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The second-generation TKIs dasatinib and nilotinib are increasingly being used as frontline therapy for CML; this expert gives imatinib only to patients with co-morbidities.
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Highlights
The second-generation TKIs dasatinib and nilotinib are increasingly being used as frontline therapy for CML; this expert gives imatinib only to patients with co-morbidities. (Analyst note: imatinib is still used frontline in the community setting, so this prescribing trend will need time to spread beyond research centers.)
Despite cardiac safety concerns, ponatinib has a major role in treating refractory/relapsed CML patients, especially those with the T315I mutation, and future directions will include mitigating risk in ponatinib patients.
A future research push in CML is complete disease elimination in patients with minimal residual disease following TKI treatment. FLT-3 inhibitors in clinical trials (e.g. quizartinib, crenolanib, midostraurin) benefit AML patients with an FLT-3 mutation. Sorafenib (branded as Nexavar; approved for other indications) is widely used off-label for AML patients, both in the research and community settings, and third-party payers frequently cover it.
Oral hypomethylating agents (e.g. oral azacitidine) are not a major advance over IV versions for AML and MDS but are an easier way to provide extended therapy; reimbursement of branded oral hypomethylating agents will play an important role in uptake.
Gazyva is possibly more efficacious than other anti-CD20 antibodies and will eventually gain widespread usage, but physicians are accustomed to using rituximab and will only gradually switch patients over.
In the future, regimens including ibrutinib and idelalisib may come close to curing patients with CLL, and these oral therapies may have a role similar to that of TKIs in CML today.
Highlights
What kind of patients are you usually treating?
What is your patient breakdown as far as percentages of different leukemia patients?
Let’s talk about CML first. How are you treating patients in different phases of CML?
You’re not using imatinib anymore, you’re only using second-generation TKIs?
Which co-morbidities are you most concerned about?
Do you think there are trends in when patients have started receiving therapy, as far as chronic phase goes?
Are most of these patients coming to you as newly diagnosed, or as referrals who have failed other treatments?
So what do you think about your current patient satisfaction with TKIs?
Which side effects do they typically complain about?
Are people looking at treatment discontinuation or lowing doses for this?
Those are mostly due to fatigue or other side effects?
One of the big pieces of ASH and pre-ASH news was ponatinib safety.1 Could you talk about the role of ponatinib in therapy today?
Can you give any details about what ways you’re trying to minimize risk of AEs?
Ariad and FDA have given different estimates of AE rates, with Ariad perhaps trying to minimize the level of risk. What has been the experience in your practice with cardiac AEs?
How about other promising mechanisms of action for CML?
So that would be after getting a major response from TKIs?
So do you use Synribo [omecetaxine] on your patients?
What kind of usage levels do you have for that on your patients?
A question about the second-generation TKIs. How do you decide which to give to patients, nilotinib vs. dasatinib?
Yes, as initial therapy.
Can you talk a little more about what co-morbidities and what dosing schedules are concerns?
So you’re speaking a little more generally. Can you give us an estimate of how you use these drugs in your own practice?
What about bosutinib usage?
Let’s move on to ALL. How do you treat your Philadelpha-chromosome positive (Ph+) ALL patients?
What do you do with patients who are Ph+ and are refractory or fail TKIs and chemo?
What percentage of adult ALL patients would you say are able to tolerate chemo?
What do you do with Ph- ALL patients?
What is the prognosis for most of your Ph+ ALL patients when they’re receiving frontline chemo with TKIs?
So they’ll be on TKIs indefinitely after that?
What do you think about clinical trials going on now with antibody-drug conjugates and bifunctional antibodies for ALL?
What other promising mechanisms of action are going to be good for ALL in the future?
Can you talk a little bit more about which antibodies you think are interesting?
This CAR thing that you mentioned – how do you think that’s going to work in the future? Is it going to be scalable?
Looking in the next five years, do you think this is going to be used mostly in refractory patients, or do you think it’s going to get moved along towards frontline?
Could you talk about how you treat your AML patients today?
Which FLT-3 inhibitor do you use?
As far as AML patients, how do you tailor therapies based on patient cytogenetics?
What percentage of patients with AML are eligible for a transplant and would be able to go through that process?
What is the average age of your AML patients?
I forgot to ask earlier – you see entirely adult patients, right?
Could you talk a little more about these FLT-3 inhibitors?
What do you think of the prospects for oral hypomethylating agents, like oral azacitidine?
What percentage of patients do you think would benefit from oral agents instead of IV?
I don’t know if you’re familiar with what’s been going on in vosaroxin. Do you have any thoughts on what happened to its prospects and the failure of the investigator-initiated trial at Cardiff, and how that may read through to the company-sponsored Phase III trial?
Do you have any insight – maybe trial design? – as to why the Cardiff study failed? I know they haven’t released details about it yet.
You also treat many patients with MDS in the MDS-AML continuum. What percentage of MDS patients are you actively treating, and what’s the distribution of severity?
As far as AML and MDS are concerned, do you see any trends with how physicians are treating patients?
How do you decide which hypomethylating agents to use on AML or MDS patients?
Which combinations of hypomethylating agents do you use?
You mentioned treatment schedule modification with azacitadine – what are people doing?
Mechanistically, do you have any thoughts on the HDAC inhibitors?
What are you currently doing for CLL?
So what do you think about the new therapies – Gazyva, for example, and the new oral therapies [ibrutinib, idelalisib] that are going to be approved?
Do you think the tolerability and safety profile of the new agents are comparable or
I heard rumors of less favorable safety with ibrutinib. Have you heard or experienced that?
What do you think Gazyva uptake, do you think it’s going to be used a lot?
So you think it’ll take a while even though Gazyva had very favorable Phase III results?
What about usage of Arzerra, the other anti-CD20 that GSK has?
A general question for all these leukemias: do you see any new combinations of drugs being developed, for example, using two different TKIs?
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