Lenalidomide

We start preparing our patients for CAR-T versus bispecific antibodies, which really are the first to three lines of therapy discussions that we're having now, with the exception being people that have never had daratumumab.

They're not refractory to DERA or Revlimid.

Sometimes we'll introduce that.

and first relapse if they have not had daratumumab.

She's just excited.

I know, I'm just so excited to have a new class of drugs with a novel mechanism of action that's easily accessible in the communi- like, this is given the same way we'll learn about how it's given as Revlimid and pomalidomide, three day... three, three weeks on and one week off.

And so I think that that's, uh, that's comfortable for patients that have been on these drugs.

But, um, so what are the some of the trials? We'll talk about that in a minute.

And Velcade came in through that, as did venalizumab.

So I'd love to understand your feeling at that point, right? Because so I was at Celgene in the mid aughts, right? And and I remember, you know, Velcade was a competitor to thalidomide originally, and it draws back your Judah Falkman angiogenesis, understanding the mechanisms there, then lenalidomide, Revlimid on that.

And but here you were starting out your career, your first ever exposure was in the hematologic malignancy space, Mount Sinai, and having an interest in there, then practicing, and then to see this kind of revolution of treatments in the market.

Tell us about that feeling of coming full circle, even though Velcade was a proteasome inhibitor, right? Not a, you know, we didn't really understand thalidomide and relevant mechanisms, now molecular glues, popular, you know, phrase, but like, you must've felt like, wow, I've actually witnessed like a front row seat of these therapies that are actually having huge impacts on disease.

And with myeloma, that's exactly the situation we were in.

You know, we had individual drugs like the alkylators like melphalan and drugs like prednisone, marginal effects.

And then we got thalidomide and Revlimid, another mechanism.

We got bortezomib Velcade with another mechanism.

Right.

Lenalidomide combined with dexamethasone has shown significant efficacy.

Lenalidomide is an immunomodulatory imid drug that directly induces apoptosis in the clonal plasma cells and profoundly alters the bone marrow microenvironment, reducing the secretion of vascular endothelial growth factor.

In a phase two trial utilizing lenalidomide and dexamethasone, the neurologic response rate was about 95%, and the three-year overall survival was about 90%.

However, the choice of the specific systemic agent requires extreme caution from the neurology team.

The bad stuff is they're a new company with a limited track record.

Revlimid, which is this cancer drug, has expired.

So it's only about 1% of their revenues this year, which is not good.

And the replacements are not really yet clear.