CD3

The 4.1BB doesn't work well.

So the further explorations we find, when you bring the CD3 and the 4.1BB together, we can do it.

So I incubate these platforms in the Liverpool Biopharma, which is likely to come back to the end of 2024.

We have opportunities because the Liverpool Biopharma wants to focus more on the development of ADC, and because there is one PD-1 approved in China, the second There's a EZLFR-based ADC already approved in China.

I know Jialun is one of IMAP, he was the first CFO of IMAP, and we bring IMAP to Nasdaq.

So I gave him a call, we have a hot pot dinner, and we decided to do it together.

We are lucky once we get the opportunity to get financing and also to bring the leading asset out and also related to CD3 platforms out.

And there is where we started from AccelerPoint.

Maziar, just to close off, when we have different bispecific antibodies, how do you pick one over the other? Epcoritumab, glufitumab, what's your go-to here? And what can we learn from this in community settings?

I think the two bispecifics, again, similarly, they target the same antigen, in this case, CD20, CD3.

So it's mainly logistics from, you know, one with BEPCO being a sub-Q with a more complicated schedule of weekly and then every two weeks and every four weeks, and it's treated until progression, not time-limited.

But it's sub-Q and patients like that.

In humans, we see a measurable increase in certain markers that tell us that the fight against cancer will probably be improved.

So we see an increase in CD3, CD4, CD8 in natural killer activity.

All of this in link with immunity and all those data depending on the different trials that were done.

Number two, increase in tumor response, so a more direct and targeted action primarily through the terpenes.

Everybody's using that term exosome.

It should be called the secretome or a conditioned media, depending on how you make it, um, because the way you isolate, you know, if you look at exosomes, what we know now, and you should be asking the questions of is, uh, is it truly an exosome following when I get it, when I thaw it, when I use it? Show me that there's the particular markers you look at Outside of the, the exosome three markers, CD3, uh, I think, yeah, CD3, 63, 81.

You look at those three, three different things and how much of that is actually in there?

Mm.

We want to sort of blind it, um, to going there.

We want to sort of redirect it towards T cells through this CD3- Uh, targeting, and on top of that, deliver the CAR.

So, you know, here we, after we targeted the T cells, then we wanted to look for whatever the cancer cell is, and in the particular case what we're discussing, it's this BCMA target in, in malignant plasma cells.

And then on top of all that, and I'll shut up because [laughs] I don't want you to take all the time, there's G-Link.

So we're trying to harness that power.

We're taking the VSVG protein and saying, "Okay, well, we no longer want to bind to the LDL receptor.

We want to bind to CD3.

How do we figure that problem out?" We, um, we, I think benefited a great deal from some really pioneering work that came out of France, and there's a group at CNRS that identified the receptor binding sites on VSVG for the LDL receptor and then started to mutate them and see, you know, do these mutations inhibit the ability of the virus to bind to the LDL receptor? [coughs] And so they, you know, they published on some of that work and I think gave the field a lot of new ideas about how to, uh, disrupt this interaction because those specific residues that were involved were now identified for everyone to see.

Cujan, $19.

CD3, $51.

Vinita Rose at $51.

The Wanda Waver at $16.

So we will talk about that.

Also, we have congressional candidate Bernie Flowers in CD3.

He'll be joining us at 10 o'clock.

We'll talk about his race, of course.

And I was hoping that at least Dr. Fauci would be held responsible, but It doesn't seem like we're going to get there anytime soon.

But with all that said, I wanted to talk to you again.

Bernie Flowers held a line with us in CD3.

I wanted to talk to you about what's currently happening in Iran.

Of course, however, not all patients respond to therapy, and those that do can acquire resistance over time.

Perhaps you can start by providing some background on what was previously understood about the resistance mechanisms of CD3, CD20 bispecific antibodies and the limitations of some of the standard platforms that have been used.

Thanks a lot for this question about the mechanism of resistance, not so much known and studied.

The major one is the low expression of the target, the CD20, and the exhaustion of T-cells.

Finally, CYMSIR-Zyming licenses its tri-specific antibody CYMO660 to Roach in a deal worth $75 million up front and up to $1.53 billion in total payments plus tiered double-digit royalties.

CYMO 660 targets CD79A, CD19, and CD3 simultaneously, pairing a CD3-engaging arm with two B-cell antigen-binding domains to drive T-cell-mediated cytotoxicity against B-cell malignancies and autoimmune diseases while limiting cytokine release.

The agreement is SimSeer's sixth major out-licensing deal, pushing the aggregate potential value of those transactions past $6.1 billion.

Thanks for listening to Pharmaceutical Executive Daily.