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Alright! I was hoping blocking SYK as a downstream mediator of (among others) FcyRI might be able to block some feedback loop or further downstream mediators. Looking forward to reading the full hypothesis once its out! Thank you for your work :)

Would we expect to be able to pragmatically test this hypothesis with a drug like fostamatinib?

It seems as though Dr. Habets has successfully treated an ME patient with low doses teclistamab. Much more cost effective than daratumumab apparently (< 1000€ per treatment course). This is the German maverick oncologist that's also treated ME patients successfully with daratumumab in the past...

Hm, I guess I'm either just much less sensitive or we're just too different. To me there's a massive difference (positively) for brainfog on low doses. As you rightly mentioned, I believe it's an inverted U shaped dose-response curve and higher doses make me feel drunk/high/stoned. I really...

That happens with common doses for me as well, they must be small enough to not reach some sort of threshold that makes everything worse for me! Do you have any experience with that? Maybe in your case 25 mg or even less? I feel like what's often discussed are doses used for neuropathic pain...

Do we have a hypothesis on what causes this soreness? In PEM currently and if I didn't know any better, I would be 100% sure I caught a cold. Every time I have PEM my throat and nose just sore the hell up.

To me it makes sense if we frame my bro-science hypothesis ("strong LTP circuits are more vulnerable to dysfunction in ME than lesser potentiated ones") somewhat like this. Very high-level hypothesis: I believe strongly LTP synapses release more glutamate per spike compared to lesser...

For sure. I guess to compare dosing purely (and we assume the main moa is binding to spike) pk would suffice actually. We wouldn't know if that reflects any situation in vivo though - so doubtful how helpful this is.

We'd also need pd data - and from pk affinity to spike, maybe something like potency for ADCC if they retain effector functions (and if ADCC would be deemed necessary for post COVID treatment).

Dose means nothing without pk/pd data. If one or the other has a higher affinity, is more potent, bioavailable (would not expect this to be different with sc and iv) or what not, the doses will be different.

I've had thoughts along these lines before. The devil's-advocate-phamaceutical-engineer on my shoulder from my previous career always asked me if this wasn't "just some sort of "bro-science" in my head" but I also believe in @Jonathan Edwards line of thinking. Somewhat akin to a clinician like...

Not even close to published (still enrolling if at all I believe) but Nancy Klimas is doing a trial with sipavibart. Will be interesting to see the results later this year.

On the other hand, in the opening talk from Amy Proal, she said something where out of reflex my first instinct was to doubt her. She said we need new methods to be able to find tiny tiny minimal amounts of viral RNA/DNA/proteins more accurately. My response being "If you need to find those...

There was some speculation from Peluso's side on whether it was "just" the wrong drug. If there is viral persistence, I believe there could be something to that idea. It lost efficacy against SARS-CoV-2 variants in the end of 2022. Many of the patients enrolled had been (re)infected after 2022...

A little last minute, but today there's the PolyBio Spring 2025 symposium. According to the agenda, it looks like among others, results from a clinical trial using anti-spike mAbs in LC will be shared at 4 pm UTC. Free registration at the top of the agenda page or here.

Could any of the findings in this paper (and DecodeME) point towards potential symptomatic treatments through drug repurposing while curative treatments are in the making?

"rearranging" data can certainly create value. We don't know if we need any red in the picture. Maybe all of the needed data has already been generated and you only need to find the right connections - who knows? AI can certainly help with that. It might even be able to suggest experiments that...

Oh I meant anti CD38 mAbs specifically, from what I can see it's only Dara and Isa, and apparently only Isa can induce apoptosis alone? Idk, just what a quick Wikipedia search said, they referred to a 2019 trial that I didn't read.

Thanks for the info! The Prof asking the question made it sound like they've been testing CAR-T cells themselves and have seen much more benign side effects in autoimmune indications. But no idea, just sharing what I heard!

I read that isatuximab can induce apoptosis directly apparently?