This is a great example of where cancer treatment is headed and why it's so hard - namely that cancer isn't one disease, it's many thousands of diseases.
This is a drug that targets lung cancer (~12% of cancers) and only one type of lung cancer (non-small cell lung cancer, ~80% of cases). It targets a particular mutated gene that occurs in about 30% of that subtype. And then, about 50% of those patients respond.
So do that math, and you end up seeing that treating one of the most common mutations in one of the most common cancers with what is considered very high efficacy still only helps with about 1.4% of all cancers. This is actually an enormous number for this kind of treatment, and there is a long tail of rare cancers that are going to be much harder to find targeted therapies for.
That all said, this currently appears to be an enormous success story, and the kind of treatment options that have been enabled by genomic sequencing of cancers, followed by many years of drug development and clinical trials. It's fantasically exciting to see us continue to chip away at the problem but by bit and grant people longer lives as a result!
Just because this approach works doesn't mean this is the only approach out there. I sincerely believe that this thought has singlehandedly retarded progress towards more generic cancer treatments. Immune checkpoint inhibition is a clear proof that you could make one drug that could attack a wide swathe of cancers. Heck even chemo is proof of that. If this is the research you want to focus on, please go ahead. But don't tell the public the continuous half truth that every cancer is unique with no commonality with any other cancer. They all literally share the same DNA, they can't be that different. Consider the possibility that the entire cancer research community is just too dumb to discover globally effective drugs. Unless you can mathematically prove its impossibility I'll say let's not make that statement.
Signed, a guy who spent most of his PhD studying cancer.
You’re both kinda right, personalized or targeted cancer therapy is definitely an incredibly promising field and the early results in various cancers are promising. Most notably in disseminated disease.
Simultaneously, one of the largest criticisms of osimertinib in resectable NSCLC has been that some oncologists got overexcited about the DFS results and patients have been unfortunately not receiving the traditional standard of care adjuvant therapy (old school platinum based drugs) which have a proven overall survival benefit (until today osimertinib did not, it now possibly does).
Targeted gene-directed therapy is cool but conventional chemotherapy is still really important.
Why shouldn't he tell the public that every cancer is unique? It's technically true, much in the same way it's technically true you studied cancer but have for years been working with entirely unrelated fields to the advancement of cancer research. You're as much of an authoritative figure on this topic as a random person on the street.
Do you mean this literally or figuratively? Isn't one of the serious problems with tumors that the mutation rate inside them goes through the roof? (And then they eventually figure out how to be metastatic?)
Isn't there a high chance that research aimed at one type of cancer will end up transferrable to other types? Either the actual treatment/drug, or at least the methods and approaches to designing the treatment.
Agreed! This specifically is for adjuvant osimertinib for EGFR+ Stage IB–IIIA completely resected NSCLC.
The headline here is really strong -- and the actual abstract is much more sober: "5-year OS rate was 88% with osimertinib vs 78% with placebo" [Full abstract is here: https://meetings.asco.org/abstracts-presentations/219805 ]
P.S. Hi Chris! (I think I picked up a summer student from you last week!)
Think about that... If the committee whose job is approving this medicine get results in on Friday, but don't sit down to approve it till the following Monday, then 4098 people die unnecessarily.
It always surprises me how little effort we put into getting things from the lab to the people quicker.
As soon as we have compelling data some discovery (medical or otherwise) might help lots of people, it should be almost a manhattan project type effort to get it into the hands of everyone worldwide asap.
Not sure if you're specifically referring to the drug in this article but osimertinib has been FDA approved for ~8 years and has been part of routine clinical practice for quite a while now.
The system is actually really fast at getting promising cancer therapies into the hands of patients, especially when there aren't good alternatives.
Even if something isn't yet approved and the patient is ineligible for a clinical trial, an intervention can be offered to patients under compassionate grounds/special access.
the FDA face an unenviable challenge: how to promote healthcare innovation without endangering patients?
regulations that are too loose may cause suffering and death while regulations that are too strict will delay or block prevent helpful treatments.
regulating healthcare is extremely difficult and largely a thankless job.
one solution is to approach national healthcare like national security and let people volunteer for treatments like volunteering for the army.
in short, overstate risks but let patients decide.
adopt cigarette-simple consent forms that state in bold words that an experimental treatment is likely to cause death or crippling side-effects like paralysis, blindness, stroke, Alzheimer's, or worse.
perhaps require multiple signatories from family members to guard against irrational behavior.
this protects the FDA while minimizing barriers to innovative therapies and treatments.
Although that is suspiciously large. Looking at the numbers I think it should be much lower. A 51% reduction doesn't mean it helps 51% if the people. In this case it looks like about 10% of the people are effected given the 88% vs 78% survival rates, right? Maybe something like .28% of all cancer?
These are ballpark numbers to be sure, and yeah, my off the cuff comment didn't get that exactly right. I also simplified things quite a bit to try to get the broader point across - Thanks for following up!
I mean, the people who die of cancer are the problem. If 88% survive instead of 78%, 55% of those who would have died survived (taking these numbers just from your comment).
The way forward then seems to be personalized therapy for each case. There have been some limited trials with CRISPR that look promising, but mainstream adoption is still likely years away.
Personalized therapy might possibly not work for a really long time. Consider each drug to be a code change at heart of the most critical code running the code of your body. Clinical trials are the integration testing and ab testing equivalent of making sure this change doesn't have side effects. Personalized therapy means you have no way of testing in a comparable system. Unless you're gonna clone babies of yourself give them the same cancer and see if it treats them and doesn't kill them (and then pull a Prestige)
My mother in law has stage 4 lung cancer. Tagrisso is extending her life. The cancer has been shrinking since going on it with few side effects.
Unfortunately stage 4 cannot be cured, and at some point tagrisso stops working. My understanding is the cancer mutates and eventually develops resistance. Then she will go on chemo and her quality of life will go down.
I am thankful for modern medicine that we get some extra time with her.
My father is in this situation with prostate cancer. First line therapies have stopped working and now its on to chemo. I am hoping chemo won't damage him too much.
There are also radioligand therapies like lutetium 177 but they haven't been sequenced on chemo naive patients yet. So soc is chemo first.
I wasn’t involved in this study but the cancer center I just left was one of the sites for the upfront Lu177 vs chemotherapy trial. Speaking casually with the physician involved recently he said the results weren’t promising thus far.
I don’t think this is published yet and I’m not familiar with prostate ca treatment literature so take this with a grain of salt.
The really crappy part of lung cancer is that it's very uncommon to detect it because there aren't really any symptoms to speak of.
Eventually it will metastasize so some other part of the body and THAT will give symptoms.
When my Mum was diagnosed the Dr. said the bad news is you have cancer in the bones in your neck. The really bad news is that it started in your lungs, and it's way, way to far along to do anything about.
Not really. Lung cancer is mostly due to smoking or radon. So don’t smoke and get your house tested.
Outside of that, it’s a crap shoot. My mom in law didn’t have either risk factor. PET scans can pick up but each one exposes you to radiation which can also cause cancer. So they generally don’t screen for low risk patients.
My mother is on what sounds like a similar pill (in result, if not mechanism of action) for a different cancer. Had a poor prognosis, genetically tested several times and after a few rounds of conventional chemo the test indicated she could take a daily pill. It’s wonderful, I’m so glad she is alive for her grandchild, for me, and for herself of course. I think she will probably still die “of” her cancer but at this point it has completely stopped the progression of it for several years. The side effects are a bit weird, and a bit bad, but not even THAT bad. Really came out of the blue for us, an unexpected outcome.
I’m writing this live from the ASCO meeting where this was just presented. Osimertinib (TAGRISSO) has truly transformed the way we treat EGFR-mutant NSCLC, having repeatedly redefined standards of care. I don’t have a source handy, but osi used to hold a record in oncology as being the fastest drug to go from IND (trial-enabling) to approval - less than 18 months.
Osimertinib did $5.44B in global sales last year, leading AstraZeneca’s oncology portfolio [0]
"After five years, 88% of patients who took the daily pill after the removal of their tumour were still alive, compared with 78% of patients treated with a placebo. Overall, there was a 51% lower risk of death for those who received osimertinib compared with those who received placebo."
So 88% instead of 78% without the pill were still alive five years on. I assume that is the maximum range they could test. How was the 51% then calculated?
Edit: thank you all for the explanation. That makes a lot of sense!
If 22% of patients in the placebo group died, and 12% in the test group, then that's a reduction of 1 - (12/22) = 45% in the risk of death over that time interval.
The true value could easily be 51% if the percentages reported in the Guardian were rounded.
You could subtract both percentages by the baseline average risk of death for 5 years at the age group that people are most likely to get this type of cancer.
The article makes the assumption that those that took the placebo represent the typical post removal patient (an assumption).
So, for 100 untreeated patients 22 would die. Now for these 100 placebo patients, if they took the pill, they would die 12 (another assumption that the two populations are the same).
The reduction is (22-12) / 22 = 10/22 is the risk of death if untreated.
The complementary percentage is
12/22 approx 51%.
However this does not come with confidence intervals.
If you think about the numbers as 12% died vs 22% died, then the 51% intuitively makes more sense, although I don’t know if this is the correct explanation. My guess is that 12 and 22 are rounded numbers.
I actually think the other explanations are wrong. They are probably reporting the Hazard Ratio, which is more often used as primary outcome for efficacy of drug than 5 year survival. (See for example: https://en.wikipedia.org/wiki/Hazard_ratio)
The hazard ratio, under some assumptions, tries to estimate the relative risk of dying per unit of time. The benefit of this measure is that there is not some artificial cutoff (the difference between a death at 4 years and 364 days and 5 years and 1 day is neglible).
The pricing of drugs is always weird to me. Is there a good book / article / primer on why a drug can cost the price of a good house per person ? Is it just about recouping R&D, does manufacturing requires very rare raw materials, is the bill going up because of regulation, etc... ?
How big a check would a government have to do to just "buy" the rights to a drug ? (Both in the "legal" and in the "an offer the CEO can't refuse" version ?)
All of the above, but my guess would be that the most expensive part is usually running the phase III clinical trial. You have to pay data managers to perform the randomization, train doctors and nurses to administer it, and the hospital for the added time it takes them to run the trial, pay the statisticians that perform the analysis, an agency that helps prepare the application, etcetera. You have to recruit patients, gather informed consent (though that is sometimes done by doctors and nurses). Also, you have to give the drug for free, since insurance companies do not cover experimental drugs. Sometimes patients also receive a fee for participating in the trial. All in all, the median cost of pivotal trials is 50 million dollars. This is the cost after you already did studies to discover the drug, and determine the dosage. Half of these trials fail, and all the previous investments are lost in that case.
the pricing is partially due to a lack of collective negotiation
the government programs carry a lot of weight as a large client but are currently barred from negotiating on prices
part of some US universal healthcare proposals are to just allow existing government programs to negotiate on prices, while simultaneously extending coverage to more people
It costs about $7000 in Europe (the price seems to be similar in different country even though there is no EU wide collective negotiation).
The price in the US seems to be around double in the US. But maybe that just pharma companies do PPP adjusted pricing? e.g. it seems to cost ~1500 in India for instance. Americans are simply much richer and also significantly more on healthcare than people in other countries.
According to the CDC, 80-90% of lung cancer deaths are linked to cigarette smoking (1). It seems like a simple solution for people to just not smoke...
'Nicotine releases a chemical called dopamine in the same regions of the brain as other addictive drugs. It causes mood-altering changes that make the person temporarily feel good. Inhaled smoke delivers nicotine to the brain within 20 seconds, which makes it very addictive—comparable to opioids, alcohol and cocaine. This "rush" is a major part of the addictive process.
'When the person stops using tobacco, nicotine levels in the brain drop. This change triggers processes that contribute to the cycle of cravings and urges that maintains addiction. Long-term changes in the brain caused by continued nicotine exposure result in nicotine dependence, and attempts to stop cause withdrawal symptoms that are relieved with renewed tobacco use.'
The data isn’t published yet (presumably this was shown during the ASCO conference this weekend) but this is a bit misleading and the results seem underwhelming.
The DFS numbers are not new and known, the reason this is in the news as it’s the first report of OS numbers from the initial ADAURA trial.
I can’t be definitive without seeing the data yet but:
1. Osimertinib is not that new, in the context of curative intent disease (i.e. resectable stage II-IIIA) it is currently (ideally) used post adjuvant chemotherapy (the only treatment to date with an overall survival benefit).
We need clarification on what the placebo arm is and what the subgroup analysis showed. What it should be (and presumably) is an “active surveillance protocol” where patients underwent short course adjuvant platinum based therapy and then followed with imaging. Recurrences are then treated with systemic or locoregional therapy.
As this is an update of the ADAURA trial we know that only 40% of patients received the standard of care platinum adjuvant therapy, this article claims an OS benefit was seen in all groups but we don’t have the numbers for the subset of patients who received appropriate adjuvant treatment.
2. Main criticism of the ADAURA trial thus far has been that the results only report “disease free survival”, while that intuitively makes sense as a metric what we really care about is “overall survival”. There are several reasons but to keep it simple this is now the third generation tyrosine kinase inhibitor, the first 2 also had DFS improvements (albeit not as dramatic) but failed to show OS benefits.
3. Osimertinib is expensive. Following the ADAURA protocol (3 years of adjuvant therapy) would have an incremental cost (ICER) somewhere around ~$3-450,000 per patient. “Willingness to pay” is variable, in most places it’s $50,000/quality adjusted life year. Some in the US are pushing for this to be ~$190,000/QALY (3x GDP).
Based on extrapolated DFS and earlier OS data in the last year it was estimated that the OS would be around 5-6%, based on this threshold a system would need a willingness to pay of ~$320,000/QALY. Conversely, to meet the GDP threshold above OS would need to be ~20%.
In a recent Canadian economic analysis they modelled 6% OS at 10 years and arrived at a ICER of ~$40,000 suggesting this protocol makes economic sense. To my knowledge this is the first report suggesting cost effectiveness and contradicted the Health Canada modelling.
4. Based on this news article, there was an absolute reduction in OS of 10% at 5 years which seems underwhelming given that we know most of the patients did not receive adjuvant platinum based chemotherapy, the OS in the subgroup that received both treatments is what matters here.
From the US analysis, this would still not meet the willingness to pay threshold. The Canadian one would need to be re-run with 5 year numbers to see what the ICER is.
Overall, it’s potentially a very positive result but at face value the OS numbers seem less impressive than anticipated.
If someone has the $ and an EGFR ex19 mutation there is definitely benefit but it remains unclear whether this is cost-effective for a system vs other treatment options we have.
(N.B. These numbers are approximate from my recollection of the literature but I can dig up references if something seems off. For background I’m a radiologist focused on oncologic imaging, this has been a hot topic in rounds/case conferences for a few years now hence my familiarity.)
I don’t know much about pharmaceutical pricing or drug discovery to offer an informed opinion as to why it’s so expensive ($300/day) or whether that’s justified.
AstraZeneca’s patent expires in 2035 and as a cash cow ($2B in revenue) I would expect they continue to aggressively fight competitors in court.
Imatinib (the 1st gen drug of the same class) went generic a few years ago and is 99% cheaper now.
I assume we’ll see something similar with osimertinib but I can’t comment on whether there’s any secret sauce that makes it different.
Perhaps one of the pharma/biochem HN commenters can offer more insight.
Readit News
This is a drug that targets lung cancer (~12% of cancers) and only one type of lung cancer (non-small cell lung cancer, ~80% of cases). It targets a particular mutated gene that occurs in about 30% of that subtype. And then, about 50% of those patients respond.
So do that math, and you end up seeing that treating one of the most common mutations in one of the most common cancers with what is considered very high efficacy still only helps with about 1.4% of all cancers. This is actually an enormous number for this kind of treatment, and there is a long tail of rare cancers that are going to be much harder to find targeted therapies for.
That all said, this currently appears to be an enormous success story, and the kind of treatment options that have been enabled by genomic sequencing of cancers, followed by many years of drug development and clinical trials. It's fantasically exciting to see us continue to chip away at the problem but by bit and grant people longer lives as a result!
Signed, a guy who spent most of his PhD studying cancer.
Simultaneously, one of the largest criticisms of osimertinib in resectable NSCLC has been that some oncologists got overexcited about the DFS results and patients have been unfortunately not receiving the traditional standard of care adjuvant therapy (old school platinum based drugs) which have a proven overall survival benefit (until today osimertinib did not, it now possibly does).
Targeted gene-directed therapy is cool but conventional chemotherapy is still really important.
ICIs are magic when they work.
Do you mean this literally or figuratively? Isn't one of the serious problems with tumors that the mutation rate inside them goes through the roof? (And then they eventually figure out how to be metastatic?)
The headline here is really strong -- and the actual abstract is much more sober: "5-year OS rate was 88% with osimertinib vs 78% with placebo" [Full abstract is here: https://meetings.asco.org/abstracts-presentations/219805 ]
P.S. Hi Chris! (I think I picked up a summer student from you last week!)
Interested to see their detailed results but I’m mildly suspicious this will be AstraZeneca PR buffing underwhelming results.
Think about that... If the committee whose job is approving this medicine get results in on Friday, but don't sit down to approve it till the following Monday, then 4098 people die unnecessarily.
As soon as we have compelling data some discovery (medical or otherwise) might help lots of people, it should be almost a manhattan project type effort to get it into the hands of everyone worldwide asap.
Deleted Comment
The system is actually really fast at getting promising cancer therapies into the hands of patients, especially when there aren't good alternatives.
Even if something isn't yet approved and the patient is ineligible for a clinical trial, an intervention can be offered to patients under compassionate grounds/special access.
regulations that are too loose may cause suffering and death while regulations that are too strict will delay or block prevent helpful treatments.
regulating healthcare is extremely difficult and largely a thankless job.
one solution is to approach national healthcare like national security and let people volunteer for treatments like volunteering for the army.
in short, overstate risks but let patients decide.
adopt cigarette-simple consent forms that state in bold words that an experimental treatment is likely to cause death or crippling side-effects like paralysis, blindness, stroke, Alzheimer's, or worse.
perhaps require multiple signatories from family members to guard against irrational behavior.
this protects the FDA while minimizing barriers to innovative therapies and treatments.
This actually seems large to me.
Although that is suspiciously large. Looking at the numbers I think it should be much lower. A 51% reduction doesn't mean it helps 51% if the people. In this case it looks like about 10% of the people are effected given the 88% vs 78% survival rates, right? Maybe something like .28% of all cancer?
Unfortunately stage 4 cannot be cured, and at some point tagrisso stops working. My understanding is the cancer mutates and eventually develops resistance. Then she will go on chemo and her quality of life will go down.
I am thankful for modern medicine that we get some extra time with her.
There are also radioligand therapies like lutetium 177 but they haven't been sequenced on chemo naive patients yet. So soc is chemo first.
I don’t think this is published yet and I’m not familiar with prostate ca treatment literature so take this with a grain of salt.
Why would we give higher dose of the cure at start ? Wouldn’t the body handle it ?
Eventually it will metastasize so some other part of the body and THAT will give symptoms.
When my Mum was diagnosed the Dr. said the bad news is you have cancer in the bones in your neck. The really bad news is that it started in your lungs, and it's way, way to far along to do anything about.
Cancer sucks.
https://www.cdc.gov/cancer/lung/basic_info/screening.htm
https://www.uspreventiveservicestaskforce.org/uspstf/recomme...
Do you smoke? quit smoking. Do you live in areas with lots of air polution? High levels of radon where you live? Move.
Do you work with a bunch of carcinogenic chemicals? Find something else to do.
You can also get a gene test do see if you're suspectable to certain cancers.
But most importantly: listen to your body. If you feel that something is wrong, take it up with your doctor.
Outside of that, it’s a crap shoot. My mom in law didn’t have either risk factor. PET scans can pick up but each one exposes you to radiation which can also cause cancer. So they generally don’t screen for low risk patients.
Osimertinib did $5.44B in global sales last year, leading AstraZeneca’s oncology portfolio [0]
[0] https://www.astrazeneca.com/content/dam/az/PDF/2022/fy/Full-...
"After five years, 88% of patients who took the daily pill after the removal of their tumour were still alive, compared with 78% of patients treated with a placebo. Overall, there was a 51% lower risk of death for those who received osimertinib compared with those who received placebo."
So 88% instead of 78% without the pill were still alive five years on. I assume that is the maximum range they could test. How was the 51% then calculated?
Edit: thank you all for the explanation. That makes a lot of sense!
The true value could easily be 51% if the percentages reported in the Guardian were rounded.
So, for 100 untreeated patients 22 would die. Now for these 100 placebo patients, if they took the pill, they would die 12 (another assumption that the two populations are the same).
The reduction is (22-12) / 22 = 10/22 is the risk of death if untreated.
The complementary percentage is
12/22 approx 51%.
However this does not come with confidence intervals.
I actually think the other explanations are wrong. They are probably reporting the Hazard Ratio, which is more often used as primary outcome for efficacy of drug than 5 year survival. (See for example: https://en.wikipedia.org/wiki/Hazard_ratio)
The hazard ratio, under some assumptions, tries to estimate the relative risk of dying per unit of time. The benefit of this measure is that there is not some artificial cutoff (the difference between a death at 4 years and 364 days and 5 years and 1 day is neglible).
Deleted Comment
Deleted Comment
How big a check would a government have to do to just "buy" the rights to a drug ? (Both in the "legal" and in the "an offer the CEO can't refuse" version ?)
[1] https://bmjopen.bmj.com/content/10/6/e038863
the government programs carry a lot of weight as a large client but are currently barred from negotiating on prices
part of some US universal healthcare proposals are to just allow existing government programs to negotiate on prices, while simultaneously extending coverage to more people
The price in the US seems to be around double in the US. But maybe that just pharma companies do PPP adjusted pricing? e.g. it seems to cost ~1500 in India for instance. Americans are simply much richer and also significantly more on healthcare than people in other countries.
(1) https://www.cdc.gov/cancer/lung/basic_info/risk_factors.htm#....
'When the person stops using tobacco, nicotine levels in the brain drop. This change triggers processes that contribute to the cycle of cravings and urges that maintains addiction. Long-term changes in the brain caused by continued nicotine exposure result in nicotine dependence, and attempts to stop cause withdrawal symptoms that are relieved with renewed tobacco use.'
https://www.camh.ca/en/health-info/mental-illness-and-addict...
The DFS numbers are not new and known, the reason this is in the news as it’s the first report of OS numbers from the initial ADAURA trial.
I can’t be definitive without seeing the data yet but:
1. Osimertinib is not that new, in the context of curative intent disease (i.e. resectable stage II-IIIA) it is currently (ideally) used post adjuvant chemotherapy (the only treatment to date with an overall survival benefit).
We need clarification on what the placebo arm is and what the subgroup analysis showed. What it should be (and presumably) is an “active surveillance protocol” where patients underwent short course adjuvant platinum based therapy and then followed with imaging. Recurrences are then treated with systemic or locoregional therapy.
As this is an update of the ADAURA trial we know that only 40% of patients received the standard of care platinum adjuvant therapy, this article claims an OS benefit was seen in all groups but we don’t have the numbers for the subset of patients who received appropriate adjuvant treatment.
2. Main criticism of the ADAURA trial thus far has been that the results only report “disease free survival”, while that intuitively makes sense as a metric what we really care about is “overall survival”. There are several reasons but to keep it simple this is now the third generation tyrosine kinase inhibitor, the first 2 also had DFS improvements (albeit not as dramatic) but failed to show OS benefits.
3. Osimertinib is expensive. Following the ADAURA protocol (3 years of adjuvant therapy) would have an incremental cost (ICER) somewhere around ~$3-450,000 per patient. “Willingness to pay” is variable, in most places it’s $50,000/quality adjusted life year. Some in the US are pushing for this to be ~$190,000/QALY (3x GDP).
Based on extrapolated DFS and earlier OS data in the last year it was estimated that the OS would be around 5-6%, based on this threshold a system would need a willingness to pay of ~$320,000/QALY. Conversely, to meet the GDP threshold above OS would need to be ~20%.
In a recent Canadian economic analysis they modelled 6% OS at 10 years and arrived at a ICER of ~$40,000 suggesting this protocol makes economic sense. To my knowledge this is the first report suggesting cost effectiveness and contradicted the Health Canada modelling.
4. Based on this news article, there was an absolute reduction in OS of 10% at 5 years which seems underwhelming given that we know most of the patients did not receive adjuvant platinum based chemotherapy, the OS in the subgroup that received both treatments is what matters here.
From the US analysis, this would still not meet the willingness to pay threshold. The Canadian one would need to be re-run with 5 year numbers to see what the ICER is.
Overall, it’s potentially a very positive result but at face value the OS numbers seem less impressive than anticipated.
If someone has the $ and an EGFR ex19 mutation there is definitely benefit but it remains unclear whether this is cost-effective for a system vs other treatment options we have.
(N.B. These numbers are approximate from my recollection of the literature but I can dig up references if something seems off. For background I’m a radiologist focused on oncologic imaging, this has been a hot topic in rounds/case conferences for a few years now hence my familiarity.)
AstraZeneca’s patent expires in 2035 and as a cash cow ($2B in revenue) I would expect they continue to aggressively fight competitors in court.
Imatinib (the 1st gen drug of the same class) went generic a few years ago and is 99% cheaper now.
I assume we’ll see something similar with osimertinib but I can’t comment on whether there’s any secret sauce that makes it different.
Perhaps one of the pharma/biochem HN commenters can offer more insight.