Tyrosine kinase inhibitor
Pharmaceutical drugWikipedia
125
MENTIONS
33
EPISODES
22
PODCASTS
Search complete. 125 mentions across 33 episodes found for "Tyrosine kinase inhibitor".
Sep 12, 2026
Neil LoveHOST
So I want to get into some of the clinical issues that come up in daily practice.
Neil LoveHOST
And one thing you were commenting on, and I'm not sure, I'd be curious whether or not you feel that typically general medical oncologists are aware of it, the fact that some patients in initial diagnosis of chronic fake CML don't fit into sort of the pattern you would expect in terms of excellent response to TKIs.
Neil LoveHOST
You said that 2% or 3% of patients actually should be prepared for early transplant.
Neil LoveHOST
What specific abnormalities are you talking about? And do you think that these are picked up in the community?
Andreas HochhausGUEST
Therefore, I don't ask for an NGS in all the patients.
Andreas HochhausGUEST
We do it in clinical trials, but in the community, it's not mandatory.
Neil LoveHOST
So let's talk a little bit about the mechanism of action of the available TKIs, and also you mentioned some new developments or new strategies, combinations, et cetera.
Neil LoveHOST
First of all, can you talk a little bit about the way you conceptualize the mechanism of action of the first and second generation TKIs, and then how, at a molecular level, siminib is fundamentally different?
Neil LoveHOST
I want to get into some of the clinical issues that come up in daily practice.
Neil LoveHOST
And one thing you were commenting on, and I'm not sure, I'd be curious whether or not you feel that typically general medical oncologists are aware of it, the fact that some patients in initial diagnosis of chronic fake CML don't fit into sort of the pattern you would expect in terms of excellent response to TKIs.
Neil LoveHOST
You said that two or three percent of patients actually should be prepared for early transplant.
Neil LoveHOST
What specific abnormalities are you talking about? And do you think that these are picked up in the community?
Andreas HochhausGUEST
Therefore, I don't ask for an NGS in all the patients.
Andreas HochhausGUEST
We do it in clinical trials, but in the community, it's not mandatory.
Neil LoveHOST
So let's talk a little bit about the mechanism of action of the available TKIs, and also you mentioned some new developments or new strategies, combinations, et cetera.
Neil LoveHOST
First of all, can you talk a little bit about the way you conceptualize the mechanism of action of the first and second generation TKIs, and then how, at a molecular level, siminib is fundamentally different?
RachelHOST
Like who would have thought? And not just
CandiceHOST
the TKIs.
CandiceHOST
But the Bruton kinase inhibitors that are for people with MCAS, so it's not working on the SM pathway, but really shutting down that overactivation of the mast cell through this other...
CandiceHOST
this other pathway, which I think is so amazing.
14 MINS LATER
RachelHOST
But I I've been in all three and I I swear there's been actual things that I've like I've seen literal change, like change.
RachelHOST
We didn't used to call SM a cancer.
RachelHOST
And I think some of the conversations that took place in the first and second Heroes Summit really may have had an impact on how the TKIs coming out were marketed.
RachelHOST
And that really helped change the way that that's framed.
Wade T. IamsHOST
I'm the Director of Lung Cancer Research at Tennessee Oncology in Nashville, Tennessee.
Wade T. IamsHOST
Welcome to this podcast that's called Management of Adverse Events Associated with MET TKIs in Patients with Advanced Non-Small Cell Lung Cancer.
Wade T. IamsHOST
hosted by Targeted Oncology.
Wade T. IamsHOST
And we're going to be discussing safety considerations specifically for met TKIs, tapotinib and catmetinib in particular is going to be our focus for this discussion.
Wade T. IamsHOST
We'll talk about safety considerations generally and in the context of switching and end with a couple of patient cases.
Wade T. IamsHOST
So I'll turn it over to my colleague, Dr. Flores.
Wade T. IamsHOST
So the epidemiology here is key.
Wade T. IamsHOST
And as we all know, in oncology, next generation sequencing is really the technology that's opened the door for all these therapeutic advances.
Neil LoveHOST
So I want to get into some of the clinical issues that come up in daily practice.
Neil LoveHOST
And one thing you were commenting on, and I'm not sure, I'd be curious whether or not you feel that typically general medical oncologists are aware of it, the fact that some patients in initial diagnosis of chronic fake CML don't fit into sort of the pattern you would expect in terms of excellent response to TKIs.
Neil LoveHOST
You said that 2% or 3% of patients actually should be prepared for early transplant.
Neil LoveHOST
What specific abnormalities are you talking about? And do you think that these are picked up in the community?
Andreas HochhausGUEST
Therefore, I don't ask for an NGS in all the patients.
Andreas HochhausGUEST
We do it in clinical trials, but in the community, it's not mandatory.
Neil LoveHOST
So let's talk a little bit about the mechanism of action of the available TKIs, and also you mentioned some new developments or new strategies, combinations, et cetera.
Neil LoveHOST
First of all, can you talk a little bit about the way you conceptualize the mechanism of action of the first and second generation TKIs, and then how, at a molecular level, siminib is fundamentally different?
Steve HarrisonGUEST
And because this type of...
Steve HarrisonGUEST
this type of exon 19 deletion has a treatment, a TKI inhibitor, osminotib, or commonly known as Tigriso.
Steve HarrisonGUEST
So he suggested that I go with, there was a study done, I think it was called FLORA2, and he suggested we follow that protocol because it has the highest success rate rather than just doing one versus the other.
Steve HarrisonGUEST
So once I had that diagnosis, that was kind of the treatment he suggested, and that's the treatment that I followed.
Solange PetersGUEST
So if you have a patient with brain mets, you will have a slightly more confidence to give adagracib as compared to sotiracib because you have data in untreated brain mets.
Solange PetersGUEST
And that's what I want to stress, comparing against lorlatinib and all the other TKIs we know for oncogene addiction.
Solange PetersGUEST
So brain efficacy, by the way, is not so fantastic, right? The intracranial response rate in untreated brain mets is not 60%, it's 20, 30%.
Solange PetersGUEST
So we still need to learn about these compounds, right? A bit more data for adagracib and sotoracib in the brain, but still not fantastic results.
Solange PetersGUEST
So if you have a patient with brain mets, you will have a slightly more confidence to give adagracib as compared to sotoracib because you have data in untreated brain mets.
Solange PetersGUEST
And that's what I want to stress, comparing against lorlatinib and all the other TKI's we know for oncogene addiction.
Solange PetersGUEST
So brain efficacy, by the way, is not so fantastic, right? The intracranial response rate in untreated brain mets is not 60%.
Solange PetersGUEST
It's 20, 30%.
31 MINS LATER
Solange PetersGUEST
And we're really looking forward to see this data stratified and properly collected.
Solange PetersGUEST
Because still, it's not lorlatinib, right? We need to see the magnitude of efficacy of this drug in the brain because it's not going to be perfect.
Solange PetersGUEST
It's going to be something between lorlatinib and nothing, right? It's not going to be impeccable as we expect for TKI's in the past.
Solange PetersGUEST
So this is all the things.
Solange PetersGUEST
So if you have a patient with brain mets, you will have a slightly more confidence to give adagracib as compared to sotoracib because you have data in untreated brain mets.
Solange PetersGUEST
And that's what I want to stress, comparing against lorlatinib and all the other TKI's we know for oncogene addiction.
Solange PetersGUEST
So brain efficacy, by the way, is not so fantastic, right? The intracranial response rate in untreated brain mets is not 60%.
Solange PetersGUEST
It's 20, 30%.
31 MINS LATER
Solange PetersGUEST
And we're really looking forward to see this data stratified and properly collected.
Solange PetersGUEST
Because still, it's not lorlatinib, right? We need to see the magnitude of efficacy of this drug in the brain because it's not going to be perfect.
Solange PetersGUEST
It's going to be something between lorlatinib and nothing, right? It's not going to be impeccable as we expect for TKI's in the past.
Solange PetersGUEST
So this is all the things.
Dana T. AftabGUEST
So cabozantinib was a great story, as is zanzulitinib, which was the, the, the drug that came after it that has a similar target profile.
Dana T. AftabGUEST
Um, you know, we had a belief in that target profile, just the fact that we were hitting more HIF targets than just VEGF, which all the other TKIs seem to, to be focused on.
Dana T. AftabGUEST
Uh, the fact that we were hitting other key targets of HIF that n-no other tyrosine kinase inhibitor was hitting, that to us was compelling biology, right? It had to work.
Dana T. AftabGUEST
Um, and then we got clinical data that showed it does work.
23 more episodes mention Tyrosine kinase inhibitor.
Create an account to see the whole feed, search across every transcript, and follow the entities you care about.