🧩Educational discussion of historical market structure & liquidity. No buy/sell/hold recommendations. Liquidity ≠ prediction. Not signals. Not financial advice
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Tracking liquidity & technical behavior across sessions.
Patterns repeat. Notes remember. Liquidity forgets.
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$CRBU — NBA Finals energy, Michael Jackson “Jam” in the background, and one message for EHA:
Show the world why allogeneic CAR-T still has a kingdom — and why Caribou may be sitting on the throne.
Just signed up. I know that does not solve the bigger economics, but I wanted to support the work because your voice is original and the DD has real depth.
The quick-returns crowd is loud, but some of us are here for the opposite: under-the-radar names, longer-duration setups, and frameworks we would not have found on our own. That is the edge. I hope you keep posting in whatever form still makes sense for you.
In other words: potential blockbuster.
Not because it lowers LDL alone.
Because if the outcomes data confirm the signal, $NAMS may hit LDL, Lp(a), glycemic risk, small-particle biology, and brain-aging biomarkers in one oral drug.
Long $NAMS. My personal notes. Not financial advice.
I don’t own $ABVX, but this biology is fascinating.
Whether obefazimod becomes first-line, second-line, or third-line in UC clearly matters commercially.
But my bigger question is biological:
Is $ABVX touching a real immune-dose lever?
Bullish defense: the short parent-drug half-life is a relief. Obefazimod itself clears quickly.
But the active metabolite, ABX464-N-Glu, appears to have a much longer half-life and is also pharmacologically active.
So the question is not simply:
“Could a short half-life drug create cancer in under a year?”
The better question is whether chronic miR-124 pathway tuning changes immune signal-to-noise over time.
Too much inflammation can become biological noise.
Too much immune dampening may reduce surveillance.
Looking at the 25 mg and 50 mg cohorts makes you wonder:
Maybe 25 mg is the Goldilocks dose.
Maybe the true immune-modulation window is even lower.
Completely unproven — but this is the question the safety debate opens up.
Purely a mechanistic hypothesis — not medical or financial advice.
This is why the dose-escalation data matters so much: it is not just about Wilson disease — it is about whether PRME’s liver-editing chassis can become reusable.
Prime building a printer?
Printer = GalNAc liver LNP + Prime Editor system
File = pegRNA / nicking guide RNA
Document = corrected liver gene
Wilson disease is the first liver document.
AATD is the second.
GSD1b is the third.
If every document needs a brand-new printer, the business is weaker.
But if the printer largely stays the same and only the file changes, the platform becomes much more valuable.
Scenario math — personal estimates, not company guidance:
CGD: $100M–$400M peak annual potential as a human Prime Editing validation bridge
Wilson: $500M–$1.5B peak annual potential
AATD: $1B–$4B+ peak annual potential
Other liver documents: $100M–$500M each
Platform / partnering value: meaningful optionality
If the printer works safely in humans, the revenue math stops being “one rare disease” and becomes:
How many liver mutations can this system print?
My personal notes. Not financial advice. No current PRME position; watching closely.
@LennaertSnyder@WatcherGuru For now, I’m currently net short BTC, but my bias is flexible and may flip long if liquidity/structure changes.
My personal notes. Not financial advice.
@LennaertSnyder@WatcherGuru Jusy having fun.
64.5k is what i am watching. Lets see if there is any bounce left?
My personal notes. Not financial advice
Agree with this. OA desperately needs something beyond pain management, injections, and eventual joint replacement.
GLP-1s may already be helping the load/inflammation side, and Cartigenix HP/RestorCel has interesting joint-biomarker data, but neither is the same as rebuilding lost joint architecture.
If the animal regeneration signal translates into durable human cartilage/bone repair, that could be a totally different category for orthopedics.
Thanks for sharing