviable problem of effective treatments, we can start to pull back. Just like we had a debate about, “Well, how long is too long for immunotherapy, and can we do as well with less treatment?” I think we can start to ask that about the financial toxicity. We should ideally not have to choose between effective drugs and unfathomably ridiculous pricing. While I appreciate that we want to incentivize companies to innovate, we are too far on the end of unchecked price restraints, and have very little incentive to control costs. There’s plenty of room for companies to still make a healthy profit, for us to respect and protect that, while not giving away all controls to the point of bankruptcy and forcing us to make choices we shouldn’t have to make, considering how much money we dedicate to health care.

Thank you all. One final thought that I would render, and we didn’t have a chance to talk about this, is that if we’ve learned anything over the past couple of decades, we’ve learned that in oncology, one size doesn’t fit all. All of us would be happily willing to use a drug—I’m not saying without cost concerns—if we knew the drug was going to be highly effective. And if we knew the drug was going to have no effect, we wouldn’t use it. That brings up the issue of biomarkers, and if we can truly personalize medicine and say, “This therapy is going to work, or this therapy is not going to work,” to a greater degree than we do today. We are certainly better than we were 20 years ago, but we’re not where we would like to be with regard to using ineffective therapy in patients, which isn’t attractive to any of us. If we would have a greater ability to identify the patients who are truly going to benefit, that would go a long way to helping us with the cost effectiveness of all these things. That’s my parting comment.

I want to thank all 3 of you. It’s been a great discussion. I also want to thank our viewing audience. We hope you found this 

 discussion to be useful and informative. Thank you.

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Experts in cancer management share their final thoughts on effective treatment and individualized care vs financial toxicity.

Final Thoughts on Effective Therapy and Financial Toxicity

: Let me bring up a slightly different perspective. In lung cancer, I can’t remember the last time—I think it was probably bevacizumab—that a cooperative group led to drug approval. We’ve transitioned from our government, and I think this happened, in my opinion, when Bristol Myers Squibb acquired paclitaxel in the 1980s. Drug development went from the NCI [National Cancer Institute] to the pharmaceutical industry, so if I were on the industry side, I would say, “Do you know how many dollars we spend on negative trials that never become FDA approved?” I don’t know what that figure is, but I’m sure it’s eye-popping in terms of the dollars that are spent on clinical trials for the development of drugs that never reach FDA approval, and therefore are never able to be reimbursed. So, how do you balance? We ask industry to be innovative and to bring us all these new drugs. For industry, many of the large companies are as good as any academic medical center we can think of; they have a cadre of PhD-type people who figure this out, much like our great universities and cancer centers do. How much do we balance this innovation and say, “Well, OK. We want you to be innovative, but we want cheap drugs at the same time.”

: We don’t want cheap drugs, we want drugs that are fairly priced. The way we have the system today, drugs aren’t fairly priced. What’s the ideal price of a movie theater ticket? We know what that is because there’s an open market. There’s not only 1 company making movies, there are a number of different companies making movies. You have competition in the market and the market sets that price. We have a right to patent, which is the way we used to incentivize those pharmaceutical companies to bring those drugs to the market, but we cannot abuse that patent process. We have to be cognizant that we need to bring competition to the market, and the place to bring competition is where we have several drugs for the same indication. Historically, companies have protected their turf by not bringing the prices of those drugs down. We will need new entrants that have more to win. We will need new companies not in the medium to be able to break that stalemate.

: I want to add one comment. There’s something in health economics that’s called “price elasticity.” Price elasticity for the pharmaceutical industry does not exist. What does that mean? It means that the competition doesn’t set the price for the pharmaceutical industry. The reason for that is the way the pharmaceutical industry is set up. They aren’t set up to sell to an individual, which would then drive the market to set the price. They are set up with big contracts that the individual, who is the end user, is not able to influence. So if you look back at the hypertension market, which is a big market, the lack of price elasticity is actually well described in the antihypertensive market. In oncology, we’re getting there, but price elasticity doesn’t exist. The only thing that can change that, I think, with the competition between the United States and the European market, is the introduction of Chinese companies bringing forward products with cost differences that can be drastic. Giving an example, going from $10,000 to $5,000, would redirect the contracts, and is the only thing that can potentially introduce price elasticity to a market that isn’t open to this competition to set the price of drugs.

: Let me ask you 2 questions. Do you believe that will impact innovation? And do you believe that it will have an impact on how quickly we get those drugs to market?

: If you look at the global market as innovation—the entire globe and how we innovate—it won’t change the innovation because there will be other companies in other countries with lower running costs that would still bring new products to the market. If you look at the United States, potentially, I think one thing that needs to be looked at is the cost of running the trials. When I wrote my first investigator-initiated trial in 2011, the cost per patient for the trial was in the $5000 to $8000 range, and that was with biomarkers. Now, we are talking about a cost of $30,000 to $40,000 per patient.

: I started at $1500. Mark probably started at less than that.

: That’s the problem, and we’re generating data that we aren’t using. The FDA is asking for PRO [patient-reported outcome] and quality of life that we aren’t using. We have to step back and ask, “How much of the data that we are generating are we actually using?” Maybe we should take the waste off the plate in the design of our trials. That may result in keeping the innovative market in place without impacting the cost and financial toxicity.

: And the speed to market, yes. We’re generating this massive amount of data but we never go back to use it.

I think that’s getting back to your point about flooding the market with other choices. It was part of the strategy with the FDA, to allow submission of external United States data in considerations for the drug, particularly in the PD-1, PD-L1space, where we have all these antibodies. That seems to be the most effective strategy, assuming that someone takes that first step and changes the price of the drug. If everyone has the same price because no one wants to take the step forward, then I don’t think we can get anywhere in this setting.

: I agree with Afsaneh. I think it’s going to take disruptors from outside of the United States and Western Europe, and it could be China, it could be India, or it could be Brazil. However, it looks like it’s going to be China.

: The other issue is that when they come forward, what pricing would they put on their product? Are they going to select pricing that looks at the United States market, and therefore it’s not going to make a big change? Or are they going to come in with prices that are truly different?

: Time will tell, and if they do, are we going to take them?

: I don’t know. Remember, we are not the decision-makers. That’s the complexity of health care, there are so many layers that it makes it hard for any of these things to happen.

How do we think about this in terms of moving beyond cancer? We have a bunch of diseases, such as rheumatologic diseases. There are so many TV [television] commercial for psoriasis. It’s incredible how many there are, I can’t keep track of them. I should keep a list of TV commercials that I see of all these other diseases, but I think the same issue is ongoing in other areas.

A panel of experts debate the cost of innovation vs disruptive pricing of therapy.

Innovation of Therapies vs Disruptive Pricing

Gilberto, I’m going to ask you to address this next point. We talked a little about the role of TKIs [tyrosine kinase inhibitors], certainly as the standard of care in patients with 

-mutant disease but also in terms of the financial toxicity. Are there mitigating strategies that are appropriate for these populations, or is this not a major issue because we have 1 leader in this field, and without other competitors, it’s hard to mitigate the financial toxicity?

 Absolutely. There are situations in which we see patients suffer from this financial toxicity, especially in terms of co-pays. Yes, the company that sells osimertinib has access programs that often will help patients pay that co-pay. Having said that, there are situations in which patients still need to pay a significant amount of money out of pocket. That’s the biggest barrier that we have in the United States, and when we look at access in different situations, in different countries, the situation is even more complex, so I’m not going to address that. Most of our audience is in the United States. I agree with what Dr [Afsaneh] Barzi had mentioned before. He mentioned that if CMS [Centers for Medicare & Medicaid Services] was able to negotiate prices, then this might help. It certainly may benefit the market as a whole to have some competition if osimertinib gets approved, based on the data that we saw and discussed earlier today. There are situations where that has happened.

We talked earlier about the use of gefitinib [Iressa] in Asia vs erlotinib [Tarceva] being a little cheaper a decade and a half ago. With that, gefitinib is getting a significant lead on the market. We also have drugs that have been developed in countries that have never gotten approved in the United States or Western Europe, like icotinib [Conmana], which is the EGFR inhibitor that has been approved in China for the better part of a decade. This has also included an increased competition in that country and has brought prices down. It’s not that we don’t know that it happens, but it’s in the United States, so we have only 1 option—there’s absolutely no competition.

Unfortunately, when we look at other situations with competition among PD-L1 inhibitors, we don’t see a significant decrease in price. Every company is trying to protect them and is worried that if they create competition in this indication, come 5, 10 years, you have a new indication. Their competitors would do the same and would cut prices more. It’s a difficult conundrum that companies have, and that’s when regulators come in. Competition really doesn’t bring prices down. This is something that we don’t have an easy answer to, and we certainly have to be here, informing our communities, our colleagues, and society in general, so that we can address this difficult situation.

 I was going to ask Gilberto, or anybody, to comment on what if 1 company breaks ranks and lowers the cost. Let’s be honest, if the drug is priced at $10,000 instead of $18,000 a month, and you capture a big part of the market, you’re still going to be making money hand over fist. There’s a ton of meat on the bone here. Everyone has to put their toes on the line, and if 1 company breaks that pattern, can that be constructive? I don’t know. It’s not like a race to the bottom, because there’s a ton of profit to be made and no one would begrudge a pharmacy company a healthy profit. It’s an extortionate circumstance that we don’t want.

Jack West, MD, and Gilberto Lopes, MD, share their thoughts on mitigating strategies of therapy associated with financial toxicity.

Mitigating Strategies Appropriate for EGFR Therapy and Financial Toxicity

 Let me make a statement, and get a consensus opinion, about the significance of PD-L1 testing in this disease. I assume we all agree that it’s the standard of care. Everyone gets it.

 If they stopped doing PD-L1 tomorrow, I don’t know if I would miss it that much.

That’s where I was going with this. I’ve evolved in my practice. Even if you’re greater than 50%, I want you to be greater than 90%, so what’s the true cutoff point? Many patients who fall into the indication for the 3 drugs here have lots of symptoms, and when you look at the scans and if they have a big tumor burden, they really need a response. I’m not doing single-agent immunotherapy. I’d do chemo-immunotherapy of some flavor—depending upon other factors, obviously—but I’ve said that PD-L1 is useful only for finding those 90% to 100% expressers that have relatively low-volume disease and minimal symptoms, where you might give immunotherapy too. That’s how my practice has evolved. Otherwise, everyone is getting chemotherapy–I/O [immuno-oncology] of some flavor. Does anyone disagree with that or want to challenge me on that?

 Actually, I’d do it a little differently. I certainly agree with the principle that you’re never going to be wrong giving chemotherapy-immunotherapy if you don’t have a driver mutation, but we discussed that we don’t want to overtreat these people either. Pemetrexed-carboplatin-pemetrexed is a great regimen, but there’s a reason it’s not in the water supply. This is a medication that you’d want patients to get if they needed it, and not before then if they’re destined to do well on immunotherapy alone. I don’t want them to be on an ongoing vestigial pemetrexed acid and pembrolizumab [Keytruda], for 4 years potentially, when only 1 is doing the heavy lifting, and you don’t know because you automatically, reflexively gave 1. I wouldn’t hesitate if someone was losing weight on repeated visits every 2 weeks, or had escalating pain, or their scan showed that their tumor significantly grew from their initial ER [emergency department] visit that led to the start of their work-up. But if someone has pleural studding as their advanced disease and isn’t very symptomatic, I don’t think 75%, 80% of patients with high PD-L1 necessarily need to get chemotherapy pembrolizumab. I don’t know exactly what it is—it may be south of 50%—but even if it’s not a wrong choice, I’d say that you’re consigning people to a lot of gratuitous chemotherapy that may just be alligator repellent.

 We have to be cognizant of the consequences of saying, “Don’t do PD-L1 testing.” Are people going to stop doing other testing? Are they going to equate that we don’t need testing? That’s not the idea. We should be careful about the talk about testing. If you say, “PD-L1 testing probably doesn’t change the treatment with regard to the immunotherapy space,” then I don’t want people to think, “Maybe we can skip testing if we don’t need it right away.” That’s 1 thing that you have to be careful about.

A panel of experts in cancer treatment review the need for PD-1/PD-L1 testing for immunotherapy. 

Significance of PD-L1/PD-1 Testing in NSCLC

Gilberto, in your neck of the woods, to your patients and to your health care system, what are the pharmacoeconomic considerations for I/O [immuno-oncology] therapy?

 Without a doubt, I/O includes and increases cost. In terms of formal cost-effectiveness evaluations, these have been better than what we see in marketing, but they’re still in place for settings where cost is a bigger issue. I/O therapy is still not cost effective, but depending on the trial and the competitor medication used, I/O is considered cost effective in many situations. Having said that, as an IV [intravenous] drug, as long as it’s FDA approved, it’s included in formulary. Usually we don’t have a big issue in terms of access to I/O at the University of Miami Health System Cancer Center, but in our community hospital and our county hospital, that’s an issue sometimes—in particular for situations where the benefits are relatively smaller. We sometimes have issues with getting patients access to it. Sometimes we’re able to get patients assistance programs, but other times we can’t, so it’s an issue in terms of access because of I/O’s high cost in some settings, even in the United States.

 One of the major issues that I struggle with, at least in lung cancer, is the duration of therapy. How much therapy do we need in these patients that have remarkable responses and do well for periods on end? Do they need 2 years of therapy? I don’t know what the literature says in melanoma or other tumors, but they seem to have shorter durations and get away with it.

 It’s beyond 2 years—is that too much? But then when you reach 2 years of therapy, we’re still angst ridden about whether to stop at 2 years. That’s an empiric process. It’s very common to treat beyond 2 years because you don’t know.

 It’s hard to make patients stop. It’s lung cancer we’re talking about, so in melanoma, it’s interesting that there are data that aren’t randomized, but some data suggest that if you get a CR [complete response] and you treat beyond 6 months with a CR, you’re safe to stop. In lung cancer, we don’t have a lot of data. We have small subsets of the clinical trials that have reached 3 to 5 months and sometimes a little longer. But in melanoma there’s a consensus, especially if you have a very good response for a CR, that you could stop therapy at about a year or so. In lung cancer, I don’t know. I have trouble making my patients stop therapy at 2 years.

It’s funny because most of my patients are very comfortable stopping and after seeing very small data sets, the KEYNOTE-024 update at ESMO [European Society for Medical Oncology Congress] last year reassured me that you can always start therapy again. But if you believe in the immunity cycle and you induce an immune response, your immune system should be able to generate memory in a continued immune response, and that’s what we’re seeing with these people who have long durations of therapy. My greatest success story is a lady with second-line small cell cancer whom I gave nivolumab-ipilimumab chemotherapy to. She developed grade 3 hepatitis, so I stopped therapy. She was pretty much a CR, she resolved. She was fine, she felt fine, and her scans looked great. I said, “Why do we have to risk it and restart?” That was 2 years ago, and she’s still without progression of disease 2 years later. Yeah, she progressed right after 4 cycles of platinum-etoposide, so she had a resistant small cell cancer, and here we are.

 There’s no question. It gets to a point, which you made earlier, that’s different from when patients say, “I’ve achieved a good response on osimertinib [Tagrisso], so can I stop now?” And you say, “No, because”—saying this isn’t the same as the sustained responses that you can get after stopping. A fraction of patients can do well, for years, after stopping therapy—there’s no question—but the question has to do with that fraction of patients, who are doing well post-therapy, and it’s 3, 4, 5 years higher if they were still on therapy. We know that some patients do well, and some will respond if you rechallenge that they need it, but the response rates are less than 50% when you do that. It’s a half-empty, half-full situation. It’s a question of whether more patients could have done better continuing therapy. We don’t want to “overtreat” people who don’t need it, but we don’t want to undertreat either. That’s a question for the next generation of trials: with a patient cutting back on 2 years of therapy, can they do just as well? Can you do less frequent immunotherapy as a booster, as they did with the rituximab [Rituxan] studies? At this point, we just don’t have those data, and we’re left with patient discretion and individual judgment with the doctors. I have a lot of patients who are more like Gilberto mentioned: they’re reluctant to keep going if they’re tolerating therapy.

Gilberto Lopes, MD, Jack West, MD, and Mark Socinski, MD, provide their insight on the pharmacoeconomic considerations for immunotherapy.

Pharmacoeconomic Considerations for Immunotherapy

 I’ll ask Gilberto to give us a brief overview of I/O [immuno-oncology] options in this setting and explain the impact that it’s had on the standard of care. It’s changed everything in the first-line setting.

 Absolutely. When we look back 10 years, when we had median survivals of less than 10 months without chemotherapy, and 10 to 12 months with chemotherapy, without a doubt that we have much better situation today. That started with the target agents EGFR, ALK, and so on. But for the majority of patients we still don’t have target agents. Chemotherapy plus immunotherapy has become the standard of care for patients that don’t have a PD-L1 equal to or greater than 50%. In that specific subpopulation, we now have the option of using immunotherapy alone, and we’ve already alluded to the 3 approved drugs: imatinib [Gleevec], atezolizumab [Tecentriq], and pembrolizumab [Keytruda]. As you mentioned, Mark, I’d be very comfortable using any of those. I tend to use pembrolizumab more than anything else in that situation, because we’ve been using it from the beginning and it was the first agent to be approved in that specific subpopulation. We also have questions in terms of using pembrolizumab in the earlier settings, but I’m not going to discuss that too much. We now have IMpower110 trial data suggesting that there’s a benefit, at least in disease-free survival, in patients who are PD-L1 1% or more and especially 50% or more. I’d be very comfortable using atezolizumab for patients in the advanced setting, who express PD-L1 at 50% or greater. I’m waiting for the approval to start pushing for patients with 1% or greater. I don’t think I’ll use it for patients that don’t express any PD-L1.

 It’s important for our audience to know, and it’s something that all of us probably see on a weekly basis in our practices, but we never saw these patients who would have these deep responses that would last for years. I’m sure all of us can tell stories, and some people that I thought didn’t have a very good prognosis and were quite sick with I/O therapy—either alone or with chemotherapy—get through 2 years. Every time I see them in the third year to get a scan every 3 months, I’m keeping my fingers crossed, but things are holding up and people are doing well. We didn’t see that before.

 What’s remarkable is a few things: No. 1, we have a bunch of targets and therapies for nonsmokers with an adenocarcinoma, but we had 10, 15 years without very much to suggest for people who didn’t fit that demographic. Some patients have a driver mutation with a smoking history, and even somewhat squamous, but not most. Too many of our breakthroughs are great news for the same sliver of patients, but this is something that’s applicable to a big, broad swath of patients. If you’re practicing in Kentucky, you see a ton of patients who can benefit from these therapies, whereas you don’t see that many Asian nonsmokers, as we do in California or up and down the West Coast. That’s great, and it’s common, in addition to the 28% to 30% of patients with high PD-L1, and immunotherapy combined with chemotherapy benefits other patients too. You’re talking about a big population of patients who have the potential to redefine what we thought was possible for metastatic cancer and get in a realm similar to what we’ve seen with targeted therapies that blew our minds 10 to 15 years ago.

I love targeted therapies—don’t get me wrong, they’re highly effective—but I don’t view them necessarily as curative. But I’m beginning to think that we might be curing some of these patients who we were all trained to believe weren’t curable. It’s very different. Dr Barzi, I want to invite you back into the conversation and get your perspective on the general concept of immuno-oncology in GI [gastrointestinal] tumors. Where do you use it? What are your thoughts? Has it been as impactful as you hear the lung cancer crowd endorse its impactfulness? What are your thoughts?

 Unfortunately, it hasn’t been as impactful in GI as it’s been in lung cancer—with the exception of HCC [hepatocellular carcinoma] or liver cancers—and it probably has changed its standard of care. In other parts of GI, not so much, but in MSI [microsatellite instability]–high site-agnostic cancer—remember, the approval for pembrolizumab for MSI-high is site agnostic—that’s the meaning of tumor biology. It’s the tumor biology that drives the outcome, regardless of where the site is. I always say that’s as close to a cure as we get. For these are patients who I’ve treated, when I get to 2 years, I stop their treatment. You still see things on their imaging, but they do fine and I don’t think we’ve seen, in oncology, at least in my area, the term of cure without surgery. Now we’re seeing that. That’s remarkable, and we shouldn’t forget about it. When you look at the immuno-oncology in other fields, immuno-oncology has a footstep in every cancer—solid or liquid—that we look at. Many trials have established their efficacy, many with guidelines. Even in small diseases—rare diseases by guideline case studies, case cohorts, or smaller studies—there isn’t an area of oncology that you look at and can’t see a footstep of some form of immuno-oncology.

Experts in cancer care management review PD-1/PD-L1 immunotherapy for patients with NSCLC and GI cancers.

Impact of Immunotherapy on Standard of Care for NSCLC and GI Cancers

 We need to distinguish between a cosmetic improvement in something that’s remarkably less expensive, and notably so, a game changer. A treatment coming in as a second or much later entrance in the EGFR market and still being 85% or 90% the cost, isn’t going to be enough to displace our general, strong affinity for osimertinib [Tagrisso].

One of the hats I continue to wear is the cochair of what used to be the Oncology Pathways

 Camidgeand I cochair the lung committee, and Elsevier asked us to make a decision about 1 pathway choice, based first on efficacy, second on toxicity, and third on cost. I can think of at least 3 instances in which we couldn’t differentiate a lung cancer treatment based on efficacy or toxicity, but we made a decision based purely on cost. Sometimes the cost difference was only 6%, in the case of 1 of the immunotherapeutic agents. But in 1 of the driver subsets, there was a 50% difference in the cost of the 2 drugs that were in the class.

One of the drugs came first, and that was on the pathway, so we took it off the pathway because when the other drug was approved, it was priced 50% less. It was priced 50% less because in addition to the indication we were considering, the drug also had a second indication in lung cancer. Maybe our lung cancer people can figure out which drugs I’m talking about, but the drug was priced more to compete with drugs in the other driver subsets vs the driver subset that only had a single drug in that setting.

The point is that these costs can influence pathway decisions or guideline decisions in this setting. Let me ask my 2 friends, Jack and Gilberto—I often use this as an example in the high PD-L1 expressors. Let’s assume this agent was approved in the United States. They need your recommendation. You see a patient with exon 19, and your recommendation is to give osimertinib as your first-line choice. Two days later, your office calls you, or your clinic calls you, and says, “The patient’s insurance company doesn’t cover osimertinib, but it does cover aumolertinib.” Knowing what we know now, would you say, “That’s not acceptable. We have to fight this because osimertinib is a better drug.” Or would you say, “The patient will be financially better off sticking with their insurance payer’s choice”?

 This is a discussion I would definitely have with the patient. Without a doubt, I’d be more comfortable once we see overall survival data. But if the option is between getting aumolertinib vs gefitinib plus erlotinib, I’d be very happy going with aumolertinib if we can’t get osimertinib.

I agree. There are things we would love to have, to be as comprehensive as possible, and there are things we do because it’s a preference. I—and I suspect both of you do as well—generally use pembrolizumab [Keytruda] in first-line setting for high PD-L1. I haven’t used atezolizumab [Tecentriq] or cemiplimab [Libtayo] in this setting. The data look very comparable, but why would I change? It has to break a pattern, and there hasn’t been a reason not to. If an insurance company says that it’s significant and that they’re going to cover 1 but not the other, I’m not going to die on that yolk. That’s fine.

 I’m not going to do that peer-to-peer call as well.

 We’ve taken the path of least resistance, and using the cemiplimab where the atezolizumab vs the—

 Exactly. If a company doesn’t necessarily have to be 50% less expensive, if it’s enough that a company or an insurer will intervene and say, “We preferentially use 1 but not the other,” then I’ll say it works for me. That’s good enough.

I’ve used that example specifically in the high PD-L1 space, and there’s an opportunity for some price disruption. We’ll see if it happens because we know that there are other PD-1, PD-L1 compounds coming in the future.

A panel of experts discuss treatment options based on efficacy and out-of-pocket cost for patients.

Place for EGFR Agents and Comparison of Costs 

Gilberto Lopes, MD, a medical oncologist at the Sylvester Comprehensive Cancer Center, University of Miami Health System, discusses findings from the KEYNOTE-042 trial of frontline treatment with pembrolizumab (Keytruda) for patients with squamous and nonsquamous non—small cell lung cancer in an interview with 

KEYNOTE-042 assessed the efficacy of pembrolizumab versus standard chemotherapy in patients with PD-L1 expression with a tumor proportion score of 1% or greater. This trial was designed for patients with either squamous or nonsquamous histology, as well, Lopes explains. The primary endpoint was overall survival (OS) which was tested sequentially for those with either PD-L1 expression of 1% or greater, 20% and greater, and 50% and greater. OS was improved across subgroups. In addition, progression-free survival was not positive at this interim analysis. The duration of response with pembrolizumab, he adds, was improved in all subgroups.

Combinations of chemotherapy and immunotherapy have also demonstrated improvements in survival outcomes for patients with NSCLC. Lopes advises that patients with high-volume disease and low PD-L1 expression should receive the combination regimen, while those with low-volume disease and high PD-L1 expression are appropriate candidates for pembrolizumab monotherapy.

Gilberto Lopes, MD, a medical oncologist at the Sylvester Comprehensive Cancer Center, University of Miami Health System, discusses findings from the KEYNOTE-042 trial of frontline pembrolizumab (Keytruda) as a treatment for patients with squamous and nonsquamous non–small cell lung cancer in an interview with OncLive during the 2018 ASCO Annual Meeting.

Gilberto Lopes, MD

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