A roundtable discussion on anemia management in myelodysplastic syndromes. Featuring moderator Guillermo Garcia-Manero, MD, of the University of Texas MD Anderson Cancer Center; Amy DeZern, MD, MHS, Johns Hopkins Medicine; Tiffany Tanaka, MD, of the University of California San Diego; and Uma Borate, MBBS, of Ohio State University.
We don’t know why they need more transfusions. And so it’s a little intimidating to give a drug. And then the patient’s platelets go from 150 to 50. In an 80 year old. And so I, I love that there’s an option, but there was no option in this space. In the U.S, the go to was HMAs. And you’ve done some of the pioneering work with low dose HMAs in the space, and I think they are very effective.
So the typical patients, once this label, this indication was approved in my practice, are patients who’ve seen everything and they’ve seen HMAs, which we don’t, we have some data on, but not a lot of data. They were not enrolled in the study. So the patients that we’ve been giving this drug to have seen everything. And so we are learning how to use the drug, how to manage the toxicities.
We’ve had few patients on this drug so far with mixed results. So I’ll just stop there and see what other people think.
I have limited experience with the compound. Exactly. For the same reasons that you’re talking. Also, maybe this may resonate with Amy a little bit we are concerned with targeting telomerase activity in this disease. I mean, I actually but at the ASH meeting, it’s a very nice presentation suggesting that maybe (couldn’t understand) doses is actually the true mechanism by which this drug works. So maybe, you know, we don’t know how HMA works.
And actually, I’m not sure that we 100% understand how luspatercept works. But that to me was kind of concerning, like a block in symptomatic activity I don’t think is really that positive, but it it works. And I think now we’re starting to ask these questions ESA failure, luspatercept failure. And we will learn how to use this.
And I think it’s great that now that we have a really powerful front line approach, we have second line. I think we need to learn actually what really happens to luspatercept failure treated with imetelstat. Doctor Platzbecker had apresentation Saturday with some of this data. I couldn’t believe I need to, you know, understand it a little bit better.
I think we really on some hand, I feel like sometimes I’m arguing out of both sides of my mouth. I think everybody should start earlier so they feel better, longer. But then I’m very hesitant to start something like this earlier. But given the mechanism of action and the cytopenias and the toxicity, I think holding it to multiple lines later may mean the marrow failure component is really burning out for a patient, and at that point, inhibiting telomerase activity probably is detrimental.
And I think we need more real world experience because biologically, even though we haven’t seen it, you could imagine if you continue to inhibit enzymatic activity and shorten the telomeres, we may end up with other malignant problems that we are not keen to see. And so I am sort of being quite measured and selective in my patients. And then I have very open, informed consent with individuals because I think a lot of older patients have the concern of exchanging red cell transfusion dependance for something like platelet transfusion dependance, which somehow seems worse.
And so that’s.
No, I agree with Uma. I mean, you could die from a intracranial bleed. So I think this is the cytopenia that makes us the most concerned.
