interleukin 12

There's a lot of data, but it's observational data, right? They did show that biologic use lowered the risk of future PSA by 46%, and that was significant.

It was very significant for IL-17 inhibitors, where it dropped at 35%, and the IL-23 or the IL-12-23, where it dropped it by 54%.

They, in this study, compared IL-23 inhibition to IL-17 and showed that IL-23 was superior to IL-17 inhibition by as much as 33% in preventing future PSA.

Get together with your derm colleagues.

Tridon another agent didn't work.

tried an IL-12 or IL-23 blocker, and this patient went into remission in like overnight, okay? Overnight.

And these are, you know, Stelara is what blocks IL-12 and 23, and there's several molecules that block only IL-23.

And what was very, very interesting is we had initially this one patient that had these findings that responded so dramatically to IL-1223.

And we then studied that patient as well as the other six patients that had the same phenotype.

They had very severe disease, mostly involving their colon and refractory to other medications.

But when we studied them, it turned out by deep, detailed computational analyses that that their IL-23 pathway was markedly upregulated, markedly upregulated.

So we had a group, a panel of genes by studying the blood and biopsies of these patients that when you study them all together, showed that their IL-23 and IL-12 signaling was markedly upregulated.

So I present on IL-18, Yihan on IL-36 gamma, Sebastian on some kind of features of cytokine receptors in general.

So there's obviously lots of great cytokines that have impacts on immune system, T cells, the microenvironment, IL-2, IL-7, IL-12, 15, 36, 18.

What are kind of the defining features that we should look at as designers of CARs to go, these are really the important features to be able to combine with a CAR T-cell, specifically when attacking a solid tumor cell therapy.

So I'll kind of pitch that to you all.

We covered now I think already quite a fair amount of drugs and something I always like when you talk about pregnancy the oldest drugs are usually the best because you have the highest exposure over a long long time but you already mentioned some of the newer drugs and some even if you consider the mechanisms are really safe.

So I think we have a fair amount of data with IL-12, IL-23.

Now the IL-23s come out and a lot of colleagues feel this is a very safe drug.

I should even put a patient and start with this.

How would you recommend for clinical practice you have a newly diagnosed patient who wants to become pregnant and is in a critical age to become pregnant, would you start with an IL-23 or would you better use something of the older drugs like infliximab or vidulizumab or IL-1223, ustekinumab? What is your position on this?

So I always think that the best course is to treat the patient.

So what is the drug you would use if this patient wasn't planning on pregnancy? And so for any woman, what is the best drug for her case is how you should think about it.

That's really cool.

Because the original mammalian cell-produced IL-12 is just not too much work for the bacteria.

You just look for alternative versions.

As long as they stimulate the receptor, I guess that's all you need, really.

These are infusions or injections.

And they're affecting these markers, IL-1, IL-6, IL-12, IL-17, TNF alpha blockers, for example, that when you see for Crohn's disease, ulcerative colitis, psoriatic arthritis, any of these things, you'll see them all over television.

Every day, very, very heavily marketed.

One of them is the most common.

At Strand, Tasuku and his team are developing technologies such as self-replicating RNA, circular RNA, and logic gated mRNA circuits to engineer the next generation of RNA medicines.

Strand's lead program, STX1, is designed to express IL-12 locally in tumors, and has already entered clinical testing in patients with advanced solid tumors.

I'm truly thrilled to have Dr. Kitada with us today.

Tasuku, thank you so much for joining us.

And so, yeah.

Yeah, both extremely exciting.

And, you know, it strikes me that these therapeutic mechanisms of action, right, the autologous, uh, CAR T, which you're trying to make, uh, in vivo, and, uh, you know, the IL-12, uh, you know, immunotherapy, both of these have, uh, some precedent or at least, you know, proof of concept, right? What you guys are doing is really changing the sort of delivery platform, and with that, the, the specificity, the safety profile.

So, um, I guess I'm wondering, to what extent do you see this as being a true platform that you can sort of take these RNAs, your RNAs, and, you know, program anything you want into them, right, to get tissue specificity, to get cell type specificity? Um, the thinking is that you could go anywhere, right, um, to all sorts of disease contexts.

No differences in infections, serious infections or otherwise, and no differences in a bunch of other stuff the authors thought to study.

Height, weight, vaccination responses, and serum levels of cortisone, eosinophils, IL-4, IL-10, IL-12, and IL-31.

Wow.

Yeah, I know.

Let's contrast that with AbbVie, just to be clear.

In that case, the claims were defined heavily by what the antibodies did, right? Their functional ability to bind to a specific antigen like IL-12 with a certain neutralizing capacity.

Which goes right back to your four minute mile analogy.

In AbbVie, the genus was defined functionally.