Dexamethasone

um and the payload itself is delivered to the myeloma cell it in and of itself induces cell death and the antibody is also engineered to have an immunologic cell death so not only do we have direct cell death associated with chemotherapy we have activation of the immune system from the antibody itself And so we have two sets of randomized data that show the benefit of Belomav combinations in patients with relapsed and refractory myeloma.

This is the DREAM-7 study showing an improved progression-free survival and overall survival when Belomav was combined with bortezomib and dexamethasone compared to daratumumab, bortezomib, and dexamethasone.

And you see here on the bottom of the screen, the median progression-free survival was 36 months for the Belantamab, the Belomav arm, and only 13 months with the Daratumab, Brutasmab, Dexamethasone arm.

There was a higher response rate, a higher CR rate, and all of this improvement in response and progression-free survival translated into a real and statistical and clinically important improvement in overall survival.

And when we have updated data from this, the survival improvement is maintained and the increase in quality of life is maintained over the course of therapy.

The timeline differs, but the endpoint is the same if untreated.

What about treatment beyond antibiotics? You mentioned dexamethasone.

Dexamethasone is the main adjunct.

It's given with or just before the first antibiotic dose in suspected pneumococcal meningitis.

mostly in adults in high-income settings.

A commonly used regimen is hydrocortisone 300 mg EV as a loading dose followed by 100 mg every 8 hours.

Dexamethasone, such as 8 mg per day, is an alternative.

Now, supportive treatment is not an afterthought.

It is a major part of thyroid storm management.

So first, we're going to talk about the anti-inflammatory action and how that contributes to the mechanism of decatron.

So the first question is, does dexamethasone block one of these four pathways that I described in the same way that odansetronazofran blocks 5-HT3? The answer is no, and this is the first myth we have to kill.

Dexamethasone is not a receptor blocker in any way in which we usually describe a receptor blocker.

It doesn't sit on the 5-HT3 receptor and physically stop serotonin from binding.

Its mechanisms are going to be a little bit slower, a little bit more upstream, and I think a little bit more interesting.

So the surgery itself is generating a lot of this chemical noise that's going to really turn up the volume in the vomiting circuit.

And that's where dexamethasone comes in.

Dexamethasone is a glucocorticoid, meaning that it works through intracellular glucocorticoid receptors.

And this was using the NHS patient population essentially as a big open label, randomized, but still open label, clinical study to test the impact of drug repurposing candidates.

And within six weeks, for less than £2 million, we found dexamethasone.

Dexamethasone has saved way more than a million lives now.

It became almost overnight the standard of care for severe acute COVID-19 patients.

There is absolutely no reason why we shouldn't be able to do the same thing in exactly the same way with more targeting in long COVID and ME-CFS, and in fact, a whole bunch of other diseases as well.

D-

A Decadron?

That's a Pokemon.

That's a Pokemon.

But they fundamentally alter your metabolism.

Dexamethasone drastically raises blood glucose and causes insulin resistance.

So if you are on that steroid, trying to get your glucose low enough to hit a GKI of 1.0 is literally biologically impossible.

You are fighting a losing battle against heavy-hitting pharmaceuticals.

Antibody drug conjugates like Belentamab are really moving forward.

We have now the release of the data about the novel cell modes, especially mezictumide in combination with Scarfizumab and Dexamethasone, the successor to trial.

But...

I would say one of the key highlights from this meeting, but also from the ASCO 2026 annual meeting, is about the increasing use of bispecific antibodies, namely the BCMA-targeted T-cell engages, which are now moving progressively from late relapse into earlier disease setting and earlier relapse.