SR @PatternNotes

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.

@Hstlinghosptlis @JoshuaBarzon @official_flo @FLAGALine @Floridaman @nbc6 @RonDeSantis @SunSentinel @FloridaTourism @FlaPanthers @FloridaGators 😂 thanks for the info!

@Hstlinghosptlis @JoshuaBarzon @official_flo @FLAGALine @Floridaman @nbc6 @RonDeSantis @SunSentinel @FloridaTourism @FlaPanthers @FloridaGators Food options good? Beach 🏖️? Clearwater best beach I have seen, how does it compare? Thanks

@BiomedicalRX @meremrtl No PhD here, but I grew up watching my father chase one in chemical engineering, and that shaped how I think.

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.

@Hstlinghosptlis @JoshuaBarzon @official_flo @FLAGALine @Floridaman @nbc6 @RonDeSantis @SunSentinel @FloridaTourism @FlaPanthers @FloridaGators Why? 30A/Santa Rosa Beach is hard to beat — Seaside, Grayton, Rosemary, white-sand beaches, slower pace, and enough good food without the Orlando/Miami chaos?

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

@LennaertSnyder @WatcherGuru You mean 64,5k? Lol

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

Disclosure: I’m long CRBU. This is my personal thesis based on public information only. High-risk biotech. Not financial advice. I may add, trim, or exit as facts or risk change.

The market is Wonderland. 🕰️🐇 Sometimes you have to believe in six impossible things before the opening bell rings. Impossible thing number two: The four-lane CRBU thesis The market may be missing the real CRBU structure. Caribou is not only two clinical drugs. It may be two clinical drugs plus a licensable editing architecture. CB-010 / vispa-cel has shown 82% ORR, 64% CR, and 51% PFS at 12 months in the prospectively HLA-matched confirmatory cohort. CB-011 has shown 92% ORR, 75% ≥CR, and 91% MRD negativity in early CaMMouflage data, and now has RMAT designation. Those are the clinical proof points. But chRDNA is the platform layer. Caribou invented CRISPR hybrid RNA-DNA guides to improve editing specificity and support precise, complex genome edits for off-the-shelf cell therapies. That creates a possible tollbooth model: • ex vivo CD19 drug rights • ex vivo BCMA drug rights • CD19-related platform / future modality rights • BCMA-related platform / future modality rights The FDA Platform Technology Designation Program makes this more interesting, because validated platform technologies may be able to leverage prior CMC/safety/manufacturing data across related products. But the key is rights of reference. Nobody gets to use CRBU’s platform data for free. They would need to license the IP and the data rights. That is the bull case: CB-010 and CB-011 validate the clinical layer. chRDNA becomes the licensable infrastructure layer. If Big Pharma wants the drug, they pay for the drug. If Big Pharma wants the editing architecture for future ex vivo or in vivo programs, they may need to pay again. That is the four-lane CRBU thesis. 1. Ex Vivo CD19 — CB-010 / vispa-cel Big Pharma pays for the mature, clinical-stage, off-the-shelf CD19 CAR-T asset to secure lymphoma optionality. 2. Ex Vivo BCMA — CB-011 Big Pharma pays for the RMAT-designated BCMA CAR-T asset to secure multiple myeloma optionality. 3. In Vivo CD19 — Platform License Big Pharma pays for chRDNA “scissors,” IP access, and potential rights of reference to relevant platform data for future CD19 in vivo or autoimmune applications like lupus. 4. In Vivo BCMA — Platform License Big Pharma pays for chRDNA “scissors,” IP access, and potential rights of reference to relevant platform data for future BCMA in vivo or next-generation myeloma programs. My personal notes. Not financial advice

DNA contains the IL15 gene → the cell transcribes it into IL15 mRNA → ribosomes translate that mRNA into IL-15 protein → IL-15 is used locally or presented/released to communicate with immune cells. Skeletal muscle can express that gene, especially in the context of contraction and exercise stress. The muscle then uses IL-15 as a myokine — a message to the immune system. That message helps support NK cells and CD8+ T cells, which are central to immune surveillance. Exercise turns on the IL-15 message; redox/persulfidation support may reduce inflammatory static so the immune system hears that message more clearly. High inflammation = static on the radio. Exercise = the broadcast. IL-15 = one of the key messages. Redox support = reducing the static so the message comes through cleaner. Immune labs: 1. Lymphocyte subset panel This is the first real “under the hood” immune panel. It breaks the immune system into compartments: •CD3: total T cells •CD4: helper T cells •CD8: cytotoxic T cells •CD4/CD8 ratio: immune balance / aging signal •CD19: B cells •CD16/CD56: NK cells This is more useful than a CBC because it shows whether the immune army is balanced — not just whether the total white blood cell count looks normal. 2. NK-cell activity/function assay This gets closer to the real question: Are the NK cells actually killing? NK cells are one of the immune system’s first-line cytotoxic cells. They help identify and eliminate virally infected, stressed, abnormal, or potentially cancerous cells. Counting NK cells is useful, but function matters more. NK cells are recognized for anti-viral and anti-tumor responses, which is why they are a major focus in cancer immunotherapy. 3. Granzyme B + perforin These are the weapons. Perforin helps punch holes in the target cell. Granzyme B enters and helps trigger programmed cell death. So when I think about immune surveillance, I do not just care whether NK cells and CD8+ T cells exist. I care whether they are carrying the cytotoxic machinery needed to do their job. Granzyme B and perforin are central parts of that NK/CD8 killing system. 4. IFN-γ response IFN-γ is a major Th1 / cytotoxic immune signal. This is the “immune system is awake and coordinating an attack” marker. It is produced by NK cells and T cells and helps activate macrophages, antigen presentation, and anti-viral / anti-tumor immune responses. 5. IL-15, IL-15Rα, and IL-7 These are more research-style markers, but they matter for the thesis. IL-15 helps support NK cells and memory CD8+ T cells. IL-15Rα is important because IL-15 often works through receptor-mediated “presentation,” not just floating freely in the blood. IL-7 helps support T-cell survival and immune maintenance. IL-15 is specifically known for regulating activation and proliferation of T cells and NK cells and for helping maintain memory T cells. So IL-15 is not just a “more inflammation” marker. It is closer to an immune-survival and immune-readiness signal. 6. IL-6, TNF-α, and IL-10 These help show the inflammatory background. IL-6 and TNF-α can reflect inflammatory activation. IL-10 is more regulatory / anti-inflammatory. But these are tricky. Higher is not automatically bad, and lower is not automatically good. Timing matters. Context matters. Acute exercise can transiently move cytokines. Chronic inflammation a different story. A CBC tells me the immune system is present. A lymphocyte subset panel tells me how the army is organized. An NK-function assay tells me whether the assassins can actually kill. Granzyme B and perforin tell me whether they are armed. IFN-γ tells me whether the cytotoxic network can communicate. And IL-15 tells me whether the survival and readiness signal may be active. That is the real immune-resilience dashboard. Personal hypothesis. Educational only. Not medical advice, not a diagnosis, and not a claim that any food, supplement, or protocol prevents or treats cancer.

The market is Wonderland. 🕰️🐇 Sometimes you have to believe in six impossible things before the opening bell rings. Impossible thing number one: I’m interested in whether pulsed dietary organosulfur signaling can support the hydrogen-sulfide / persulfidation axis — a redox pathway where sulfur species can modify cysteine residues on proteins and influence metabolic signaling pathways like AMPK. 🧬🔥 The hypothesis: since mechanical exercise already activates AMPK to trigger myokines like IL-15, spiking the upstream redox environment through persulfidation might make that same IL-15-related exercise signal stronger, cleaner, or more sustained. To be clear: this is not a shortcut around training. I still run. The point is not to replace the mechanical signal — it is to explore whether precision nutrition can intensify the biochemical signaling around it. Personal hypothesis. Educational only. Not medical advice, not a recommendation, and not a claim of proven human performance enhancement.

Impossible thing number one: The longevity cuisines from Japan, France, and South Korea may be speaking the same biochemical language. South Korea uses salt, raw garlic, and kimchi. Japan uses Washoku, daikon radish, miso, natto, and green tea. France uses shallots, garlic, fermented cheese, and red wine. Different cuisines. Different cultures. Same recurring pattern: dietary sulfur + fermentation + polyphenols → H₂S / persulfidation biology → AMPK / redox signaling → immune resilience. That does not prove causation. Longevity is never that simple. Medical systems, screening, blood pressure, BMI, smoking rates, and public health all matter. But the overlap is hard to ignore. France gives us the French Paradox version of the signal. The base of traditional French cooking is not just butter. It is the allium family: garlic, onions, shallots, and leeks. Alliums contain organosulfur compounds that can contribute to hydrogen sulfide biology — one of the redox-signaling pathways involved in protein persulfidation and metabolic regulation. Garlic-derived organosulfur compounds have been studied as slow H₂S-releasing agents. Then comes red wine. The point is not “drink wine to live forever.” The point is that red wine polyphenols, especially resveratrol, have long been studied for AMPK/SIRT1-related metabolic signaling. So France may be pulling the same broad lever from another angle: sulfur from alliums, polyphenols from wine, and fermentation from cheese. Japan gives us the sister-study to South Korea. Japan historically had high stomach-cancer pressure from salt-preserved foods, pickled vegetables, H. pylori, and smoked foods. But Japan also built one of the most aggressive gastric-screening cultures in the world, which is a major reason survival is so high. CONCORD-3 data showed Japan’s 5-year net survival for stomach cancer improved to about 60.3% in 2010–2014, while South Korea was even higher at about 68.9%. That matters because the “Korean- Japanese paradox” is probably not one thing. It is not just food. It is not just screening. It is not just genetics. It is the collision of all three! High local gastric stress created high stomach-cancer incidence. Aggressive screening caught cancers earlier. And the broader dietary terrain — fermented foods, alliums, crucifers, soy, sea vegetables, green tea, polyphenols, and sulfur biology — may have supported a more resilient systemic host environment. South Korea may be the most extreme version of this model. The Lancet projection estimated that South Korean women could become the first national female population to cross the 90-year average life expectancy threshold by 2030. The same projection placed France second and Japan third. That is the signal I care about. Not “kimchi cures cancer.” Not “wine is a longevity drug.” Not “natto makes you immortal.” The real thesis is cleaner: The longest-lived food cultures keep repeating the same pattern: sulfur signaling, fermented biology, polyphenols, low metabolic dysfunction, and strong medical infrastructure. Different cuisines. Same biological conversation. Personal hypothesis. Educational only. Not medical advice, not dietary advice, and not a claim that any food prevents or treats cancer.