David Young : Because there may be some intellectual property things that we’re dealing with — so I can’t comment on that right now.
Naz Rahman : Got it. And I guess my last question is on 11T irinotecan. You mentioned that you obviously see a better risk benefit profile at a 50% dose. But could you give more color on what the dosing regimen might look like? Does that mean, for example, you provide like 50% or even lower dose and increase the dosing frequency to reduce the incidents of AEs? Or are you dosing at the same volume and intervals just with a better formulation? Could just provide more color surrounding that?
David Young : Yes. So right now, what we’ve done is we’ve kept the dosing regimen, the timing of the dose, the same. And the only thing we’ve done is change the actual amount that’s been dosed, all right, in terms of the active molecule. But we have to remember, this is not a formulation change. So the formulation of these things don’t make a difference. But the key to this is this is a prodrug. So what we’ve done is we’ve taken the active molecule of irinotecan, which is SN-38, and we’ve hooked on some other molecules onto it. And those other molecules preferentially put the drug into the membrane of the cancer cells over normal cells. So it’s like — I don’t want to call it — it’s like a transporter, or in some way just loads up the drug into the cancer cells versus normal cells.
And so, we have a different balance between how much the cancer cells get this SN-38 versus normal cells compared to irinotecan, where you have a different balance. So what we’re really doing is the prodrug that makes this drug be attracted into the membrane of cancer cells.
Naz Rahman : That actually raised two questions from me. So it sounds like that your 11T, it sounds like it’s more selective. Do you have any numbers surrounding selectivity of 11T versus regular irinotecan? And also, is it also more bioavailable?
David Young : We do have numbers. I can’t share those right now, but we’ll be putting something out on that in the near future. But in terms of — the administration is parenteral administration, if not oral administration. So the bioavailability is pretty much the same. But again, I won’t — I can’t comment. There is a difference in the cancer to tissue ratio of irinotecan versus next-generation irinotecan. There is definitely a difference, a big difference. But I just can’t say the number right now at this time.
Naz Rahman : Got it. So I just have one last question, if you don’t mind. Is it possible for you to comment on what you think the Phase 2B for 6422 and Phase 2b for 3117 might cost?
David Young : That’s hard for us to do right now because a lot of it depends on the discussion and negotiations with the FDA. Of course, if they want four arms and they want a bigger study, that’s going to be more expensive. If it’s only two or three arms and not having a normal control, for example, it would be less expensive. I really can’t say because it depends on how we finalize the design, which we won’t know until after we meet for next-generation capecitabine. For next-generation gemcitabine, it’s a little different. What we are going to be looking at, we are meeting with the FDA also mid-year in that. And what we are going to be looking at is the alternative types of pancreatic cancers that we should be targeting this drug to.
