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Speaker 1: This episode is brought to you by Allogen, a company

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Speaker 1: redefining how we fight cancer and autoimmune disease. By pushing

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Speaker 1: the boundaries of cartes cell therapy. Allogen is creating next

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Speaker 1: generation off the shelf treatments designed to reach more people.

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Speaker 1: Learn more at allogen dot com. Hi everyone. Cancer treatment

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Speaker 1: has come such a long way from the blunt tools

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Speaker 1: of chemo to today's precision immunotherapies like cart or chimeric

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Speaker 1: antigen receptor T cell therapy. Our partner, Allogen Therapeutics, is

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Speaker 1: helping lead that transformation. Cart is amazing. It reprograms your

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Speaker 1: own immune cells to find and destroy cancer, and because

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Speaker 1: it's targeted, it does it without some of the most

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Speaker 1: brutal side effects of say, chemotherapy. But access has been

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Speaker 1: a real challenge. That's where Allergen comes in developing truly

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Speaker 1: off the shelf CARTI treatments made from healthy donor cells

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Speaker 1: and ready when patients need them most. Who better to

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Speaker 1: understand these exciting developments and Alergen's chief medical Officer, Doctor

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Speaker 1: Zach Roberts. We talked about how cancer outsmart some of

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Speaker 1: its fiercest opponents, but how CARTE therapy is changing the

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Speaker 1: face of the disease, but first I wanted to know

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Speaker 1: what drew him to cancer research in the first place.

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Speaker 1: Doctor Zachary Roberts. So nice to meet you. I admire

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Speaker 1: people like you so much who are cancer scientists who

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Speaker 1: are trying to come up with better treatments to save

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Speaker 1: people's lives or to at least manage their disease. I'm

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Speaker 1: curious how did you get interested in cancer research? And

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Speaker 1: by the way, thank you that I appreciate that you

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Speaker 1: did well.

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Speaker 2: Thanks Katie. This is absolutely lovely to be here with

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Speaker 2: you today. I have to say that I was interested

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Speaker 2: from a very very young age. I grew up wanting

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Speaker 2: to be a scientist, wanting to be a doctor. I

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Speaker 2: became quite fascinated with how cells kind of went wrong.

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Speaker 2: There are a normal cell one day and then there

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Speaker 2: are cancer cell the next, and so really understanding what

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Speaker 2: genes were in play, what went wrong, what switches got

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Speaker 2: turned on, which ones got turned off, all of that

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Speaker 2: was so fascinating to me as a youngster.

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Speaker 1: How old were you when you became interested in that?

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Speaker 2: Oh it's probably seven eight really? Yeah?

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Speaker 1: Wow?

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Speaker 2: Yeah. But what I was really interested in was how

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Speaker 2: the immune system interacts with cancer.

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Speaker 1: Immunotherapy used to be kind of mocked in the medical establishment, right,

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Speaker 1: and now it seems to hold the key to dealing

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Speaker 1: with a lot of cancers. But I want to go back,

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Speaker 1: if I could for a minute, to talk about how

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Speaker 1: cancer treatment has changed and how immunotherapy has been embraced.

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Speaker 1: My husband was diagnosed with stage four colon cancer in

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Speaker 1: nineteen ninety seven. He was just forty one years old,

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Speaker 1: and of course, back then, may I call you Zach,

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Speaker 1: of course I did a lot of research. I was

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Speaker 1: just desperate to figure out if there was any way

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Speaker 1: we could treat and save my husband's life. And back

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Speaker 1: then these approaches were just starting to gain a little speed.

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Speaker 1: But for the most part, everything was treated with chemotherapy.

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Speaker 1: Chemotherapy obviously was a great development in cancer treatment, but

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Speaker 1: there are a lot of things wrong with chemo. Can

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Speaker 1: you talk about that and talk about how you've seen

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Speaker 1: cancer therapies evolve in the year since.

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Speaker 2: Absolutely, so, You're right, chemotherapy is very much a double

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Speaker 2: edged sword. And if you go back a leave it

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Speaker 2: even a little further than your husband's diagnosis, maybe another

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Speaker 2: fifty years. Let's say cancer was uniformally fatal at that time,

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Speaker 2: and no matter what cancer you had, it was just

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Speaker 2: a matter of time before you would succumb. In the

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Speaker 2: middle of the twentieth century was when through serendipitous and

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Speaker 2: lots of hard work, we discovered that these class of

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Speaker 2: medicines chemotherapy could kill very rapidly dividing cells.

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Speaker 1: And we should just mention the double edged sword of

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Speaker 1: it is that it kills a lot of healthy cells too.

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Speaker 1: It's indiscriminate. I used to call it the scorch body therapy,

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Speaker 1: right because it just kills everything, and that while the

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Speaker 1: healthy cells grow back, it's pretty ravaging.

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Speaker 2: Yes body. I mean, the way that chemotherapy works is

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Speaker 2: it has a slightly more toxic effect on cells that

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Speaker 2: are rapidly dividing. So in your body, you've got cells

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Speaker 2: that are very very slowly dividing maybe once a year,

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Speaker 2: and then you've got cells that are dividing every day.

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Speaker 2: You've got cancer cells that are dividing multiple times per day.

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Speaker 2: So what we try to do with chemotherapy is just

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Speaker 2: tune it so we get the cells that are dividing

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Speaker 2: the most rapidly. But your hair cells, the lining of

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Speaker 2: your stomach, and your GI tract, those are all rapidly

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Speaker 2: dividing cells. So absolutely super super toxic, But the targeted

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Speaker 2: therapies were not. They were very well tolerated by and

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Speaker 2: large and these patients could go back to their normal lives.

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Speaker 2: And this is coming back to the first question you

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Speaker 2: asked me, the biology of cancer. In the intrinsic biology

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Speaker 2: of a cell, we know that there are certain genes

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Speaker 2: that in some cancers are activated in a way that

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Speaker 2: gives rise to the cancer in that cell. That the

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Speaker 2: ability it gives the ability of that cell to become tumorous.

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Speaker 2: And if we could design a drug that targets that

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Speaker 2: specific gene, we can arrest the cancer.

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Speaker 1: It's so amazing to me how challenging cancer is as

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Speaker 1: a disease. I used to you know, I think a

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Speaker 1: lot of people think of cancer one disease, but it's

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Speaker 1: thousands of diseases in thousands of different biologies. In other words,

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Speaker 1: I got cancer, Zach. Even if it's the same kind

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Speaker 1: of cancer. If we both got a certain cancer, the

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Speaker 1: way my body reacts to it and the way your

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Speaker 1: body reacts to it could be totally different.

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Speaker 2: Right, Absolutely, that's a most people, You're absolute right, do

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Speaker 2: not they think of cancer as a monolithic disease. But

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Speaker 2: you're right, it's thousands of diseases. I mean, there are

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Speaker 2: hundreds of phlymphomas.

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Speaker 1: So when you think of targeted therapies, is immunotherapy a

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Speaker 1: subset of targeted therapy.

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Speaker 2: So I would say, no, it's different ball of whax.

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Speaker 2: That's a different ball of wax. So in my mind,

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Speaker 2: I kind of the way I organize it, there's sort

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Speaker 2: of three pillars of cancer care. There's pillar one, which

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Speaker 2: is chemo, which still has a big role to play, yes,

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Speaker 2: you know, for better or worse.

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Speaker 1: And by the way, I don't mean to dump all

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Speaker 1: over chemo because it's so lightly.

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Speaker 2: You're not gonna hurt my feelings.

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Speaker 1: No, but you know what I mean. And I think

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Speaker 1: a lot of people benefit so much from chemo therapy.

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Speaker 2: It absolutely can prolong people's lives. And and one thing

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Speaker 2: that has really improved in the last twenty years is

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Speaker 2: the supportive care element of this.

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Speaker 1: So you have fewer side effects.

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Speaker 2: Fewer side effects, so you know, we've got growth factors

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Speaker 2: to manage low blood counts, so you feel stronger between cycles.

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Speaker 2: We've got very powerful anti nausea medicines now so and

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Speaker 2: in a way interestingly that's actually made chemo even a

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Speaker 2: little more effective because it means we can push the

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Speaker 2: dose a little bit higher and the patients are able

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Speaker 2: to to manage it. So, yes, chemo still it gets

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Speaker 2: a bad rap, but it still has a pretty big

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Speaker 2: role to play. So that's pillar one. Pillar two, I

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Speaker 2: think is this targeted therapy, which is looking for specific

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Speaker 2: regulators of cancer and targeting those directly. And then pillar

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Speaker 2: three I would put as the imminotherapy in of things,

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Speaker 2: and that targets a pathway in T cells, which are

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Speaker 2: really kind of the field generals of the immune system.

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Speaker 2: It targets what is often called the immunological break of

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Speaker 2: those cells.

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Speaker 1: Let's go back and talk about T cells because they

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Speaker 1: sort of are, as you mentioned, the warriors of immunotherapy, right,

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Speaker 1: Are there other cells other than T cells that can

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Speaker 1: act like warriors against cancer.

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Speaker 2: Absolutely so, even though it's a little cliched, I think

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Speaker 2: kind of the army sort of analogy really works for

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Speaker 2: the immune system because you actually have many different kinds

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Speaker 2: of cells. Each of them has one or several very

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Speaker 2: important roles to play. There's a lot of cooperation, there's

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Speaker 2: a lot of crosstalk between the cells. So the cells

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Speaker 2: will actually talk to each other, obviously not with voices, yeah,

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Speaker 2: but with molecules that they secrete, and a T cell

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Speaker 2: will secrete molecule that a B cell will take in,

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Speaker 2: and that B cell, with that message will act now differently,

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Speaker 2: it'll take a sort of an order from the T cell.

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Speaker 1: Is the T cell the general I like to.

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Speaker 2: Think of them as the general Now I call them

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Speaker 2: field generals, though, which is the term I may have

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Speaker 2: made up, but it means that they actually are doing

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Speaker 2: some of the work themselves. They're not sort of sitting

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Speaker 2: in a back office somewhere. They're actually on the front

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Speaker 2: lines because they have Without getting too far into the

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Speaker 2: weeds here, as I said, I'm an aemynologist, which is

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Speaker 2: really my passion.

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Speaker 1: Well, I'm really into this, so go ahead.

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Speaker 2: The T cells have, in addition to their ability to

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Speaker 2: send messages to many different other cell types B cells, macrophages,

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Speaker 2: dendritic cells, they also have a very specific molecule on

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Speaker 2: their surface called the T cell receptor, and the T

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Speaker 2: cell receptor is unique to that T cell. So let's

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Speaker 2: say you've got a billion T cells, and more likely

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Speaker 2: you've got one hundred billion T cells in your body

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Speaker 2: each one has its own unique T cell receptor, and

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Speaker 2: bodies have evolved in that way so that you can

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Speaker 2: in any infection that you encounter. Right when you're born.

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Speaker 2: It's not like you're just given a set of instructions

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Speaker 2: of all the infections that you could ever see or

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Speaker 2: all the allergens. Right you are born with a truly

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Speaker 2: naive immune system, and so you have to have this

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Speaker 2: ability to create diversity in your in your T cell

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Speaker 2: population so that you can attack anything that comes in.

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Speaker 2: So the T cell receptors have an ability to recognize infections,

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Speaker 2: and some of them have an ability to recognize tumors.

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Speaker 1: As a T sell in a car T sell the

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Speaker 1: same thing.

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Speaker 2: Great question, so and great transition. So as as our

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Speaker 2: ability to understand the function of T cells grew over

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Speaker 2: the nineteen eighties, the nineteen nineties, and then into the

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Speaker 2: two thousands. And it's really rather recent that we started

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Speaker 2: to really tease all this apart. Many Nobel prizes were

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Speaker 2: involved in this whole story in the early nineties. Someone, well,

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Speaker 2: let me fill in one other little gap here, So

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Speaker 2: I mentioned B cells as another member of this little army.

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Speaker 2: B cells are famous because, like T cells, they've each

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Speaker 2: got their own specificity. Right, there's billions upon billions of

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Speaker 2: B cells, and each one has its own special specificity

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Speaker 2: that is unique to whatever infection that you may get

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Speaker 2: or may never get. When that little molecule that's on

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Speaker 2: the surface of the B cells gets cut off and

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Speaker 2: floats around your body by itself, we call it an antibody.

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Speaker 2: So B cells make the antibodies.

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Speaker 1: We love B cells.

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Speaker 2: We love B cells. We love antibodies. They're good for

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Speaker 2: a lot of things. They're a huge part of the

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Speaker 2: immune response. And we've known how antibodies work for a

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Speaker 2: little longer than we've known how T cell receptors work.

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Speaker 2: And so One Suite began to realize the potency of

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Speaker 2: T cells and their ability to kill target cells, including

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Speaker 2: cancer sometimes. And we can do this in the lab.

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Speaker 2: We can get them to kill cancer cells in the lab,

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Speaker 2: but we couldn't really figure out how to do it

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Speaker 2: in people until we started to use the checkpoint blockers

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Speaker 2: in twenty eleven.

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Speaker 1: And the checkpoint blockers basically they basically allow the T

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Speaker 1: cells to kill the cancer cells without being told to

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Speaker 1: back off. They're like, screw you, cancer, We're coming in.

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Speaker 1: There's nothing you can do to stop us.

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Speaker 2: That's right, it's taking the break off. The checkpoint is

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Speaker 2: another term for the break. So if you block the checkpoint,

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Speaker 2: the immune checkpoint, the T cells will just go on

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Speaker 2: and kill. So in the early nineties, an Israeli scientist

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Speaker 2: named Zella Geshar got this idea that if he took

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Speaker 2: an antibody and actually stuck it onto a T cell,

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Speaker 2: an antibody of known specificity, so we know what this

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Speaker 2: antibody is targeting, and we actually put it into a

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Speaker 2: T cell.

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Speaker 1: Give me an example of an antibody like a specific one.

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Speaker 2: So remember what the first one he actually did. But

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Speaker 2: let's say let's say her too. I'm going to make

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Speaker 2: this up, right, this is making up. Her two is

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Speaker 2: a famous breast cancer marker. It's the drug trans twos

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Speaker 2: amab her septin. Her targets her two. So her two

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Speaker 2: is on the surface of breast cancer. So let's say

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Speaker 2: we had an antibody to her too, and there are many,

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Speaker 2: herceptin is one of them.

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Speaker 1: Thank you, Denny Slayman.

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Speaker 2: Yes, absolutely, Danny Slayman. So let's say let's say I

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Speaker 2: wanted to make a car te cell with her sceptin.

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Speaker 2: So this going back to the early nineties. Let's say

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Speaker 2: I have got this antibody that is un that is

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Speaker 2: targets the HER two antibody hertoo molecule, and I put

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Speaker 2: that into a T cell. And I do that by

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Speaker 2: actually creating the genetic sequence that is used to make

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Speaker 2: the antibody. Because everything comes from DNA, so the DNA

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Speaker 2: is like the blueprint. So you take that piece of DNA,

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Speaker 2: you stick it into the T cell. So the T

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Speaker 2: cell's none the wiser and it sees this piece of

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Speaker 2: DNA and it says, oh, I need to take an

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Speaker 2: antibody now. So the antibody goes to the surface of

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Speaker 2: the T cell.

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Speaker 1: It doesn't reject it. It says welcome.

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Speaker 2: It says welcome. It's just DNA. And so they are.

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Speaker 2: They are appliable in a way. We can modify them

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Speaker 2: using genetic techniques.

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Speaker 1: Which brings us to allogenic therapy because I'm like, how

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Speaker 1: do you do that?

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Speaker 2: So the basic biology is you have to modify the

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Speaker 2: T cell, right, because as I said, right, you've got

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Speaker 2: billions of T cells, they are all unique. Right, that's

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Speaker 2: not going to help you if you need to kill

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Speaker 2: a kilogram of tumor, right, you need a lot of

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Speaker 2: T cells that are all focused on the same thing.

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Speaker 2: The easiest way to do that is to modify the

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Speaker 2: T cells. Now it's not easy, it's hard to do that,

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Speaker 2: but if you can do it successfully and get them

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Speaker 2: all to see the same thing and react in the

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Speaker 2: same way, suddenly you've got an entire army that you

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Speaker 2: can deploy to eradicate this tumor. So the CAR T

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Speaker 2: cells are just that. So we take in the early days,

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Speaker 2: it was an antibody put in the T cell, and

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Speaker 2: suddenly the T cell became specific for her too. In

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Speaker 2: our example, which was itself a massive breakthrough. It took

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Speaker 2: another twenty years. We talked about Carl June before we

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Speaker 2: get started, and he was one of the pioneers in this.

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Speaker 2: It really we really had to incorporate a lot of

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Speaker 2: what we had learned about how T cells themselves work

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Speaker 2: before we do anything to them to then design a

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Speaker 2: perfect CAR. And CAR stands for chimerican, chimeric anigen receptor

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Speaker 2: chimeric because it's part T cell receptor, part antibody, so

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Speaker 2: it's a chimera and it's an anigen, which anigen is

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Speaker 2: a fancy word for the molecule that this receptor sees.

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Speaker 2: So the anogen is on the tumor cell and the

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Speaker 2: receptor sees theanogen, so chimeric anigen receptor. And so once

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Speaker 2: we designed an effective CAR we put that into T

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Speaker 2: cells using the same general techniques we can talk about that.

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Speaker 2: It's actually quite interesting. We use modified HIV virus to

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Speaker 2: do that, and we drop this DNA into the T cells.

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Speaker 2: The T cells again are none the wiser, and suddenly

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Speaker 2: you now you've got a population of T cells with

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Speaker 2: uniform specificity. They all see the same thing in this case,

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Speaker 2: her too in our example. So if you've got a

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Speaker 2: patient and there's no CART cells, effective cart cells for

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Speaker 2: her too. But we'll come back to you know, the

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Speaker 2: real situation in a moment when when the analogy is done.

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Speaker 2: If you've got a breast cancer patient who's got a

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Speaker 2: very her too positive tumor, and many do, and you

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Speaker 2: put the car T cells in them into the patients,

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Speaker 2: suddenly you've got billions of car T cells that are

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Speaker 2: all finding her too on the on the breast cancer

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Speaker 2: cells and they'll kill the breast cancer cells. So it's

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Speaker 2: remarkable how well this works in solid tumors. It's been

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Speaker 2: a little tricky. Allergen actually has has some great data

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Speaker 2: in solid tumors, but it works really well in blood cancers.

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Speaker 2: Lymphoma's leukemia is multiple myeloma.

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Speaker 1: Why you know, I always have a hard time, just

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Speaker 1: because my experience with my husband was calling cancer. My

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Speaker 1: sister pancreatic I was diagnosed with early stage breast cancer

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Speaker 1: three years ago. I always have a hard time envisioning

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Speaker 1: how cancer acts in the blood. Can you explain that.

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Speaker 2: To me, picularly blood cancer.

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Speaker 1: Yeah, Like, well, my mom had lymphoma, yes, so that

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Speaker 1: was a blood cancer, right, yes, But how I have

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Speaker 1: a hard time envisioning in the blood stream how blood

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Speaker 1: cancers were. Can you explain that to me?

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Speaker 2: Sure? So it's probably helpful to go back and realize

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Speaker 2: that all cancers start with one cell more or less,

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Speaker 2: and we give the name to the cancer depending on

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Speaker 2: which cell became the cancer. So in pancreatic cancer, it

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Speaker 2: was a pancreas cell. In blood cancers, it's often cells

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Speaker 2: of the immune system. So T cells, B cells both

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Speaker 2: can can give rise to cancer.

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Speaker 1: Wait a second, I thought they were fighting cancer.

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Speaker 2: They are, they are, but they are they are subject

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Speaker 2: to the same molecular malfunctions as any other cell in

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Speaker 2: your body, So lymphoma, non Hoskins lymphoma, almost all of

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Speaker 2: those are come from B cells. So your mom had

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Speaker 2: mantle cell. Correct, mantle cell comes from a from a

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Speaker 2: B cell. Most leukemias that are that are lymphoid in

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Speaker 2: nature come from B cells. There are some T cell

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Speaker 2: leukemias as well. Most leukemias that we think of actually

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Speaker 2: come from a different blood cell that are give rise

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Speaker 2: to macrophages and other immune cells. But they all they're

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Speaker 2: all start in the marrow or in the lymph nodes.

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Speaker 2: So you've got thousands of lymph nodes in your body.

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Speaker 2: This is where all of the immune system cells all

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Speaker 2: come to congregate and form an immune response to an infection.

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Speaker 2: So if you get a cut in your arm, you

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Speaker 2: get some bacteria. You've got a lot of lymph nodes

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Speaker 2: in your arm, and as the bacteria make their way

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Speaker 2: into your body, they find their way into the lymph

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Speaker 2: nodes and that's where the TMB cells encounter them and.

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Speaker 1: They eat it up.

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Speaker 2: They eat it, they kill it, they tell their friends

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Speaker 2: about it. The friends then get deployed and go and

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Speaker 2: get inflammation in the cut. So often B in T

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Speaker 2: cell lymphomas will start in a lymph node because there's

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Speaker 2: such an explosive proliferation of those cells in response to

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Speaker 2: an infection. But this is where those T cells and

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Speaker 2: B cell lives. So if you have lymphoma, it's not

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Speaker 2: so much circulating in the blood as it is in

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Speaker 2: the lymph nodes. And so you'll see patients come in

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Speaker 2: with very just enlarged lymph nodes throughout their body. You

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Speaker 2: do a PET scan and you'll see lymph nodes even

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Speaker 2: in their abdomen and their chest. So throughout leukemias, on

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Speaker 2: the other hand, they are often circulating. Mantle cell lymphoma

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Speaker 2: is an example that is a also has a circulating phase.

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Speaker 2: So you can actually draw blood in these leukemia patients

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Speaker 2: and find tumor cells in the blood.

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Speaker 1: But what you're saying is the T cells in the

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Speaker 1: B cells are basically not doing their jobs in the

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Speaker 1: blood cancer and that's what's creating the opportunity for blood cancer.

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Speaker 2: Or it just takes one. So you might have you

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Speaker 2: might have ninety nine point nine to nine percent of

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Speaker 2: your B cells might be doing the right thing, and

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Speaker 2: your T cells might be doing the right thing. You've

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Speaker 2: just got one bad apple in there.

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Speaker 1: This episode is brought to you by Allogen, a company

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Speaker 1: redefining how we fight cancer and autoimmune disease. By pushing

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Speaker 1: the boundaries of car T cell therapy. Allogen is creating

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00:20:52,640 --> 00:20:56,919
Speaker 1: next generation off the shelf treatments designed to reach more people.

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00:20:57,560 --> 00:21:10,360
Speaker 1: Learn more at allogen dot com. So clearly, an approach

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Speaker 1: to killing cancer is to make these T cells or

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Speaker 1: turn them into car T sells, right, which give them

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Speaker 1: the ability to attack specific cancer cells. Right, How do

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Speaker 1: you do that?

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Speaker 2: So the approved therapies that are on the market already

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Speaker 2: for blood cancers all start with the patient's T cells themselves,

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Speaker 2: and so the procedure works as follows. You. The patient

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Speaker 2: who's got the lymphoma goes and sits down for several

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Speaker 2: hours in as procedure called aphoresis, and that is it's

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Speaker 2: kind of like an enhanced blood donation where we where

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Speaker 2: we take out billions and billions and billions of circulating

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Speaker 2: normal T cells from that patient. That becomes the manufacturing

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Speaker 2: star material. We take that bag of T cells and

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Speaker 2: that's a literal bag of T cells, and then we

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Speaker 2: bring it to the lab and that's when we do

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Speaker 2: our genetic modification. We use that that that special HIV

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Speaker 2: virus to deliver this genetic material into the T cells.

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Speaker 2: The T cells then become car T cells. We wash

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Speaker 2: them and purify them and put them in a different bag,

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Speaker 2: and then they get frozen and sent back to the

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Speaker 2: hospital where the patient is receiving their care, their thought

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Speaker 2: at the bedside, and they're infused into the patient.

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Speaker 1: It is amazing.

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Speaker 2: It's amazing. It's amazing that it works as well as

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Speaker 2: it does.

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Speaker 1: So what happens when they get an infusion of their

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Speaker 1: modified car T cells, right, or their T cells that

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Speaker 1: are modified and turned into car T cells.

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Speaker 2: Yeah, okay, we often just saying it, you're nailing it.

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Speaker 2: We we often just say car T cells. They get

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Speaker 2: their cart cell infusion. So so the infusion itself, and

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Speaker 2: I've seen many is sort of little anti climactic. It

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Speaker 2: takes about five minutes. Cells just go into a normal

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Speaker 2: IV and then what happens next can be exciting. The

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Speaker 2: patients can get quite sick with the side effects of

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Speaker 2: these cart cells because, as you'd imagine, they're on overdrive.

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Speaker 2: They're on overdrive, and they all have the same specificity,

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Speaker 2: so they're all seeing the same thing at the same

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Speaker 2: exact time, within minutes of being infused, and.

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Speaker 1: It's like swarming. This the swarming, right.

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Speaker 2: And they're also dividing, so they can actually divide in

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Speaker 2: the body ten thousandfold, and so you get this massive

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Speaker 2: immune response. You feel like you have the flu. Sometimes

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Speaker 2: that can become quite serious. We learned in the early

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Speaker 2: days how to manage this pretty effectively. But once you

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Speaker 2: get through that first week or two where the toxicities

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Speaker 2: can be the side effects can be a little you know, difficult.

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Speaker 2: Once you get through that, then you begin to see

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Speaker 2: the effects of these cart cells on the tumor. And

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Speaker 2: these patients will come in often one month after their infusion,

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Speaker 2: before their infusion, you know, they're just loaded with cancer

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Speaker 2: on a scan, and they come in one month later

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Speaker 2: in a complete remission. Every visible tumor is gone.

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Speaker 1: So I was just going to ask you what is

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Speaker 1: the success rate for this kind of therapy and specifically

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Speaker 1: in blood cancers.

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Speaker 2: Yeah, so in blood cancers it works really, really well

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Speaker 2: in the best cases. You know, there's a lot of

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Speaker 2: different trials out there, but you can see remissions like

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Speaker 2: this eighty ninety plus percent of the time, depending on

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Speaker 2: the patient. The disease and the car T cell that

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Speaker 2: you're using that applies to leukemia, lymphoma, and myeloma. Myeloma

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Speaker 2: is a very common blood cancer, famously and curable, and

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Speaker 2: just earlier this year we saw data that was five

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Speaker 2: years out from the first trial using a Carte cell

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Speaker 2: for mioloma, patient's still incomplete re mission. So really astonishing efficacy.

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Speaker 2: Not only high response rates but durable. These patients can

438
00:25:08,840 --> 00:25:11,040
Speaker 2: and they're leading normal lives after a single infusion.

439
00:25:11,440 --> 00:25:17,240
Speaker 1: And what about recurrence? Is it just too early to say.

440
00:25:17,640 --> 00:25:21,000
Speaker 2: So with blood cancers, they tend to come back quickly,

441
00:25:21,080 --> 00:25:23,720
Speaker 2: usually within most most of the time within one year.

442
00:25:24,520 --> 00:25:27,920
Speaker 2: But certainly if you're beyond two years out, you generally

443
00:25:27,960 --> 00:25:29,680
Speaker 2: are in a good place. So there may be a

444
00:25:29,720 --> 00:25:34,520
Speaker 2: few relapses after two years. So if you can, you know,

445
00:25:34,560 --> 00:25:36,679
Speaker 2: certainly for leukemium film, if you're two years out with

446
00:25:36,720 --> 00:25:39,919
Speaker 2: no recurrence, you know, as on Collegist Animals has to

447
00:25:39,840 --> 00:25:42,720
Speaker 2: say it, but you're probably cured at that point.

448
00:25:43,280 --> 00:25:47,480
Speaker 1: The problem with this, I mean, it's extraordinary and so exciting,

449
00:25:48,119 --> 00:25:54,800
Speaker 1: but the process itself is is is a lot, right,

450
00:25:54,960 --> 00:25:58,760
Speaker 1: That's a lot. And I know that access has been

451
00:25:58,800 --> 00:26:01,640
Speaker 1: a problem talk about out the people who can benefit

452
00:26:01,680 --> 00:26:05,560
Speaker 1: from this and the people who aren't able to access

453
00:26:05,600 --> 00:26:08,359
Speaker 1: this kind of therapy, which is always so upsetting to me.

454
00:26:09,200 --> 00:26:14,280
Speaker 2: That's an absolutely topical question, Katie, because ten years ago,

455
00:26:14,359 --> 00:26:16,439
Speaker 2: when I was doing all of this work with the

456
00:26:16,520 --> 00:26:19,360
Speaker 2: Carte cells and we were seeing these remissions, you know,

457
00:26:19,800 --> 00:26:23,720
Speaker 2: as I just described, it was a revolution. We had

458
00:26:23,760 --> 00:26:25,960
Speaker 2: never seen anything like this before, and it was so

459
00:26:26,119 --> 00:26:28,919
Speaker 2: exciting to be doing this every single day. But what

460
00:26:29,040 --> 00:26:33,080
Speaker 2: became very clear is that it was very very few

461
00:26:33,119 --> 00:26:37,480
Speaker 2: patients who are actually able to receive this procedure.

462
00:26:37,640 --> 00:26:39,080
Speaker 1: Why because of expense.

463
00:26:39,760 --> 00:26:43,439
Speaker 2: Sometimes it's expensed. Sometimes it this whole thing with the

464
00:26:43,440 --> 00:26:46,440
Speaker 2: blood collection and the manufacturing that can take a month

465
00:26:46,520 --> 00:26:49,720
Speaker 2: or even two months, sometimes even longer. And so if

466
00:26:49,760 --> 00:26:52,679
Speaker 2: you are a patient as often as the case, who's

467
00:26:52,720 --> 00:26:56,240
Speaker 2: had a disease relapse, their cancer has come back, it

468
00:26:56,320 --> 00:26:59,600
Speaker 2: is an emergency and it is sometimes you know, galloping

469
00:26:59,640 --> 00:27:02,320
Speaker 2: along and growing very fast, and you become frankly too

470
00:27:02,400 --> 00:27:04,960
Speaker 2: sick to even receive the car T cells if they

471
00:27:05,040 --> 00:27:10,720
Speaker 2: come back. So and this bespoke manufacturing, one patient, one

472
00:27:10,760 --> 00:27:15,400
Speaker 2: manufacturing process, one product, really has been a deep limitation

473
00:27:15,840 --> 00:27:19,760
Speaker 2: to getting access. And it's only done in certain certain centers,

474
00:27:19,960 --> 00:27:24,840
Speaker 2: large academic centers predominantly, So I knew from the from

475
00:27:25,000 --> 00:27:28,320
Speaker 2: very early that we would need a new plan. And

476
00:27:28,400 --> 00:27:30,840
Speaker 2: so you know, we've talked a little bit about this

477
00:27:30,920 --> 00:27:36,000
Speaker 2: termalogenetic Allogenetic car T cell therapies are really a path

478
00:27:36,080 --> 00:27:40,040
Speaker 2: to solving this access problem. And it sounds like a

479
00:27:40,040 --> 00:27:42,840
Speaker 2: subtle difference between the regular car T cells, which are

480
00:27:42,880 --> 00:27:45,959
Speaker 2: sometimes called autologous car T cells made from the same person,

481
00:27:46,560 --> 00:27:50,439
Speaker 2: but it's actually quite different. It's we take the cells

482
00:27:50,440 --> 00:27:53,080
Speaker 2: from a healthy donor, so the T cells don't come

483
00:27:53,080 --> 00:27:56,560
Speaker 2: from the patient, they come from a healthy person, and

484
00:27:56,600 --> 00:27:58,760
Speaker 2: we take those T cells and we make them into

485
00:27:58,800 --> 00:28:02,080
Speaker 2: car T cells, and then we of that product to

486
00:28:02,160 --> 00:28:06,080
Speaker 2: a patient. Right now, even ten plus years after the

487
00:28:06,280 --> 00:28:08,400
Speaker 2: very first or close to ten years from the very

488
00:28:08,400 --> 00:28:12,520
Speaker 2: first approvals of CARTI, only twenty percent of patients who

489
00:28:12,560 --> 00:28:16,400
Speaker 2: are eligible are actually able to access this therapy. It's

490
00:28:16,800 --> 00:28:20,560
Speaker 2: a lengthy process, it's complex, there's insurance issues, it's only

491
00:28:20,600 --> 00:28:23,560
Speaker 2: given in certain centers. The majority of patients in our

492
00:28:23,600 --> 00:28:26,760
Speaker 2: country don't get their care at those centers. So there

493
00:28:26,840 --> 00:28:31,000
Speaker 2: is just multiple burials barriers that prevent a patient who

494
00:28:31,040 --> 00:28:34,240
Speaker 2: could have their life saved and their cancer cured by

495
00:28:34,240 --> 00:28:36,639
Speaker 2: car T cells, they just can't get them, which is

496
00:28:36,680 --> 00:28:42,800
Speaker 2: a tragic situation. So after we figured out how to

497
00:28:42,840 --> 00:28:45,160
Speaker 2: make car T cells in the very beginning, and we

498
00:28:45,160 --> 00:28:48,680
Speaker 2: were doing it using patients material patients T cells and

499
00:28:48,720 --> 00:28:50,920
Speaker 2: making the car T cells in the lab. During in

500
00:28:50,920 --> 00:28:55,360
Speaker 2: that process, I described one of the companies that was

501
00:28:55,400 --> 00:28:57,720
Speaker 2: at the forefront of that was a company called Kite Pharma.

502
00:28:57,720 --> 00:29:00,000
Speaker 2: It was a company that was founded by Ari Beldergrim

503
00:29:00,160 --> 00:29:03,440
Speaker 2: and David Chang, both of whom at the end of

504
00:29:03,480 --> 00:29:06,480
Speaker 2: the Kite cycle went on to form Allogen. And the

505
00:29:06,520 --> 00:29:11,120
Speaker 2: reason that Allergen came about was because even though we

506
00:29:11,120 --> 00:29:15,680
Speaker 2: were working with these carte cells at Kite, and all

507
00:29:15,720 --> 00:29:19,040
Speaker 2: three of us were working on this together, we very

508
00:29:19,120 --> 00:29:22,080
Speaker 2: quickly realized that there was going to be significant limitations

509
00:29:22,080 --> 00:29:26,760
Speaker 2: in our ability to scale this manufacturing process, and with

510
00:29:26,840 --> 00:29:29,440
Speaker 2: our inability to scale, we were going to run into

511
00:29:29,560 --> 00:29:34,000
Speaker 2: massive access problems. There just wasn't going to be the

512
00:29:34,040 --> 00:29:38,600
Speaker 2: wherewithal of the ability the manpower that would be required

513
00:29:38,640 --> 00:29:41,640
Speaker 2: to make products for all these patients that needed to

514
00:29:41,720 --> 00:29:45,240
Speaker 2: receive them. So the vision at the time was, how

515
00:29:45,280 --> 00:29:49,840
Speaker 2: can we take healthy donors and collect their T cells

516
00:29:49,880 --> 00:29:52,400
Speaker 2: and then make dozens or hundreds of doses from a

517
00:29:52,440 --> 00:29:55,840
Speaker 2: single manufacturing run instead of making one dose from a

518
00:29:55,880 --> 00:29:59,960
Speaker 2: manufacturing run. And so that was really how allogen was

519
00:30:00,120 --> 00:30:04,000
Speaker 2: born and the new field of allogenetic car T cells

520
00:30:04,240 --> 00:30:04,760
Speaker 2: was launched.

521
00:30:04,960 --> 00:30:09,120
Speaker 1: Wait a seconds, so all car T cells Zacher created

522
00:30:09,200 --> 00:30:13,520
Speaker 1: equal Like, if you needed car T therapy, I could

523
00:30:13,520 --> 00:30:18,720
Speaker 1: donate my T cells that would become car T cells

524
00:30:18,920 --> 00:30:20,880
Speaker 1: that could be used in your body. It's not like

525
00:30:20,920 --> 00:30:22,360
Speaker 1: a bone marrow donation.

526
00:30:22,680 --> 00:30:25,000
Speaker 2: It is not like a bone marrow donator. Actually crazy, Yeah,

527
00:30:25,040 --> 00:30:28,440
Speaker 2: And actually the question is a very interesting one, and

528
00:30:28,600 --> 00:30:32,120
Speaker 2: it's partly why it's been so difficult to achieve this,

529
00:30:32,640 --> 00:30:36,400
Speaker 2: to use a healthy, a healthy donor starting material to

530
00:30:36,440 --> 00:30:40,200
Speaker 2: make these cart cells. The immunology is a challenge. Our

531
00:30:40,240 --> 00:30:45,320
Speaker 2: bodies are able to recognize other people's immune systems as foreign,

532
00:30:46,160 --> 00:30:49,840
Speaker 2: and those immune systems are able to recognize our body

533
00:30:49,880 --> 00:30:54,120
Speaker 2: as foreign. Because we can use elegant gene editing technologies,

534
00:30:54,360 --> 00:30:57,640
Speaker 2: we can actually solve that immunology. And so we can

535
00:30:57,800 --> 00:31:02,080
Speaker 2: use universal donors. We can take a donor to use

536
00:31:02,120 --> 00:31:05,680
Speaker 2: your example, Yes, your cells could work for my cancer.

537
00:31:05,720 --> 00:31:08,200
Speaker 2: It's not actually how it works. We have there's a

538
00:31:08,280 --> 00:31:10,320
Speaker 2: sort of an elaborate testing and we have to make

539
00:31:10,320 --> 00:31:11,640
Speaker 2: sure that we're picking the dright donors.

540
00:31:11,680 --> 00:31:13,640
Speaker 1: And it's there and I might be too old.

541
00:31:14,760 --> 00:31:16,320
Speaker 2: There is an age limit. I don't know if it

542
00:31:16,320 --> 00:31:18,160
Speaker 2: would apply to you or not, but yes, those sorts

543
00:31:18,200 --> 00:31:21,280
Speaker 2: of attributes are are minded and therefore we can make

544
00:31:21,880 --> 00:31:25,160
Speaker 2: from a single donation. We can make up to one

545
00:31:25,160 --> 00:31:27,760
Speaker 2: thousand doses of Carte cells from a single donation.

546
00:31:28,360 --> 00:31:29,959
Speaker 1: Are we talking about a thousand patients?

547
00:31:30,000 --> 00:31:32,640
Speaker 2: A thousand patients? Wow? Yeah, the donation piece is not

548
00:31:32,760 --> 00:31:35,040
Speaker 2: the limitter for us because we can make so many

549
00:31:35,560 --> 00:31:40,040
Speaker 2: doses from a single donation. We have many many doses

550
00:31:40,440 --> 00:31:44,560
Speaker 2: frozen away. What I think the barrier that we need

551
00:31:44,600 --> 00:31:47,320
Speaker 2: to solve is we need to find better ways to

552
00:31:47,360 --> 00:31:51,320
Speaker 2: administer these products at the place where patients get their care.

553
00:31:51,600 --> 00:31:55,080
Speaker 1: Instead of just a few or academic centers all across

554
00:31:55,120 --> 00:31:57,680
Speaker 1: the country. They have to be in rural hospitals and

555
00:31:58,120 --> 00:32:01,200
Speaker 1: places low income areas, right.

556
00:32:01,000 --> 00:32:04,680
Speaker 2: I mean even yes, absolutely, but even large suburban areas.

557
00:32:04,680 --> 00:32:08,160
Speaker 2: I mean, you would be surprised at how reluctant patients

558
00:32:08,240 --> 00:32:13,440
Speaker 2: are to leave their primary oncologists to get a referral into,

559
00:32:13,680 --> 00:32:16,760
Speaker 2: you know, across town to you know, the gigantic building

560
00:32:16,880 --> 00:32:19,560
Speaker 2: and the nurses who name I don't know, right.

561
00:32:19,680 --> 00:32:23,880
Speaker 1: Can't the Cartie cells be shipped to various places.

562
00:32:23,600 --> 00:32:27,800
Speaker 2: In the context of the autologous, the the yes, kartas,

563
00:32:27,800 --> 00:32:29,600
Speaker 2: and all the ones that come from the patient them cells,

564
00:32:29,640 --> 00:32:33,440
Speaker 2: that whole apparatus to collect the T cells, to manage

565
00:32:33,480 --> 00:32:38,240
Speaker 2: the to and fro. That actually is pretty rigorous, and

566
00:32:39,120 --> 00:32:42,360
Speaker 2: there are accrediting bodies who make sure that that's done

567
00:32:42,400 --> 00:32:44,560
Speaker 2: all right, because you have to track the cells back

568
00:32:44,640 --> 00:32:47,320
Speaker 2: and forth. You can't get lost in the case of

569
00:32:47,320 --> 00:32:51,200
Speaker 2: an off the shelf analogeneic another word is off the shelf.

570
00:32:51,680 --> 00:32:54,360
Speaker 2: We could it's just we just send the product to

571
00:32:54,440 --> 00:32:54,920
Speaker 2: the patient.

572
00:32:55,160 --> 00:32:57,760
Speaker 1: And aligenetic just means it doesn't have to come from

573
00:32:57,800 --> 00:33:02,200
Speaker 1: your body, comes from somebody else, right, somebody else's T cells, right, correct,

574
00:33:02,560 --> 00:33:03,800
Speaker 1: So go ahead, I'm sorry.

575
00:33:03,880 --> 00:33:08,880
Speaker 2: So we can actually send our products to the hospitals,

576
00:33:08,920 --> 00:33:13,360
Speaker 2: the suburban, the rural hospitals where the patients receive their care.

577
00:33:13,880 --> 00:33:18,360
Speaker 2: And in fact, in our Alpha three program where we're

578
00:33:18,440 --> 00:33:23,200
Speaker 2: using this new technique of MRD to find patients who

579
00:33:23,240 --> 00:33:26,760
Speaker 2: are very high risk of relapse, those patients are remaining

580
00:33:26,840 --> 00:33:30,720
Speaker 2: with their local oncologists and they're completing their frontline care,

581
00:33:31,240 --> 00:33:33,280
Speaker 2: they're getting this MRD test, they're found to be at

582
00:33:33,320 --> 00:33:35,760
Speaker 2: high risk of relapse, and instead of being referred at

583
00:33:35,760 --> 00:33:38,680
Speaker 2: that point to the big academic center maybe hundreds of

584
00:33:38,680 --> 00:33:41,560
Speaker 2: miles away, we enroll them into the trial and we

585
00:33:41,680 --> 00:33:45,800
Speaker 2: just shipped the cart cells right to that practice. And

586
00:33:45,840 --> 00:33:49,320
Speaker 2: in fact, many of the clinicians on our trial are

587
00:33:49,760 --> 00:33:52,920
Speaker 2: giving Carte cells for the very first time. They've decided

588
00:33:53,080 --> 00:33:57,040
Speaker 2: at their practice to not invest in the infrastructure required

589
00:33:57,080 --> 00:34:00,600
Speaker 2: for the autologous programs, but for an allergen off the

590
00:34:00,640 --> 00:34:03,160
Speaker 2: shelf program, they have everything that they need ready to go.

591
00:34:03,520 --> 00:34:05,880
Speaker 2: So these patients now are getting access to this life

592
00:34:06,200 --> 00:34:10,239
Speaker 2: modality simply because we can just ship it right from

593
00:34:10,239 --> 00:34:10,840
Speaker 2: our warehouse.

594
00:34:10,920 --> 00:34:14,120
Speaker 1: What is the most important thing for patients and their

595
00:34:14,200 --> 00:34:19,200
Speaker 1: doctors to know about this exciting new possible therapy for

596
00:34:20,160 --> 00:34:22,560
Speaker 1: recurrence early in the game.

597
00:34:23,040 --> 00:34:25,440
Speaker 2: So the most important thing I think for patients and

598
00:34:25,480 --> 00:34:30,080
Speaker 2: doctors to know is that we have new techniques to

599
00:34:30,239 --> 00:34:33,520
Speaker 2: assess disease at the end of treatment, not just pet

600
00:34:33,520 --> 00:34:37,080
Speaker 2: scans and cat scans. We actually have this new class

601
00:34:37,080 --> 00:34:40,560
Speaker 2: of blood tests called MRD tests that will really give

602
00:34:40,600 --> 00:34:43,320
Speaker 2: you a much better prognosis of your likelihood of relapse.

603
00:34:44,000 --> 00:34:48,160
Speaker 2: Right now, the only option for treatment is in the

604
00:34:48,200 --> 00:34:51,640
Speaker 2: Alpha three clinical trial. So if you're a patient or

605
00:34:51,680 --> 00:34:53,960
Speaker 2: you're a doctor who takes care of patients with diffuse

606
00:34:54,040 --> 00:34:58,680
Speaker 2: large B celempoma, ask about the MRD test, Ask about

607
00:34:58,719 --> 00:35:01,960
Speaker 2: the Alpha three clinical trial. Well, because we are really

608
00:35:02,320 --> 00:35:04,879
Speaker 2: it's not widely available. We do believe it eventually will

609
00:35:04,880 --> 00:35:07,120
Speaker 2: be wildly available, but we're really at the cutting edge

610
00:35:07,120 --> 00:35:09,880
Speaker 2: here and we want to get these patients access to

611
00:35:09,880 --> 00:35:13,560
Speaker 2: the clinical trial enrollment to again, hopefully if they're in

612
00:35:13,600 --> 00:35:16,360
Speaker 2: that very high risk of relapse, that third of patients,

613
00:35:16,400 --> 00:35:18,640
Speaker 2: we can find them and treat them when we have

614
00:35:18,719 --> 00:35:19,799
Speaker 2: the best chance of care.

615
00:35:20,040 --> 00:35:22,040
Speaker 1: And patients need to be aware of this so they

616
00:35:22,040 --> 00:35:24,480
Speaker 1: can make sure their doctors give them this test.

617
00:35:24,680 --> 00:35:30,200
Speaker 2: Oftentimes, it's remarkable, Katie, as you may know how important

618
00:35:30,360 --> 00:35:33,680
Speaker 2: the patient's questions and opinions are in determining the care

619
00:35:33,800 --> 00:35:36,480
Speaker 2: and walking in and saying to your doctor, Hey, you

620
00:35:36,520 --> 00:35:39,120
Speaker 2: know I heard about this new MRD test that will

621
00:35:39,160 --> 00:35:40,960
Speaker 2: tell me whether my disease is going to come back

622
00:35:41,040 --> 00:35:43,640
Speaker 2: or not. What can you tell me, doc about this?

623
00:35:44,000 --> 00:35:47,239
Speaker 2: Just that conversation that one question often will lead to

624
00:35:49,360 --> 00:35:51,240
Speaker 2: a patient finding a way into the clinical trial?

625
00:35:51,400 --> 00:35:53,719
Speaker 1: Is this only available to people who have a high

626
00:35:53,840 --> 00:35:56,719
Speaker 1: risk of relapse. Let's say a patient comes in and

627
00:35:56,800 --> 00:36:00,359
Speaker 1: they have I don't know, one of the blood cans

628
00:36:00,400 --> 00:36:04,080
Speaker 1: you mentioned. Can they just go ahead and get the

629
00:36:04,280 --> 00:36:09,520
Speaker 1: allogeneic therapy? Is there any advantage of using your own

630
00:36:09,600 --> 00:36:13,640
Speaker 1: T cells over kind of what might be more widely available.

631
00:36:14,360 --> 00:36:18,000
Speaker 2: So right now, the only time that you would get

632
00:36:18,239 --> 00:36:20,879
Speaker 2: a product made from your own T cells is if

633
00:36:20,920 --> 00:36:24,319
Speaker 2: your disease has come fully back, so in May.

634
00:36:24,560 --> 00:36:27,880
Speaker 1: What about your very when you're initially diagnosed.

635
00:36:27,480 --> 00:36:30,720
Speaker 2: So right now there is a couple of clinical trials

636
00:36:30,760 --> 00:36:34,600
Speaker 2: testing whether the patient's own T cells made into car

637
00:36:34,680 --> 00:36:38,200
Speaker 2: T cells can actually work in what we say are

638
00:36:38,280 --> 00:36:40,480
Speaker 2: very high risk patients. So ones that we know are

639
00:36:40,480 --> 00:36:44,919
Speaker 2: going to have a tough time. But for the most part,

640
00:36:45,239 --> 00:36:49,160
Speaker 2: patients with blood cancers typically often are cured. In fact

641
00:36:49,160 --> 00:36:51,880
Speaker 2: that the case of non Hodgin's lymphoma, two thirds of

642
00:36:51,920 --> 00:36:56,920
Speaker 2: the patients are cured with standard frontline chemotherapy. And so

643
00:36:57,560 --> 00:37:00,360
Speaker 2: when you get to the end of that, the issue is,

644
00:37:00,440 --> 00:37:02,839
Speaker 2: right now we don't really know who's cured and who isn't.

645
00:37:02,960 --> 00:37:05,200
Speaker 2: All we can do is wait and we just scan

646
00:37:05,320 --> 00:37:08,000
Speaker 2: these patients every three months and wait for their tumor

647
00:37:08,080 --> 00:37:10,879
Speaker 2: to come back. With this new test that we have,

648
00:37:11,000 --> 00:37:14,920
Speaker 2: this ultra sensitive MRD test minimal residual disease, we can

649
00:37:14,960 --> 00:37:17,440
Speaker 2: actually pick you know, if we've got two patients who

650
00:37:17,520 --> 00:37:20,360
Speaker 2: both look in complete remission, one of them is MRD

651
00:37:20,480 --> 00:37:23,640
Speaker 2: positive and one is MRD negative, we know that MRD

652
00:37:23,719 --> 00:37:27,160
Speaker 2: positive patient, which means we're finding little traces of cancer

653
00:37:27,239 --> 00:37:30,200
Speaker 2: DNA and that blood. That patient is at a very

654
00:37:30,239 --> 00:37:32,800
Speaker 2: high risk of relapse, and so it could really benefit

655
00:37:32,960 --> 00:37:37,240
Speaker 2: could really benefit court. So in that case, it's really tough.

656
00:37:37,280 --> 00:37:41,040
Speaker 2: You can't really make the car T cells the way

657
00:37:41,560 --> 00:37:45,120
Speaker 2: that we've done with the patients because the own car

658
00:37:45,160 --> 00:37:47,719
Speaker 2: T cells they don't really have a lot of T cells.

659
00:37:47,760 --> 00:37:51,799
Speaker 2: They've just finished their frontline therapy. Sometimes the disease can

660
00:37:51,800 --> 00:37:53,719
Speaker 2: come back within a matter of weeks, so while the

661
00:37:53,760 --> 00:37:56,560
Speaker 2: cells are being made, the tumor comes back. So this

662
00:37:56,640 --> 00:37:59,600
Speaker 2: is really a great opportunity for an off the shelf

663
00:37:59,640 --> 00:38:02,839
Speaker 2: product to just go. At the time that we get

664
00:38:02,880 --> 00:38:06,960
Speaker 2: that MRD result, we send the car T cells that

665
00:38:07,000 --> 00:38:08,640
Speaker 2: are made from healthy donor. They're all frozen in.

666
00:38:08,640 --> 00:38:10,800
Speaker 1: Our fop residual disease.

667
00:38:10,920 --> 00:38:13,640
Speaker 2: That's the term, they mop up the residual disease. So

668
00:38:14,000 --> 00:38:16,520
Speaker 2: that is the clinical trial that we are running right now.

669
00:38:16,600 --> 00:38:20,360
Speaker 2: So this is a very fascinating area of oncology because

670
00:38:20,360 --> 00:38:24,560
Speaker 2: we are using these enhanced techniques like MRD to identify

671
00:38:24,600 --> 00:38:28,239
Speaker 2: the patients who are likely to relapse. So far, we're

672
00:38:28,280 --> 00:38:32,160
Speaker 2: only studying that in clinical trials, and so the Alpha

673
00:38:32,239 --> 00:38:34,920
Speaker 2: three trial is the one that Alergen is running, and

674
00:38:34,960 --> 00:38:37,759
Speaker 2: it's designed exactly that way. So if we find a

675
00:38:37,800 --> 00:38:40,960
Speaker 2: patient who looks to be in remission based on scans

676
00:38:41,000 --> 00:38:44,480
Speaker 2: and they feel great, but if they're MRD positive, we're

677
00:38:44,480 --> 00:38:46,480
Speaker 2: pretty sure that patient's disease is going to come back,

678
00:38:46,520 --> 00:38:47,919
Speaker 2: and it might come back in a matter of weeks

679
00:38:48,000 --> 00:38:51,240
Speaker 2: or months. So we're treating those patients in our clinical

680
00:38:51,280 --> 00:38:54,080
Speaker 2: trial right now with our off the shelf car te cells.

681
00:38:54,280 --> 00:38:59,080
Speaker 1: This is potentially a life saving intervention because if you

682
00:38:59,239 --> 00:39:04,720
Speaker 1: wait until the disease appears on a cat scan, sometimes

683
00:39:04,840 --> 00:39:09,200
Speaker 1: it's too late and the car T therapy isn't as effective.

684
00:39:09,280 --> 00:39:12,600
Speaker 2: That's exactly it. So if we were essentially bringing car

685
00:39:12,680 --> 00:39:16,720
Speaker 2: T cells to the patient much sooner, when they stand

686
00:39:16,760 --> 00:39:20,840
Speaker 2: a greater chance of benefiting, they probably will have fewer

687
00:39:20,880 --> 00:39:23,480
Speaker 2: side effects because side effects are related to how much

688
00:39:23,560 --> 00:39:25,360
Speaker 2: cancer is in the body at the time of infusion.

689
00:39:25,760 --> 00:39:28,920
Speaker 2: And really the goal here is to cure these patients

690
00:39:28,960 --> 00:39:31,080
Speaker 2: before they ever have to suffer that relapse. And that

691
00:39:31,160 --> 00:39:34,640
Speaker 2: is what makes Alpha three such a revolutionary design.

692
00:39:34,920 --> 00:39:40,640
Speaker 1: If someone's cancer has recurred and they do have evidence

693
00:39:40,680 --> 00:39:44,880
Speaker 1: of disease, right, then they can source car T therapy.

694
00:39:45,000 --> 00:39:48,120
Speaker 2: Now in that minority of cases right where there's about

695
00:39:48,200 --> 00:39:51,359
Speaker 2: fifteen to twenty percent of patients who are fortunate enough

696
00:39:51,360 --> 00:39:54,360
Speaker 2: to be have the stars aligned, yes, that would be

697
00:39:54,719 --> 00:39:57,040
Speaker 2: the standard second line, right, but there are a lot.

698
00:39:56,920 --> 00:40:00,600
Speaker 1: Of people who have this happen and they don't have access.

699
00:40:00,800 --> 00:40:02,560
Speaker 1: And that's what you're trying to tackle.

700
00:40:02,680 --> 00:40:04,520
Speaker 2: That's one hundred percent what we're trying to tackle.

701
00:40:04,680 --> 00:40:06,960
Speaker 1: So how are you trying? How are you tackling it?

702
00:40:07,120 --> 00:40:09,440
Speaker 1: Are you can you go the seven to eleven and say,

703
00:40:09,480 --> 00:40:11,080
Speaker 1: I like those card cells.

704
00:40:11,320 --> 00:40:16,120
Speaker 2: No. So, this MRD story is developing across oncology, not

705
00:40:16,200 --> 00:40:18,520
Speaker 2: just in blood cancers where we're studying with Alpha three,

706
00:40:19,040 --> 00:40:21,520
Speaker 2: and so patients more and more are starting to ask

707
00:40:21,560 --> 00:40:24,160
Speaker 2: for these tests. More tests are becoming available. So even

708
00:40:24,200 --> 00:40:27,680
Speaker 2: in your community oncology practices, at the end of a

709
00:40:27,719 --> 00:40:31,799
Speaker 2: treatment cycle. The oncologist will often order this MRD test

710
00:40:31,800 --> 00:40:34,000
Speaker 2: to see how do we do did we get every

711
00:40:34,080 --> 00:40:37,400
Speaker 2: last cell? You know, in a manner of speaking. And

712
00:40:37,480 --> 00:40:42,080
Speaker 2: so if in the context of our clinical trial, they

713
00:40:42,120 --> 00:40:44,640
Speaker 2: send this test, which is very sensitive, and they find

714
00:40:44,640 --> 00:40:48,640
Speaker 2: that it is that there is residual tumor there, then

715
00:40:48,719 --> 00:40:51,360
Speaker 2: that patient is potentially eligible to enroll in our study.

716
00:40:51,480 --> 00:40:53,600
Speaker 2: And so what we're trying to see here is whether

717
00:40:54,360 --> 00:40:58,520
Speaker 2: us treating the patient when they only have that molecular

718
00:40:58,600 --> 00:41:02,000
Speaker 2: disease nothing on scan the MRD alone, if we treat

719
00:41:02,000 --> 00:41:05,520
Speaker 2: with our car T cells at that moment, are we

720
00:41:05,640 --> 00:41:08,640
Speaker 2: able to cure the patient and have the disease never

721
00:41:08,680 --> 00:41:09,160
Speaker 2: come back.

722
00:41:09,920 --> 00:41:14,840
Speaker 1: Car T therapy is really effective when there's residual disease?

723
00:41:15,080 --> 00:41:18,799
Speaker 1: Is it also effective, Zach if your tumor comes back

724
00:41:18,840 --> 00:41:20,360
Speaker 1: and you see something on a scan.

725
00:41:21,160 --> 00:41:24,560
Speaker 2: So almost all the data that we have so far,

726
00:41:24,880 --> 00:41:27,520
Speaker 2: including all the approvals for the car T cells, have

727
00:41:27,640 --> 00:41:30,480
Speaker 2: been in that exact situation when your tumor has come

728
00:41:30,520 --> 00:41:32,920
Speaker 2: fully back. So this would be a time when we

729
00:41:32,920 --> 00:41:35,360
Speaker 2: would take a patient to a BOEM or transplant, for example,

730
00:41:35,400 --> 00:41:38,319
Speaker 2: if you gave them car T cells instead. This is

731
00:41:38,320 --> 00:41:40,840
Speaker 2: what has led to those miraculous outcomes that we discussed

732
00:41:40,880 --> 00:41:44,920
Speaker 2: a little early when their tumoror has come back. But

733
00:41:45,040 --> 00:41:47,799
Speaker 2: what we do know is that car T cells work

734
00:41:47,920 --> 00:41:52,040
Speaker 2: better when you have very little disease. We've known that

735
00:41:52,160 --> 00:41:54,879
Speaker 2: for a long long time. So what the Alpha three

736
00:41:54,920 --> 00:41:58,120
Speaker 2: trial is designed to do is actually find the patients

737
00:41:58,120 --> 00:42:03,359
Speaker 2: with the lowest imaginable amount of disease, just the microscopic disease.

738
00:42:03,120 --> 00:42:05,280
Speaker 1: And what percentage of patients are those.

739
00:42:05,600 --> 00:42:11,520
Speaker 2: So most likely ninety to probably close to one hundred

740
00:42:11,520 --> 00:42:15,840
Speaker 2: percent of patients who eventually relapse will have an interval

741
00:42:15,880 --> 00:42:19,120
Speaker 2: of time where they have MRD only disease, where you

742
00:42:19,160 --> 00:42:21,480
Speaker 2: can only find it in the blood using a very

743
00:42:21,480 --> 00:42:25,719
Speaker 2: specific molecular test. Relapse doesn't typically happen out of the

744
00:42:25,760 --> 00:42:29,160
Speaker 2: clear blue sky. So if we time things well, as

745
00:42:29,160 --> 00:42:31,839
Speaker 2: we're trying to do with Alpha three, the patients get

746
00:42:31,840 --> 00:42:35,759
Speaker 2: the MRD test at the right time, their doctors order it.

747
00:42:36,239 --> 00:42:39,000
Speaker 2: If it's found to be positive, we act on it.

748
00:42:39,120 --> 00:42:41,760
Speaker 2: In this case, we enroll in our clinical trial. But eventually,

749
00:42:41,760 --> 00:42:44,879
Speaker 2: if this trial is positive, we hope that this off

750
00:42:44,920 --> 00:42:48,600
Speaker 2: the shelf car T cell will be available commercially, so

751
00:42:48,680 --> 00:42:50,319
Speaker 2: this could become a standard of care.

752
00:42:50,680 --> 00:42:54,480
Speaker 1: But you're hoping that if you're able to introduce CARTI

753
00:42:54,719 --> 00:42:59,160
Speaker 1: therapy much earlier with the help of this test that

754
00:42:59,200 --> 00:43:03,080
Speaker 1: will indicate your risk of relapse, that it is much

755
00:43:03,120 --> 00:43:03,800
Speaker 1: more effective.

756
00:43:03,880 --> 00:43:06,720
Speaker 2: That's one hundred percent. If we can find these folks

757
00:43:06,960 --> 00:43:10,319
Speaker 2: when there are disease is at its weakest point and

758
00:43:10,680 --> 00:43:13,760
Speaker 2: mop it up with the Carte cells at their local

759
00:43:13,800 --> 00:43:17,880
Speaker 2: institution without a big onerous referral or blood collection, just

760
00:43:17,920 --> 00:43:20,600
Speaker 2: take care of it right then and there. Does that

761
00:43:20,640 --> 00:43:24,040
Speaker 2: improve long term cure? Does that improve outcomes and you

762
00:43:24,160 --> 00:43:29,560
Speaker 2: prevent the horrific relapse. That's a terrible moment for everybody

763
00:43:29,920 --> 00:43:33,120
Speaker 2: when you think you're cured of your lymphoma and then

764
00:43:33,160 --> 00:43:36,480
Speaker 2: suddenly you go to a clinic one day and you

765
00:43:36,520 --> 00:43:38,839
Speaker 2: get a scan and the doctor comes in and says

766
00:43:38,840 --> 00:43:41,920
Speaker 2: that your cancers come back. What we're trying to do

767
00:43:42,040 --> 00:43:46,600
Speaker 2: with this trial by deploying these Carte cells early, is

768
00:43:46,680 --> 00:43:49,080
Speaker 2: to prevent that from ever happening and get those patients

769
00:43:49,080 --> 00:43:51,479
Speaker 2: into a cured state. That is really what we're trying

770
00:43:51,520 --> 00:43:55,360
Speaker 2: to do. If we are successful here, this will be

771
00:43:55,640 --> 00:44:02,400
Speaker 2: the most impactful change to first line outcomes in almost

772
00:44:02,440 --> 00:44:05,840
Speaker 2: thirty years. That's how hard it's been to improve outcomes

773
00:44:06,120 --> 00:44:09,880
Speaker 2: in frontline non HODGKINSLM foma. So Alpha three is really

774
00:44:10,040 --> 00:44:12,040
Speaker 2: potential to be revolutionary here.

775
00:44:12,480 --> 00:44:16,399
Speaker 1: Most people are cured with the standard of care when

776
00:44:16,440 --> 00:44:20,319
Speaker 1: you have these blood cancers, correct, correct, But there is

777
00:44:20,360 --> 00:44:23,360
Speaker 1: a subset of people who relapse, and we don't know

778
00:44:23,400 --> 00:44:24,839
Speaker 1: who they are, right and.

779
00:44:24,719 --> 00:44:27,400
Speaker 2: It's about a third about a third of patients with

780
00:44:27,800 --> 00:44:31,160
Speaker 2: the most common type of non HODGKINSLM foma that we're studying,

781
00:44:31,160 --> 00:44:35,440
Speaker 2: it's a disease called diffuse large B cellmphoma, pretty common

782
00:44:35,480 --> 00:44:39,680
Speaker 2: blood cancer. About ninety percent of these patients will achieve

783
00:44:39,719 --> 00:44:43,520
Speaker 2: a remission to frontline care, which is the standard regimen

784
00:44:43,520 --> 00:44:47,120
Speaker 2: that we've been given for thirty years, but a third

785
00:44:47,200 --> 00:44:50,440
Speaker 2: of those patients will eventually have a relapse. And the

786
00:44:50,480 --> 00:44:52,480
Speaker 2: standard of care right now is you get to the

787
00:44:52,640 --> 00:44:56,279
Speaker 2: end and then you watch and wait. These patients will

788
00:44:56,320 --> 00:44:58,839
Speaker 2: come back every three months for a clinic visit, they

789
00:44:58,840 --> 00:45:01,400
Speaker 2: get scanned every three to six months, and essentially you're

790
00:45:01,480 --> 00:45:04,080
Speaker 2: kind of on pins and needles waiting for this tumor

791
00:45:04,160 --> 00:45:04,560
Speaker 2: to recur.

792
00:45:04,840 --> 00:45:07,400
Speaker 1: Can you tell me a little bit, Zach, about how

793
00:45:07,480 --> 00:45:10,760
Speaker 1: this specific trial that you're running came about.

794
00:45:12,080 --> 00:45:17,080
Speaker 2: Certainly a very cutting edge trial and in fact, even

795
00:45:17,239 --> 00:45:19,799
Speaker 2: just a few years ago, we wouldn't have been able

796
00:45:19,800 --> 00:45:22,319
Speaker 2: to run this trial. There really needed to be a

797
00:45:22,400 --> 00:45:26,120
Speaker 2: confluence of new technologies all coming to the four at

798
00:45:26,280 --> 00:45:30,040
Speaker 2: roughly the same time. So the example first that I'll

799
00:45:30,320 --> 00:45:35,799
Speaker 2: lead with is the MRD platform. This test and this

800
00:45:35,880 --> 00:45:39,000
Speaker 2: class of tests is pretty new. It's only been around

801
00:45:39,040 --> 00:45:41,640
Speaker 2: for a few years in this iteration that it is

802
00:45:41,719 --> 00:45:44,600
Speaker 2: right now, and it's only recently begun to be used

803
00:45:44,600 --> 00:45:48,680
Speaker 2: in patients with lymphoma. So that advent was something that

804
00:45:48,760 --> 00:45:52,480
Speaker 2: was required. The next big thing was because we need

805
00:45:52,520 --> 00:45:55,759
Speaker 2: to act so quickly on the MRD positive result. You know,

806
00:45:55,800 --> 00:46:00,279
Speaker 2: we can't spend months referring patients to cartee centers having

807
00:46:00,360 --> 00:46:03,440
Speaker 2: their products manufactured. We have to act really within days.

808
00:46:04,120 --> 00:46:06,760
Speaker 2: We needed to have an aalogenetic off the shelf therapy

809
00:46:06,840 --> 00:46:07,239
Speaker 2: ready to go.

810
00:46:07,400 --> 00:46:10,760
Speaker 1: And when you say allogenetic, just remind people what that needs.

811
00:46:10,880 --> 00:46:13,600
Speaker 2: That means it's coming from a healthy donor, but it

812
00:46:13,680 --> 00:46:17,120
Speaker 2: means from a practical perspective, from a patient perspective, that

813
00:46:17,160 --> 00:46:18,279
Speaker 2: it's off the shelf.

814
00:46:18,239 --> 00:46:20,080
Speaker 1: And it's ready, it's ready to need.

815
00:46:19,960 --> 00:46:23,040
Speaker 2: It when the patient needs it. It's ready to go.

816
00:46:23,080 --> 00:46:25,160
Speaker 2: It can be there literally in days because time is

817
00:46:25,160 --> 00:46:27,680
Speaker 2: of the time is of the essence. For these MRD

818
00:46:27,800 --> 00:46:31,640
Speaker 2: positive patients, we know their disease could come back any day,

819
00:46:32,719 --> 00:46:35,160
Speaker 2: and it actually can happen very very quickly within weeks,

820
00:46:35,960 --> 00:46:38,239
Speaker 2: so we really have to act very rapidly on.

821
00:46:38,160 --> 00:46:40,640
Speaker 1: That is the reason a trial like this hasn't been

822
00:46:40,719 --> 00:46:46,279
Speaker 1: done before, because all these technologies didn't exist and all

823
00:46:46,280 --> 00:46:48,680
Speaker 1: the pieces of the puzzle weren't there yet.

824
00:46:49,640 --> 00:46:53,760
Speaker 2: That is essentially it. We needed enough time for these

825
00:46:53,800 --> 00:46:57,719
Speaker 2: technologies independently to mature to a point where we could

826
00:46:57,760 --> 00:47:01,120
Speaker 2: combine them into what is really a very cutting edge

827
00:47:01,120 --> 00:47:05,080
Speaker 2: and revolutionary design. To be able to act upon a

828
00:47:05,160 --> 00:47:08,239
Speaker 2: disease before you can see it on a scan. That

829
00:47:08,360 --> 00:47:10,520
Speaker 2: is kind of a new concept, but it makes a

830
00:47:10,560 --> 00:47:15,319
Speaker 2: lot of sense because drugs and cart cells tend to

831
00:47:15,320 --> 00:47:17,400
Speaker 2: work better when there's not very much cancer around.

832
00:47:18,160 --> 00:47:21,560
Speaker 1: Let's talk about the patients that will benefit from this

833
00:47:21,880 --> 00:47:27,720
Speaker 1: right now. Is it a specific lymphoma patient you're looking

834
00:47:27,800 --> 00:47:31,000
Speaker 1: for to participate in this trial? Is it people with

835
00:47:31,160 --> 00:47:33,440
Speaker 1: leukemia who are you looking for?

836
00:47:33,960 --> 00:47:37,680
Speaker 2: Yes? So, in the Alpha three trial, it is for

837
00:47:37,840 --> 00:47:41,680
Speaker 2: a group of patients with non Hodgkins lymphoma, and it's

838
00:47:41,719 --> 00:47:45,600
Speaker 2: actually the greatest or most prevalent non Hodginson foma, which

839
00:47:45,640 --> 00:47:49,040
Speaker 2: is a disease called diffuse large diffuse large B cell

840
00:47:49,080 --> 00:47:53,560
Speaker 2: lymphoma or DLBCL. So that is the main type of

841
00:47:53,600 --> 00:47:56,680
Speaker 2: cancer that is eligible for Alpha three. There are a

842
00:47:56,680 --> 00:48:00,319
Speaker 2: couple other non Hodginson foma which are less common, but

843
00:48:00,400 --> 00:48:02,360
Speaker 2: that's the majority of patients that we're looking for at

844
00:48:02,400 --> 00:48:03,600
Speaker 2: DLBCL patients.

845
00:48:03,800 --> 00:48:07,800
Speaker 1: What is the standard of care right now for people

846
00:48:08,040 --> 00:48:12,280
Speaker 1: with diffuse large B cellomphoma.

847
00:48:12,160 --> 00:48:17,480
Speaker 2: So everyone gets the same treatment. It's a five drug

848
00:48:17,520 --> 00:48:24,799
Speaker 2: regimen that's chemotherapy our CHOP, and it's given every three weeks.

849
00:48:24,880 --> 00:48:27,759
Speaker 2: Those five drugs are given together, all on the same day,

850
00:48:29,400 --> 00:48:32,960
Speaker 2: six times three weeks apart, and at the end of

851
00:48:32,960 --> 00:48:37,200
Speaker 2: that six cycles of our CHOP, you undergo a cat

852
00:48:37,200 --> 00:48:40,600
Speaker 2: scan to see whether your disease has gone into remission

853
00:48:40,680 --> 00:48:44,279
Speaker 2: or whether it hasn't. The majority of patients will have

854
00:48:44,480 --> 00:48:47,480
Speaker 2: entered or remission, and about two thirds of them are cured.

855
00:48:48,160 --> 00:48:50,480
Speaker 2: They never need another drop of treatment ever again in

856
00:48:50,520 --> 00:48:52,239
Speaker 2: their lives and they're not going to hear from their

857
00:48:52,320 --> 00:48:56,200
Speaker 2: lymphoma again. There is a third of patients, however, who

858
00:48:56,280 --> 00:48:59,120
Speaker 2: will eventually have their disease come back and right now.

859
00:48:59,200 --> 00:49:02,760
Speaker 2: The problem is with our PET scans and our cat scans,

860
00:49:03,080 --> 00:49:06,480
Speaker 2: the way we measure disease activity is we can't distinguish

861
00:49:06,480 --> 00:49:09,080
Speaker 2: who's who right when they complete treatment.

862
00:49:09,480 --> 00:49:13,839
Speaker 1: So will this expand to other blood cancers do you think,

863
00:49:13,920 --> 00:49:18,160
Speaker 1: in other words, leukemia patients or other people who might

864
00:49:18,280 --> 00:49:18,719
Speaker 1: need it.

865
00:49:19,680 --> 00:49:26,560
Speaker 2: Absolutely so. If the Alpha three trial is successful and

866
00:49:26,680 --> 00:49:30,640
Speaker 2: we are able to show that preventing relapse leads to cures,

867
00:49:31,920 --> 00:49:33,560
Speaker 2: I think it would make a lot of sense for

868
00:49:33,600 --> 00:49:37,160
Speaker 2: Allergen or other drug developers to start to replicate this

869
00:49:37,280 --> 00:49:41,640
Speaker 2: study in other settings like B cell leukemias, like other

870
00:49:41,719 --> 00:49:45,799
Speaker 2: types of lymphoma. It is such a revolutionary way to

871
00:49:45,920 --> 00:49:51,120
Speaker 2: look at treating cancer, preventing relapse before it occurs, and

872
00:49:51,239 --> 00:49:55,319
Speaker 2: using this MRD test to really segregate patients who are

873
00:49:55,560 --> 00:49:58,480
Speaker 2: very high risk versus those who are probably cured and

874
00:49:58,520 --> 00:50:00,520
Speaker 2: you don't need to worry about them as much anymore.

875
00:50:00,840 --> 00:50:05,839
Speaker 1: What about beyond oncology, do you see this therapy as

876
00:50:05,960 --> 00:50:08,160
Speaker 1: efficacious for other diseases?

877
00:50:10,120 --> 00:50:14,000
Speaker 2: So we have seen the last three years an explosion

878
00:50:14,320 --> 00:50:19,359
Speaker 2: of work into treating autoimmune disorders with cart cells. So

879
00:50:19,520 --> 00:50:24,120
Speaker 2: diseases like lupus and systemic sclerosis are scleroderma and others

880
00:50:25,280 --> 00:50:28,680
Speaker 2: multiple sclerosis, for example, there's been some proof of concept there.

881
00:50:28,719 --> 00:50:34,839
Speaker 2: So these same products that have demonstrated such power in

882
00:50:34,920 --> 00:50:39,800
Speaker 2: oncology are now bringing to patients with refractory autoimmune disease

883
00:50:40,800 --> 00:50:43,600
Speaker 2: for the first time in many years, an opportunity for

884
00:50:43,640 --> 00:50:47,000
Speaker 2: a drug free remission. These patients are entering remissions, their

885
00:50:47,040 --> 00:50:50,160
Speaker 2: disease activity is going significantly down, if not all the

886
00:50:50,160 --> 00:50:52,440
Speaker 2: way down to zero, and they're able to come off

887
00:50:52,440 --> 00:50:54,239
Speaker 2: of their drugs that they've been on for in some

888
00:50:54,320 --> 00:50:59,120
Speaker 2: cases decades. This is poised to become yet another revolution

889
00:50:59,520 --> 00:51:02,960
Speaker 2: in car just like we saw in oncology, and so

890
00:51:03,280 --> 00:51:06,000
Speaker 2: I think that it's a very exciting moment here. There's

891
00:51:06,320 --> 00:51:09,480
Speaker 2: hundreds upon hundreds of thousands of patients who could potentially

892
00:51:09,560 --> 00:51:14,160
Speaker 2: benefit from this intervention, and so companies like Allergeen are

893
00:51:14,400 --> 00:51:17,799
Speaker 2: trying to come up with ways that are tailored to

894
00:51:17,920 --> 00:51:24,480
Speaker 2: this patient segment that is oncology patients are different rheumatology patients,

895
00:51:24,480 --> 00:51:28,080
Speaker 2: and trying to meet the needs of those individuals directly

896
00:51:28,200 --> 00:51:29,960
Speaker 2: through our product design and study design.

897
00:51:30,920 --> 00:51:35,200
Speaker 1: Well, it's really thanks to scientists like you who work

898
00:51:35,360 --> 00:51:39,960
Speaker 1: tirelessly trying to figure out how to help patients so on,

899
00:51:40,040 --> 00:51:43,520
Speaker 1: behalf of so many people who I'm sure might be

900
00:51:43,640 --> 00:51:48,520
Speaker 1: listening to this and really being grateful for your work.

901
00:51:48,680 --> 00:51:52,359
Speaker 1: I'd like to say thank you first and foremost. And

902
00:51:52,400 --> 00:51:57,120
Speaker 1: where can people go to find more information that could

903
00:51:57,160 --> 00:52:00,720
Speaker 1: potentially really help them in the future or right now?

904
00:52:01,320 --> 00:52:04,480
Speaker 2: Certainly so, We've put together website Alpha threetrial dot com

905
00:52:04,520 --> 00:52:07,920
Speaker 2: that has a lot of different resources for both patients

906
00:52:07,960 --> 00:52:10,160
Speaker 2: and for physicians to learn about the trial and all

907
00:52:10,200 --> 00:52:12,680
Speaker 2: the various technologies that we're using in the study.

908
00:52:12,960 --> 00:52:15,399
Speaker 1: Doctor Zachary Roberts, thank you so much for the work

909
00:52:15,440 --> 00:52:19,719
Speaker 1: you're doing for sharing this potentially life saving information with

910
00:52:19,840 --> 00:52:21,360
Speaker 1: the public. I really appreciate it.

911
00:52:21,640 --> 00:52:22,880
Speaker 2: Thank you, Katie, It's been a pleasure.

912
00:52:26,560 --> 00:52:29,759
Speaker 1: Thanks for listening. Everyone. If you have a question for me,

913
00:52:30,160 --> 00:52:32,640
Speaker 1: a subject you want us to cover, or you want

914
00:52:32,680 --> 00:52:36,040
Speaker 1: to share your thoughts about how you navigate this crazy world,

915
00:52:36,400 --> 00:52:39,600
Speaker 1: reach out send me a DM on Instagram. I would

916
00:52:39,680 --> 00:52:42,720
Speaker 1: love to hear from you. Next Question is a production

917
00:52:42,840 --> 00:52:47,320
Speaker 1: of iHeartMedia and Katie Kuric Media. The executive producers are Me,

918
00:52:47,640 --> 00:52:52,320
Speaker 1: Katie Kuric, and Courtney Ltz. Our supervising producer is Ryan Martz,

919
00:52:52,840 --> 00:52:57,640
Speaker 1: and our producers are Adriana Fazio and Meredith Barnes. Julian

920
00:52:57,719 --> 00:53:02,840
Speaker 1: Weller composed our theme music. For more information about today's episode,

921
00:53:03,000 --> 00:53:05,399
Speaker 1: or to sign up for my newsletter, wake Up Call,

922
00:53:05,840 --> 00:53:08,760
Speaker 1: go to the description in the podcast app, or visit

923
00:53:08,840 --> 00:53:12,040
Speaker 1: us at Katiecuric dot com. You can also find me

924
00:53:12,120 --> 00:53:15,839
Speaker 1: on Instagram and all my social media channels. For more

925
00:53:15,880 --> 00:53:21,200
Speaker 1: podcasts from iHeartRadio, visit the iHeartRadio app, Apple Podcasts, or

926
00:53:21,239 --> 00:53:26,480
Speaker 1: wherever you listen to your favorite shows. This episode is

927
00:53:26,520 --> 00:53:29,920
Speaker 1: brought to you by Alogen, a company redefining how we

928
00:53:29,960 --> 00:53:34,120
Speaker 1: fight cancer and autoimmune disease. By pushing the boundaries of

929
00:53:34,200 --> 00:53:38,640
Speaker 1: cartes cell therapy. Allogen is creating next generation off the

930
00:53:38,680 --> 00:53:43,160
Speaker 1: shelf treatments designed to reach more people. Learn more at

931
00:53:43,200 --> 00:53:46,960
Speaker 1: allogen dot com.