Jonathan Aschoff: Okay. Any of the docs that have treated these salvage MM patients convey to you that, in their view, this is a no-brainer to use this in that setting?
Andrei Shustov: Thank you for that question. We are hearing from our KOLs in multiple myeloma field that we do have clear and significant advantages, again, based on MOA, depth to responses we see, especially in very highly refractory patients. They’re very encouraged with coming — to their patients with novel MOA after all available treatment options are exhausted. And that excitement certainly is very visible and encourages us to continue our development.
Jonathan Aschoff: Great. So basically, Jim, you’ve just set a prominent stage upon which to release your data in January, and you have real-time data from a single arm trial — just on single arm. So explain to me how this could possibly blow up in your face.
James Caruso: I’m not sure — as you think about it, there’s really a few, if any, pathways to, as you said, where — I guess, a disastrous outcome, right? So when you think about the data that we have presented and that Andrei presented again today in that patient population, albeit initial 6, but very broad across a highly refractory patient population in WM across a variety of genome types, certainly the most difficult to treat at the MYD88, CXCR4, nonmutated, as Andrei described, and you saw the responses that were provided there. As I think we’ve shared publicly in the past, our patient population in this pivotal study, obviously, would be very similar to that patient population. And the mechanism of action for our drug, obviously, is the same for the pivotal study patient population as well as those initial 6 patients.
Then you take a look at the product profile, which quite frankly, would compare favorable to those few agents that are indicated currently for WM and for, quite frankly, any of the salvage therapies and chemotherapeutic [indiscernible] that are used as a desperate treatment attempt for these patients. Then you take a look at the patient demographic, the older patient population, the challenges associated with comorbidities in those late-60s to 70s. You look at the adverse events associated with those treatment modalities I just cited, the BTKi’s as well as the chemotherapeutic [indiscernible] and other related salvage therapies and the continuous nature of treatment. It’s a challenge, Jonathan, for those patients. And then you look at our product profile.
We look at the 4 single 15 to 20-minute infusions. You look at the highly manageable and very predictable adverse event profile, which, oh, by the way, is transitory upon completion of the second cycle. So those cytopenias, which are very manageable and both lymphoma and hematologists experts will tell you very comfortable in terms of the management of that, you have a really nice product profile. Now on top of that, you have a level of activity that we believe, quite frankly, will compare very favorable to those aforementioned treatment modalities or options that currently exist. And I think it’s a function of, as Andrei just mentioned, our mechanism of action, where we really have an opportunity to have a meaningful impact on the course of the disease.
I mean when you think about currently the #1 prescribed class of medication in this space, it’s suppressing IgM, which in turn — the concept is to reduce the sequela associated with the disease by maintaining a lid on IgN. Iopofosine I-131, just based on its mechanism of action and capacity to ultimately kill tumor cells, will, in fact, have, we believe, a meaningful impact on the course of the disease. Now having said all that, what does that mean? It means there’s a potential here for complete remission, which really doesn’t exists certainly in the relapsed/refractory setting in monotherapy, nor in combination and even the best and most controlled clinical trials upfront — I think there’s a 3% to 5% CR rate in combination in naive patients, potentially self-selected as well.
