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Venture Global, Inc. engages in the provision of United States liquefied natural gas sourced from resource rich North American natural gas basins. It operates through the following segments: Calcasieu Project, Plaquemines Project, CP2 Project, and Sales and shipping. The company was founded by Michael Sabel and Robert Pender in 2023 and is headquartered in Arlington, VA.

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Venture Global Inc

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Hunter Biden’s Laptop (LAPTOP) is a memecoin referencing the eponymous Hunter Biden laptop sensation that’s been a fixture in global media news cycles for the past six years. LAPTOP is a fungible, freely transferable, non-yield-bearing ERC-20 token on Base. As a memecoin, LAPTOP has no utility, but incorporates two novel distribution mechanics designed to promote long-term community growth: a large community airdrop and an event-based supply mechanism.

Hunter Biden's Laptop

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Paramount Skydance Corp. - Ordinary Shares - Class B

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Johnson & Johnson

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General Motors Company

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Tidal Trust II - YieldMax Semiconductor Portfolio Option Income ETF

YieldMax Semiconductor Portfolio Option Income ETF

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Ford Motor Co.

Ford Motor Co

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Aduro Clean Technologies Inc

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$SLS My final DD before the readout. A tour through how GPS was built, from the first mouse experiments to where we stand now. Bench research was never my thing, but this decades long story is pretty incredible and had to start somewhere.  
 
The initial wall: Why WT1 was considered almost undruggable as a vaccine. 
 
WT1 (Wilms&#39; Tumor 1) is a transcription factor, a master control protein, that sits overexpressed in the vast majority of acute myeloid leukemia, and in mesothelioma, ovarian, and other cancers. In 2009 a National Cancer Institute panel ranked 75 cancer antigens by how good a target each would make. WT1 came in first. Number 1 out of 75. 
 
So why did it take decades to build a vaccine against the best target in oncology? Because WT1 is a self-antigen, an &quot;oncofetal&quot; protein your own healthy cells express at low levels. Your immune system is trained during development to tolerate self. T-cells that react too strongly to your own proteins get deleted before they ever reach your bloodstream. So the T-cells that can see WT1 tend to be low-avidity, weak binders, the leftovers that slipped through tolerance. Vaccinating with plain WT1 mostly wakes up that weak, tired &quot;army&quot;. That&#39;s the wall. It&#39;s the same wall Stimuvax (MUC1) and MAGE-A3 crashed into, you can&#39;t rally a strong army against a target the army was built to protect. 
 
The first proof it could even work: the Japanese mouse experiments. 
 
Before GPS existed, the foundational question was simply: can you immunize against WT1 at all without the immune system attacking the body&#39;s own healthy WT1-expressing tissue? The answer came largely from Japanese groups (Sugiyama and colleagues, PMID 12188920). 
 
They immunized mice with WT1 peptides, then challenged them with WT1-expressing tumors. The vaccinated mice rejected the tumors, and survived, with no signs of auto-aggression against their normal organs that physiologically express WT1. That last clause is the whole ballgame for safety: the immune system could be pointed at WT1 on cancer without turning on the kidneys, marrow, and other tissues that also carry it. That preclinical result, tumor rejection without autoimmunity, is the reason a WT1 vaccine was worth pursuing in humans at all, and it foreshadows the clean safety profile GPS has carried through every trial since. 
 
The MSK insight: don&#39;t use the real target, use a sharpened decoy. 
 
Here&#39;s where Dr. David Scheinberg&#39;s group at Memorial Sloan Kettering enters. Their move was borrowed from their own earlier work on a different cancer target, bcr-abl in CML, where they&#39;d already shown you could vaccinate with native AND modified (&quot;heteroclitic&quot;) peptides. They ported that strategy to WT1 (Pinilla-Ibarz et al., Leukemia 2006, &quot;Improved human T-cell responses against synthetic HLA-A0201 analog peptides derived from the WT1 oncoprotein&quot; PMID 16990779). 
 
The concept: take the WT1 peptide and substitute a single amino acid at the &quot;anchor&quot; position, the spot that plugs into the HLA groove your cells use to display the peptide to T-cells. The right substitution makes the peptide bind the HLA groove more tightly and stably. A more stable, longer-displayed peptide is a louder alarm. It recruits stronger, higher-avidity T-cells than the native version ever could, and critically, those T-cells still cross-recognize the native WT1 on the actual tumor. You sharpen the decoy, and the response transfers to the real thing. 
 
The bench data, with the actual numbers. 
 
This is the study that shows the trick works. May, Dao, Pinilla-Ibarz, Maslak, Scheinberg et al., Clinical Cancer Research 2007 (PMID 17671141): &quot;Peptide Epitopes from the Wilms&#39; Tumor 1 Oncoprotein Stimulate CD4+ and CD8+ T Cells That Recognize and Kill Human Malignant Mesothelioma Tumor Cells.&quot; 
 
They ran a classic 51-chromium release cytotoxicity assay, radiolabel the tumor cells, add the T-cells, measure how much label gets released as cells are killed, against a WT1-positive human tumor line (JMN) and a WT1-negative control line (MeWo). The result: 
 
T-cells raised on the native WT1-A peptide: 19% lysis of the WT1-positive tumor vs 9.2% of the WT1-negative control. 
T-cells raised on the heteroclitic WT1-A1 analogue: 44.8% lysis of the WT1-positive tumor vs 22.2% of the control. P &lt; 0.001. 
 
Yup. The single-amino-acid modification more than doubled the tumor killing, from 19% to nearly 45%, while preserving specificity (it consistently killed WT1-positive cells harder than WT1-negative). That is direct, peer-reviewed, quantified proof that the core design choice does exactly what it was engineered to do.  
 
Why four peptides, and why that&#39;s the real innovation. 
 
A single killer-T-cell peptide, even a good one, tends to burn out. Immunology has a rule: durable, memory cytotoxic (CD8+ &quot;killer&quot;) responses require CD4+ &quot;helper&quot; T-cell support. This isn&#39;t a minor detail, it&#39;s arguably the lesson of the field. Earlier WT1 vaccine approaches that leaned on killer-cell epitopes without robust helper support repeatedly produced responses that were real but short-lived, strong for a few weeks, then fading, which is a leading explanation for why so many peptide vaccines generated measurable immune responses that never translated into clinical benefit. You can wake up the killers; the hard part is keeping them awake. 
 
GPS was built specifically to solve that. It contains four peptides: 
 
WT1-A1, a heteroclitic short peptide, the sharpened CD8+ killer trigger. 
 
WT1-331 and WT1-427, native long peptides that recruit CD4+ helper T-cells across many HLA types. 
 
WT1-122A1, a heteroclitic long peptide that stimulates both killers and helpers. 
 
The class-II helper epitopes were selected using the SYFPEITHI prediction algorithm for high binding affinity across many HLA-DRB1 molecules, deliberately, so the helper response works in a broad, genetically diverse patient population rather than only those with a lucky HLA type. That&#39;s why GPS is described as &quot;non-HLA-restricted.&quot; It&#39;s engineered breadth. 
 
And GPS&#39;s own Phase 2 immune monitoring suggests the design does what it was meant to: after six vaccinations, CD4+ helper T-cell responses were sustained through the vaccination period, with proliferation to the individual peptides rising 6- to 13-fold (p=0.008). The helper architecture, the piece earlier killer-only designs lacked, showed up and held. That&#39;s the durability bet, and in Phase 2 it cashed. 
 
The class-II helper epitopes were chosen using the SYFPEITHI prediction algorithm for high affinity across many HLA-DRB1 molecules, deliberately, so the vaccine works across a broad, genetically diverse patient population rather than only the lucky ones with the right HLA type. That&#39;s why GPS is described as &quot;non-HLA-restricted.&quot; It&#39;s engineered breadth, not luck. 
 
Proof it translates to humans. 
 
The next question is whether vaccinated patients actually generate these killers. They do. In the thoracic-cancer trial (Cancer Immunol Immunother, PMID 20532500), T-cells drawn from patients after vaccination killed WT1-positive tumor cells but not WT1-negative controls, and cytotoxicity was absent before vaccination and present after. The vaccine installed a killing capacity that wasn&#39;t there before. 
 
Then the AML Phase 2 (Maslak/Scheinberg, Blood Advances 2018): after 6 vaccinations, T-cell proliferation to the peptides rose 6- to 13-fold (p=0.008); 86% of tested HLA-A*02 patients mounted CD8 responses against the native WT1 (proving the decoy-to-real cross-reactivity held in patients); and the median overall survival in that CR1 cohort reached 67.6 months. Single-arm, so a signal rather than proof, but an extraordinary one. 
 
Why REGAL is the trial the FDA practically drew a map for. 
 
In 2011 the FDA published its only guidance dedicated to therapeutic cancer vaccines. Four core instructions: (1) treat in minimal residual disease, not bulky active cancer, because the immune response needs time and room; (2) use multiple antigens/epitopes to prevent tumor escape; (3) expect the survival curves to separate late, because immune memory builds slowly, and pick statistics accordingly; (4) use overall survival, not tumor response, as the endpoint. 
 
REGAL: enrolled in second remission (minimal disease). Four epitopes. Overall survival as the primary endpoint. And a pooled survival timeline that has stretched far past the original model, the exact late-emerging pattern the FDA said a working vaccine would produce. The failed vaccines of the 2000s violated those principles, single antigen, active disease, response endpoints. GPS reads like it was built from the guidance line by line, because the science underneath it was solving those exact problems a decade before the trial locked. 
 
Where we actually stand, honestly. 
 
Put the whole tour together. The #1-ranked target in cancer. A tolerance-breaking design proven at the bench to more than double tumor killing. Mouse data showing tumor rejection without autoimmunity. A four-peptide architecture built to fix the durability problem that sank earlier attempts. Cross-reactivity and killing confirmed in actual patients. A 67.6-month survival signal in Phase 2. And a Phase 3 designed almost exactly the way the FDA says these trials should be designed. 
 
The data is what decides. It always was. 
 
But this is not hope stacked on hope. This is fifteen-plus years of deliberate science, every design choice made to solve a specific problem that killed the vaccines before it, walking up to the finish line. If you ever wanted a front-row seat to the moment the field finds out whether the immune system can be taught to remember cancer, you have one. 
 
78 (79) of 80. Almost home team.

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$SLS 
@Stocktwits @tctranfo @StocktwitsHelp 
Could we get this important post below pinned to the Sellas board for the week ahead? Thanks.

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$SLS Incredible post, and I wanted to add to this in regards to a study just from June 2026 for WT1 that I haven&#39;t seen anyone bring up yet, which is Hashi 2026 
 
I discovered it just a week ago.  While in pediatric AML and post-transplant, it is perhaps most compelling clinical evidence that WT1 vaccination translates immune response into survival benefit.   They achieved a 91% 3-Yr OS compared to the normal 40%. 
 
1) 17 pediatric patients with post-transplant AML received WT1 peptide vaccines for maintenance 
2) Primary endpoint met: 3-year OS of 70.6% (95% CI 43.1–86.6%), exceeding the 30% historical control benchmark 
3) 12 clinical responders (sustained CR at 1 year) had 3-year OS of 91.7% (95% CI 53.9–98.7%) 
4) Immune responders vs. non-responders: 3-year OS 90.9% vs. 40.0% (p=0.027) 
 
The low-burden remission setting and the heteroclitic modification works. Hashii used a heteroclitic WT1-235 peptide (M to Y), and it successfully induced WT1-specific CTLs that recognized the native WT1 epitope

Bruno Ferdinand

$SLS @LeftyMD BEST POST EVER, read this, sleep well, our time is coming. Thanks Lefty

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SLS The science behind the investment…lengthy, but a must read. 😎🏦

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$SLS One should not post anything else here today out of respect for this great post!

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$SLS Magnificent work—it commands admiration! It also reminds us why we are here. 
I have a question... are you suggesting that the vaccine is particularly effective in our case because it is used on patients with low WT1 expression (due to their remission status, and as explicitly recommended by the FDA)? So, we might be looking at a vaccine that isn&#39;t limited to AML in second complete remission (CR2), but could potentially become a universal, preventative treatment?    @LeftyMD

Ludo

$SLS outstanding dd 🎩 off &amp; thanks for all you share with us.

$SLS Can’t wait for tomorrow! And check out the greatest DD this board has ever seen!

Juhana Tikkanen

SELLAS Life Sciences Group Inc

 My final DD before the readout. A tour through how GPS was built, from the first mouse experiments to where we stand now. Bench research was never my thing, but this decades long story is pretty incredible and had to start somewhere.  
 
The initial wall: Why WT1 was considered almost undruggable as a vaccine. 
 
WT1 (Wilms' Tumor 1) is a transcription factor, a master control protein, that sits overexpressed in the vast majority of acute myeloid leukemia, and in mesothelioma, ovarian, and other cancers. In 2009 a National Cancer Institute panel ranked 75 cancer antigens by how good a target each would make. WT1 came in first. Number 1 out of 75. 
 
So why did it take decades to build a vaccine against the best target in oncology? Because WT1 is a self-antigen, an "oncofetal" protein your own healthy cells express at low levels. Your immune system is trained during development to tolerate self. T-cells that react too strongly to your own proteins get deleted before they ever reach your bloodstream. So the T-cells that can see WT1 tend to be low-avidity, weak binders, the leftovers that slipped through tolerance. Vaccinating with plain WT1 mostly wakes up that weak, tired "army". That's the wall. It's the same wall Stimuvax (MUC1) and MAGE-A3 crashed into, you can't rally a strong army against a target the army was built to protect. 
 
The first proof it could even work: the Japanese mouse experiments. 
 
Before GPS existed, the foundational question was simply: can you immunize against WT1 at all without the immune system attacking the body's own healthy WT1-expressing tissue? The answer came largely from Japanese groups (Sugiyama and colleagues, PMID 12188920). 
 
They immunized mice with WT1 peptides, then challenged them with WT1-expressing tumors. The vaccinated mice rejected the tumors, and survived, with no signs of auto-aggression against their normal organs that physiologically express WT1. That last clause is the whole ballgame for safety: the immune system could be pointed at WT1 on cancer without turning on the kidneys, marrow, and other tissues that also carry it. That preclinical result, tumor rejection without autoimmunity, is the reason a WT1 vaccine was worth pursuing in humans at all, and it foreshadows the clean safety profile GPS has carried through every trial since. 
 
The MSK insight: don't use the real target, use a sharpened decoy. 
 
Here's where Dr. David Scheinberg's group at Memorial Sloan Kettering enters. Their move was borrowed from their own earlier work on a different cancer target, bcr-abl in CML, where they'd already shown you could vaccinate with native AND modified ("heteroclitic") peptides. They ported that strategy to WT1 (Pinilla-Ibarz et al., Leukemia 2006, "Improved human T-cell responses against synthetic HLA-A0201 analog peptides derived from the WT1 oncoprotein" PMID 16990779). 
 
The concept: take the WT1 peptide and substitute a single amino acid at the "anchor" position, the spot that plugs into the HLA groove your cells use to display the peptide to T-cells. The right substitution makes the peptide bind the HLA groove more tightly and stably. A more stable, longer-displayed peptide is a louder alarm. It recruits stronger, higher-avidity T-cells than the native version ever could, and critically, those T-cells still cross-recognize the native WT1 on the actual tumor. You sharpen the decoy, and the response transfers to the real thing. 
 
The bench data, with the actual numbers. 
 
This is the study that shows the trick works. May, Dao, Pinilla-Ibarz, Maslak, Scheinberg et al., Clinical Cancer Research 2007 (PMID 17671141): "Peptide Epitopes from the Wilms' Tumor 1 Oncoprotein Stimulate CD4+ and CD8+ T Cells That Recognize and Kill Human Malignant Mesothelioma Tumor Cells." 
 
They ran a classic 51-chromium release cytotoxicity assay, radiolabel the tumor cells, add the T-cells, measure how much label gets released as cells are killed, against a WT1-positive human tumor line (JMN) and a WT1-negative control line (MeWo). The result: 
 
T-cells raised on the native WT1-A peptide: 19% lysis of the WT1-positive tumor vs 9.2% of the WT1-negative control. 
T-cells raised on the heteroclitic WT1-A1 analogue: 44.8% lysis of the WT1-positive tumor vs 22.2% of the control. P < 0.001. 
 
Yup. The single-amino-acid modification more than doubled the tumor killing, from 19% to nearly 45%, while preserving specificity (it consistently killed WT1-positive cells harder than WT1-negative). That is direct, peer-reviewed, quantified proof that the core design choice does exactly what it was engineered to do.  
 
Why four peptides, and why that's the real innovation. 
 
A single killer-T-cell peptide, even a good one, tends to burn out. Immunology has a rule: durable, memory cytotoxic (CD8+ "killer") responses require CD4+ "helper" T-cell support. This isn't a minor detail, it's arguably the lesson of the field. Earlier WT1 vaccine approaches that leaned on killer-cell epitopes without robust helper support repeatedly produced responses that were real but short-lived, strong for a few weeks, then fading, which is a leading explanation for why so many peptide vaccines generated measurable immune responses that never translated into clinical benefit. You can wake up the killers; the hard part is keeping them awake. 
 
GPS was built specifically to solve that. It contains four peptides: 
 
WT1-A1, a heteroclitic short peptide, the sharpened CD8+ killer trigger. 
 
WT1-331 and WT1-427, native long peptides that recruit CD4+ helper T-cells across many HLA types. 
 
WT1-122A1, a heteroclitic long peptide that stimulates both killers and helpers. 
 
The class-II helper epitopes were selected using the SYFPEITHI prediction algorithm for high binding affinity across many HLA-DRB1 molecules, deliberately, so the helper response works in a broad, genetically diverse patient population rather than only those with a lucky HLA type. That's why GPS is described as "non-HLA-restricted." It's engineered breadth. 
 
And GPS's own Phase 2 immune monitoring suggests the design does what it was meant to: after six vaccinations, CD4+ helper T-cell responses were sustained through the vaccination period, with proliferation to the individual peptides rising 6- to 13-fold (p=0.008). The helper architecture, the piece earlier killer-only designs lacked, showed up and held. That's the durability bet, and in Phase 2 it cashed. 
 
The class-II helper epitopes were chosen using the SYFPEITHI prediction algorithm for high affinity across many HLA-DRB1 molecules, deliberately, so the vaccine works across a broad, genetically diverse patient population rather than only the lucky ones with the right HLA type. That's why GPS is described as "non-HLA-restricted." It's engineered breadth, not luck. 
 
Proof it translates to humans. 
 
The next question is whether vaccinated patients actually generate these killers. They do. In the thoracic-cancer trial (Cancer Immunol Immunother, PMID 20532500), T-cells drawn from patients after vaccination killed WT1-positive tumor cells but not WT1-negative controls, and cytotoxicity was absent before vaccination and present after. The vaccine installed a killing capacity that wasn't there before. 
 
Then the AML Phase 2 (Maslak/Scheinberg, Blood Advances 2018): after 6 vaccinations, T-cell proliferation to the peptides rose 6- to 13-fold (p=0.008); 86% of tested HLA-A*02 patients mounted CD8 responses against the native WT1 (proving the decoy-to-real cross-reactivity held in patients); and the median overall survival in that CR1 cohort reached 67.6 months. Single-arm, so a signal rather than proof, but an extraordinary one. 
 
Why REGAL is the trial the FDA practically drew a map for. 
 
In 2011 the FDA published its only guidance dedicated to therapeutic cancer vaccines. Four core instructions: (1) treat in minimal residual disease, not bulky active cancer, because the immune response needs time and room; (2) use multiple antigens/epitopes to prevent tumor escape; (3) expect the survival curves to separate late, because immune memory builds slowly, and pick statistics accordingly; (4) use overall survival, not tumor response, as the endpoint. 
 
REGAL: enrolled in second remission (minimal disease). Four epitopes. Overall survival as the primary endpoint. And a pooled survival timeline that has stretched far past the original model, the exact late-emerging pattern the FDA said a working vaccine would produce. The failed vaccines of the 2000s violated those principles, single antigen, active disease, response endpoints. GPS reads like it was built from the guidance line by line, because the science underneath it was solving those exact problems a decade before the trial locked. 
 
Where we actually stand, honestly. 
 
Put the whole tour together. The #1-ranked target in cancer. A tolerance-breaking design proven at the bench to more than double tumor killing. Mouse data showing tumor rejection without autoimmunity. A four-peptide architecture built to fix the durability problem that sank earlier attempts. Cross-reactivity and killing confirmed in actual patients. A 67.6-month survival signal in Phase 2. And a Phase 3 designed almost exactly the way the FDA says these trials should be designed. 
 
The data is what decides. It always was. 
 
But this is not hope stacked on hope. This is fifteen-plus years of deliberate science, every design choice made to solve a specific problem that killed the vaccines before it, walking up to the finish line. If you ever wanted a front-row seat to the moment the field finds out whether the immune system can be taught to remember cancer, you have one. 
 
78 (79) of 80. Almost home team.

LeftyMD

@LeftyMD 🫡 Outstanding breakdown of the science. Most retail investors just chase the line on the chart, but understanding central tolerance and why the heteroclitic peptide design works is what separates real high-conviction longs from momentum traders. 

The shift from a simple killer T-cell trigger to adding CD4+ helper architecture is exactly why GPS didn’t suffer the same fate as Stimuvax. 

Excellent summary of the MSK research before the readout. Till Buyout 🥂

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Bercovici Adrian

 🫡 Outstanding breakdown of the science. Most retail investors just chase the line on the chart, but understanding central tolerance and why the heteroclitic peptide design works is what separates real high-conviction longs from momentum traders. 

The shift from a simple killer T-cell trigger to adding CD4+ helper architecture is exactly why GPS didn’t suffer the same fate as Stimuvax. 

Excellent summary of the MSK research before the readout. Till Buyout 🥂