PD

Dangerous-Retard

Goddammit. Was gonna grab PD puts at the end of the day but decided to inverse myself. Shoulda just REversed myself the fuck outta there.

MediumSinger8088

[Decline of olfactory function in Parkinson's disease: A ten-year longitudinal study - PubMed](https://pubmed.ncbi.nlm.nih.gov/40383932/)"....When excluding patients with an MMSE score below 24, reflecting cognitive deficits that might interfere with olfactory test performance, UPSIT score still decreased by almost 7 points over the follow-up period. Conclusions: Olfactory function in PD declines more rapidly with increasing disease duration than can be explained by aging or cognitive decline alone. As such, olfactory function appears to be a clinical marker of disease progression in PD that can be measured non-invasively and deserves consideration as part of multimodal phenotyping to monitor disease progression." Evidently there is a vetted test for this, and could be included in future trial design.

MediumSinger8088

The FDA has nuked numerous studies citing historical or external controls, which are only justified in cases of rare disease - muscular dystrophy, Huntington's (QURE recent debacle), etc. There are plenty of PD patients. For my part, if biomarkers show statistical significance (or even close in this small N), I will look for a strategic point to increase my exposure - just saying I hope the company plays by the book with the FDA.

MediumSinger8088

Caveats about biomarkers and their limitations: Novo Nordisk semaglutide failed in AD trials despite "positive" biomarker data - though the specific data was not disclosed, and stock tanked 6% (for a $200B company = 10 billion). Remember c. 2013 Lily's Segamacestat failed in AD despite very clear biomarker data for target engagement. AD-directed monoclonals approved largely based on biomarkers don't work and have risks. Biomarkers have value; certainly, if the target is validated (IMO amyloid in AD is NOT) and the markers show engagement that is reassuring. NFL and alpha synuclein in some forms of PD have meaning... but ultimately it'll have to be gold-standard placebo-controlled trials with objective clinical endpoints to prove disease modification in PD, AD or other major prevalent indications. IF that can happen - judging by NVO- the valuation would be worth many billions of dollars.

Correct_Proposal_409

My base-case is that this at least works for the GBA1 subpopulation, which would be worth multiples of Gain's current market cap. But all signs point to GT-02287 working for a wide range of PD patients.

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MediumSinger8088

Yes, this table summarizes clinical chemical variables that quantitatively separate early and intermediate-stage PD patients from matched normal controls. AI-assisted summary : Maybe a dozen PD trials report on-treatment biomarker effects of some sort. Most historically have not used biomarkers, report only baseline CSF, or don't collect CSF at all. Per ChatGPT 5.2: "If you restrict to: * **Phase 1–3 interventional drug trials in PD**, * with **published human data**, * showing **statistically or clearly described on-treatment changes in CSF biomarkers** that are: * either direct target-engagement (e.g., CSF α-syn, CSF LRRK2/pRab10, CSF GCase), * or mechanistically relevant inflammatory / neurodegeneration markers, then as of late **2025** the literature supports **roughly 7–12 distinct trials/programs worldwide** that meet this bar: * Inosine (SURE-PD) – urate * Ambroxol (AiM-PD + PDD trial) – GCase * Early nilotinib studies – HVA / protein markers (not replicated in NILO-PD) * Buntanetap – exploratory CSF panel changes * MEDI1341/TAK-341 – free CSF α-syn ↓ * BIIB094/ION859 – CSF LRRK2 & pRab10 ↓ + lysosomal proteins * VTX3232 – CSF IL-18 and related inflammatory markers ↓ * a small number of other GBA-, LRRK2- or α-syn-targeted early studies with limited or abstract-only CSF results." MEDI1341 is the most relevant and best results, but it is a monoclonal anti-alpha synuclein antibody being developed by Astra Zeneca and Takeda. Astra-Zen and Sanofi seem to be the biggest players with advanced programs in this area. Note one wants to find increased a-synuclein in therapy-receiving patient CSF, indicating the a-syn is being washed out of the brain.

Correct_Proposal_409

Well, with all the recent emphasis on α-synuclein in Gain’s posters and presentations, it wouldn’t surprise me if the internal data already show reductions in α-synuclein–related pathology. That’s been a consistent theme in their preclinical work. Regarding RT-QuIC — isn’t that mainly used to identify PD by detecting misfolded α-syn seeds, not to measure whether a therapy is repairing the underlying disease process (like reductions in α-syn aggregates)?

MediumSinger8088

Beware biomarkers. Correlation is not the same as causation. Some biomarkers are more likely related to etiology (causal basis than others). Among the possible markers being assayed, the alpha-synuclein is likely to be most important. The table below ranks the biomarker separation of PD vs. non-PD, in general (thanks ChatGPT... I generally agree with the summary). https://preview.redd.it/84wg7k1b9i2g1.png?width=1032&format=png&auto=webp&s=bc4706dfb303c4cb0a871c7cb5dfad66425af780

Careless-Sleep4527

Their Phase 1b trial is testing the drug "in people with PD with or without a GBA1 mutation" - so they're already exploring the broader opportunity. If it only works in GBA1 patients it'll be smaller market (\~$1-2B opportunity) but if the drug works for a larger group without GBA1 its a potential blockbuster (\~$10B+ opportunity)

stylebros

For real. The elites seemed to bought up shit housing stock as well. The burnt down house still sits there diminishing property value of the block. I asked my local PD who owns it as they do squatter checks there occasionally, and it's some company. They pay the property taxes so they're not in trouble, but the building is fully condemned. I don't get why they're holding a burnt husk or a house since 2021.

MediumSinger8088

Decent summary and comparison to Bial and Vanqua Bio: [Gain Therapeutics: Valuation Remains Low In Light Of Recently Reported Functional Improvement In PD Patients (NASDAQ:GANX) | Seeking Alpha](https://seekingalpha.com/article/4840077-gain-therapeutics-valuation-remains-low-in-light-of-recently-reported-functional-improvement-in-pd-patients)

MediumSinger8088

Interview about 10 minutes... Baseness asks what comes next "Is it partnership, is it going it to the clinic alone into Phase 2...." Mack says "If the data is there at the end of the year, it's choose your own adventure... we'll have spirited conversations about whether we want to go it alone with the cash we can raise...or a partnership... maybe a combination of those two things". One could imagine all kinds of way to divide the pie among indications (Gaucher's isn't being talked about nearly enough - I'm surprised they didn't go straight for this as a fast track to approval but chose to swing for the fences on PD).

Correct_Proposal_409

https://preview.redd.it/liydunxc5f1g1.jpeg?width=1284&format=pjpg&auto=webp&s=362b3c2f535995f3532c48efbe6ef92200e357a0 You’re right that dilution is common in biotech, and it in fact has been happening some via Gain’s ATM recently — but in Gain’s case it’s looking less and less likely that there will be a large, go-it-alone cash raise for P2. Gain has been in active discussions with a handful of mid- and large-cap pharmas for at least the last year, probably longer. Management has made it clear they do not want to run Phase 2 or Phase 3 alone, and these potential partners have already completed nearly all of their due diligence. At this point, the only missing piece is the biomarker data… and realistically, these companies either already have early access to it or will see it next week at Neuroscience behind closed doors. GT-02287 went into Phase 1b already mostly de-risked, with: • strong mechanistic clarity (ER → lysosome → mitochondrial rescue) • 53% GCase activity increase in healthy humans • full motor rescue in multiple animal models • dose-dependent reversal of α-syn and toxic lipids • safety and CNS penetration already proven The upcoming biomarker readout is essentially the final confirmation… no meaningful downside risk and enormous upside potential. Even (what I believe is) the base-case scenario (highly effective in GBA1 patients) is a multibillion-dollar market. Big pharma clearly does not necessarily wait for P2 anymore (see slide). If you’re Merck, AbbVie, Lilly, or Roche… why would you risk letting the first disease-modifying Parkinson’s drug in history slip to a competitor? Especially when: • 90%+ of PD patients have lysosomal / GCase pathway dysfunction • Early signals already include improved smell and balance — the rarest and strongest markers of disease modification • Gain’s market cap is \~$100M I this is exactly the point in development where large pharma steps in: after the biology is validated but before the price goes up 10×. Dilution is possible— but a partnership or acquisition is far more likely, and far more rational, given the competitive landscape and what’s at stake. Btw, they still have a significant amount of their ATM available, which they’ve been using strategically to add runway space.

MediumSinger8088

Biomarker data can't confirm reversal of pathology - by definition this must be done by postmortem histology or in some cases neuroimaging. Regarding olfaction, this is interesting. Evidently hyposmia or anosmia (loss of smell) occurs in 90% of idiopathic PD patients, early in the disease but isn't always reported. This feature seems to map to alpha synuclein accumulation in the olfactory lobe but not to dopaminergic cell loss ([Non-motor features of Parkinson disease - CORE Reader](https://core.ac.uk/reader/111018871?utm_source=linkout)), which gets around the argument that "dead dopaminergic neurons can't come back to life". If so, 02287 may indeed engage fundamental processes in clearance of protein aggregates that would suggest broader utility beyond PD.

Correct_Proposal_409

Thanks for the response. Any thoughts on how neurogenesis and neuroplasticity play into the equation, depending on the circuitry (and patient)? Theoretically, if a PD patient has lost most of their neurons in a given system, but the existing neurons recover function, that could create the right environment for neurogenesis, which once was thought to be possible only in young brains. Neuroplasticity could also support further recovery, similar to what is seen in stroke patients, where surviving neurons reorganized and take over lost functions.

MediumSinger8088

Correct. Of those 50% or so living neurons (really, judge histologically at death - say when a person who had PD died of a heart attack or something), they may only have 50% function. The degree of functional recovery is not known because, well, there's never been a way to functionally recover them in vivo in a human.

MediumSinger8088

The data on the poster is very transparent - with N=9, nonparametric stats, the median baseline on MDS-UPDRS part III (the objective physician evaluation) is 19 and 90 day change is -5; p = 0.14, which is not formally significant but indicates 14% probability of type 1 statistical error (saying there is a change when there isn't). So 86% chance of a treatment effect with this small N, early time. The anecdotal stuff is interesting but I want numbers - hopefully that will all be forthcoming. No risk, no reward. The real important thing IMO will be if there is a reduction in the rate of conversion to moderate or severe PD over 6, 12, 18 months based on MDS-UPDRS... and in a placebo-controlled study. It takes a lot of time to get a drug to clinic.

MediumSinger8088

Dogma is that, AT TIME OF DIAGNOSIS of PD, 50-70% of the dopaminergic neurons in the substantia nigra have died and 80% of dopaminergic function has been lost. Those aren't coming back. Now there may be restoration of function in remaining neurons, reduction in gliosis, non-dopaminergic things happening (cholinergic disinhibition of D1 pathways) etc that are more important and therapeutically addressable than previously thought. Importantly, GBA1 deficient patients seem to have earlier and greater cholinergic involvement. If this thing works textbooks will need to be re-written, med school curricula revised. Which would be very exciting.

ImaginationRoutine96

You’re framing this like Gain is clueless about whether the drug gets into the brain, but that shows you haven’t actually looked at the data. They already measured CNS penetration in humans in the Phase 1 MAD cohort. It’s right there in the deck. Healthy volunteers showed clear CSF exposure of GT-02287 — 3.1 ng/mL on average, which matches the levels that worked in rodent models. The rodents actually had 2–8x higher drug levels in actual brain tissue than plasma, which is exactly what you want for a CNS drug. So no, they’re NOT “waiting to find out” if it crosses the BBB. They already know it does. The upcoming readout isn’t about basic penetration; it’s about confirming that long-term dosing in Parkinson’s patients produces consistent CNS levels and that those levels tie into: GCase activation, lysosomal + mitochondrial restoration, sphingolipid reduction and alpha-synuclein-related biomarkers On top of that, they’ve already shown functional improvement by Day 90 in the Phase 1b group. That alone sets them apart from pretty much every symptomatic PD treatment and most early “disease-modifying” attempts. And yes, other companies are working on Parkinson’s. That’s not the point. AskBio’s gene therapy is a totally different approach which is invasive, risky, and expensive. GT-02287 is an oral small molecule that restores GCase function across the entire disease cascade. If you actually compare mechanisms, they aren’t even in the same category. So the idea that Gain is behind or “doesn’t know” whether the drug hits the brain is just wrong. They already proved CNS exposure. What they’re about to share is the translation whether that CNS exposure, in actual PD patients, lines up with biomarkers and functional benefit. That’s the data big pharma waits for before writing a check.

MediumSinger8088

The p-value for the MDS-UPDRS III data in the poster is 0.14 by non-parametric stats with N=9. So 86% chance of a real treatment effect, not formally significant but encouraging. Notably the placebo effect on phase 3 is small; typically about 1 pt or less (pretty objective); median baseline MDS-UPDRS was 19, median change at 90 days was -5. Real tell would be rate of conversion to moderate-severe PD at timepoints 6 months, 12 months, 18 months. There are 21 patients who will reach 90d in 12/2025 and will be followed for 9 more months so it shouldn't take long to see if the early stage results hold true.

MediumSinger8088

Typically in a severe progression if a drug has an effect it has it at some early-intermediate stage then loses efficacy. When a PD patient shows symptoms they've already lost 80% of their dopaminergic neurons. Those aren't coming back. If there is a persistent separation between placebo and control that increases in magnitude at 6, 12, 18 months... the textbooks will have to be re-written.

Correct_Proposal_409

I think you are right, if a little conservative. If I'm one of the handful of big pharmas-- say Merck, who doesn't want any of their competition to own the first disease modifying PD drug-- I might not mess around, knowing other bids will end up being much higher. A lowball would create bad will and distrust. I think one of the serious pharmas might come in big on the first offer in the hopes of making a strong first impression and building good will.

Responsible-Meringue

Jfc you're a fucking brick wall, if you're even human. I was asking you, since you know so much about the smell & PD clinical relationship. I know the answer to the first third, & we haven't discovered the last 2/3rds. I was at least cursoraly interesting in what you had to say. But you don't have anything to say.  Humanity is cooked. Your AI link is just an agent wrapper to the big providers foundation models. A 4 day old product with spurious claims at best, spun up from a PE acquisition when Edison Scientific went bankrupt 3 years ago. Literally AI circlejerk slop. Can't believe bot farms are pulling 13yo accounts now, and engaging in ways that are far too natural to quickly scrutinize. We are most definitely in dead Internet territory now.  

Correct_Proposal_409

You’re not wrong that an n of 9 in only 90 days can’t prove anything definitive by itself, but calling the data meaningless misses what this trial was designed to do. It was meant to see if the biology that worked in animals actually shows up in people. And it does look like it’s showing up. Biomarkers will confirm if this is the case, and it sounds like they will have that. The 4-to-5-point improvement on MDS-UPDRS after 90 days matters because untreated PD patients typically worsen 3–5 points per year. Seeing that direction reverse — and only start improving at 90 days, not 30 — fits a disease-modifying mechanism, not a placebo effect. A small change in part 2 is also positive since they didn’t feel worse after 3 months. Btw, the majority of the patients, and their clinicians, asked to be included in the 9 month extension. Why would they want another lumbar puncture and a nasty daily drink if they didn’t think it was working? Mean age was 63 and mean disease duration was 3 years. That’s not exactly cherry-picking. And the return of smell and balance in at least multiple patients is the opposite of noise. Over 90 % of PD patients lose smell permanently and spontaneous recovery is virtually nonexistent. When something that rare shows up in multiple patients on the same drug, it’s a pretty clean biological signal that α-syn pathology is being cleared. Obviously we need more data on that. What other Parkinson’s drugs that are not purely symptomatic showed full motor function recovery in animal models, made meaningful improvements in UPDRS pt 3 scores, and returned sense of smell in a significant number of PD patients? I haven’t found any. Tough crowd!

Responsible-Meringue

Everyones an armchair scientist now. Ill wait till you can describe how the molecular mechanisms of smell sensation are impaired by the loss of dopaminergic neurons in the substantia niagra and your hypothesis on how the likely MOA of this drug causes the restoration of smell, and how that is an direct indicator of  reversal of the PD pathology. 

Responsible-Meringue

Generalizing a single MOA across idiopathic disease of any kind is idiocy at best. Moreover, the read out of a single efficacy metric is n=9. Fucking 9, that's barely a study in an in-vitro clonal cell-line where literally evey replicate is assumed identical. Effect size is ridiculously small, only the observer half (pt3) of the MDS-UPDRS is changing... The patients themselves are reporting no change QoL from reduction in symptoms (pt2). I see the MDS-UPDRS results graph on their poster and immediately concluded "cool, to the outside world it looks like their motor issues are getting better, but they still feel like shit inside. This drug ain't working". Also asterisk the fuck out of the score scale too. The pt3 scores reported are on the lower fifth of disability ranges in PD trials (lower half of early onset however you want to define that bucket), and the delta is like 5. Of course this makes sense cause ph1 is safety/tolerability so they pick people with less-severe PD as to not interfere with AE reports.  I might bookmark this as something to check in on if pt2 had any change, but this readout doesn't pass the sniff test for promising or even surprising results.  AI is a really decent textbook, but you still need the years of scientific training & honing your critical thinking, and tempering your emotional bias to interpret data correctly. Honestly a AP science high-school student would do a better analysis. 

leadbetterthangold

My dad passed from PD and a smart investor friends told me about this one. I only own like 1,000 shares but have been in like a year or two. Mostly like that it reminds me of my pops.

Fabulous_Mission1070

ALL IN!!!lets double whammy improvements in life for PD patients and make some $$ what a gift

Correct_Proposal_409

BTW, it wasn't just a fluke. GT-02287 was designed to do exactly this, and they did a ton of pre-clinical work which also predicted that it should work in humans with PD. Every step along the way has been further confirmation that it works. The only surprises along the way were to the upside. For example, they were very confident it would work in the GBA1 subset, but weren't confident about idiopathic populations. Now they are seeing it helps both.

Additional-Rich-7216

Company Progress • The DOJ/SEC investigations are closed, and CYDY was not the focus of the case. • The company has treated over 1,600 patients and is submitting its safety profile and supporting data for publication. • The Phase 3 MDR-HIV trial achieved statistical significance. • The Phase 2 MSS-CRC trial builds upon promising basket-trial data showing tumor size reduction, modulation of the tumor microenvironment, and PD-L1 up-regulation—potentially enabling synergistic combinations with checkpoint inhibitors. Management has communicated that PD-L1 data is expected in January 2026, which could pave the way for partnership funding or collaboration opportunities. ⸻ Conclusion Given the company’s strengthened fundamentals, clinical progress, and the closing of its regulatory challenges, CYDY appears significantly undervalued at current levels. Based on peer comparisons alone, a near-term valuation in the $3–$5 per share range seems reasonable even before accounting for additional indications or future developments.

Additional-Rich-7216

Company Progress • The DOJ/SEC investigations are closed, and CYDY was not the focus of the case. • The company has treated over 1,600 patients and is submitting its safety profile and supporting data for publication. • The Phase 3 MDR-HIV trial achieved statistical significance. • The Phase 2 MSS-CRC trial builds upon promising basket-trial data showing tumor size reduction, modulation of the tumor microenvironment, and PD-L1 up-regulation—potentially enabling synergistic combinations with checkpoint inhibitors. Management has communicated that PD-L1 data is expected in January 2026, which could pave the way for partnership funding or collaboration opportunities. ⸻ Conclusion Given the company’s strengthened fundamentals, clinical progress, and the closing of its regulatory challenges, CYDY appears significantly undervalued at current levels. Based on peer comparisons alone, a near-term valuation in the $3–$5 per share range seems reasonable even before accounting for additional indications or future developments.

Additional-Rich-7216

Company Progress • The DOJ/SEC investigations are closed, and CYDY was not the focus of the case. • The company has treated over 1,600 patients and is submitting its safety profile and supporting data for publication. • The Phase 3 MDR-HIV trial achieved statistical significance. • The Phase 2 MSS-CRC trial builds upon promising basket-trial data showing tumor size reduction, modulation of the tumor microenvironment, and PD-L1 up-regulation—potentially enabling synergistic combinations with checkpoint inhibitors. Management has communicated that PD-L1 data is expected in January 2026, which could pave the way for partnership funding or collaboration opportunities. ⸻ Conclusion Given the company’s strengthened fundamentals, clinical progress, and the closing of its regulatory challenges, CYDY appears significantly undervalued at current levels. Based on peer comparisons alone, a near-term valuation in the $3–$5 per share range seems reasonable even before accounting for additional indications or future developments.

Additional-Rich-7216

Company Progress • The DOJ/SEC investigations are closed, and CYDY was not the focus of the case. • The company has treated over 1,600 patients and is submitting its safety profile and supporting data for publication. • The Phase 3 MDR-HIV trial achieved statistical significance. • The Phase 2 MSS-CRC trial builds upon promising basket-trial data showing tumor size reduction, modulation of the tumor microenvironment, and PD-L1 up-regulation—potentially enabling synergistic combinations with checkpoint inhibitors. Management has communicated that PD-L1 data is expected in January 2026, which could pave the way for partnership funding or collaboration opportunities. ⸻ Conclusion Given the company’s strengthened fundamentals, clinical progress, and the closing of its regulatory challenges, CYDY appears significantly undervalued at current levels. Based on peer comparisons alone, a near-term valuation in the $3–$5 per share range seems reasonable even before accounting for additional indications or future developments.

Additional-Rich-7216

Company Progress • The DOJ/SEC investigations are closed, and CYDY was not the focus of the case. • The company has treated over 1,600 patients and is submitting its safety profile and supporting data for publication. • The Phase 3 MDR-HIV trial achieved statistical significance. • The Phase 2 MSS-CRC trial builds upon promising basket-trial data showing tumor size reduction, modulation of the tumor microenvironment, and PD-L1 up-regulation—potentially enabling synergistic combinations with checkpoint inhibitors. Management has communicated that PD-L1 data is expected in January 2026, which could pave the way for partnership funding or collaboration opportunities. ⸻ Conclusion Given the company’s strengthened fundamentals, clinical progress, and the closing of its regulatory challenges, CYDY appears significantly undervalued at current levels. Based on peer comparisons alone, a near-term valuation in the $3–$5 per share range seems reasonable even before accounting for additional indications or future developments.

badinvesta

They also sell PD's as a service and then give those PD's shit information that leads to false arrests

0dteSPYFDs

It already has and UNH YTD stock price reflects that loss of goodwill. When you deal with indemnity for 3rd party BI&PD there are different expectations than with healthcare. You’re kind of shit out of luck if you get sick and your insurance provider tells you to kick rocks, but you also have healthcare advocates who fight for it. If you read more about what’s happened with tort reform in Florida it would give you a better picture of what would happen. Basically people were assigning their rights to sue to roofers. Those roofers would go through neighborhoods repair roofs after a storm, whether or not they needed to be or had existing damage that would have been denied by the insurer because insurance doesn’t cover wear and tear. In turn exchange for the right to collect from insurers property owners wouldn’t have to pay for the new roofs. Roofers would then go after their insurers for repayment, have to pay legal fees and punitive damages. Because of those jurisdictions being plaintiff friendly, they kept losing their pants in court, even when there was no bad-faith on their part. Basically a racket to extort insurers, but some of those loopholes have closed. You see the same types of problems with bodily injury from auto claims and billboard lawyers. Some places it’s the tort climate and others like southern Louisiana, it’s straight up collusion and fraud between claimants and personal injury attorneys. Long winded way of explaining it, but basically insurance for a lot of things is expensive, not because insurers have to pay for the losses, but because of frivolous litigation.

WordWriterGuy

The Hyperscale Series D or E preferred stocks are not the same tickers as $GPUS. D IS GPUS-PD and its like 23 dollars a share not 67 cents for example. You won't get dividends on the $GPUS ticker.

DisonanciaCognitiva

What i've done is trading some research and estimated correlations among assets, its simply how all assets behave in different economic periods, of course last 10 years have been massive growth years and the BEST brhaving security in growth is stock. When recession hits, for example 2008 bonds actually were a safe net (and even appreciated a bit) during stagflation 70s and 2022 both bonds and stocks behave poorly, thats why i introduces some MF and arbitrage, thats the quick rundown of why i chose this stuff, mainly correlations and a sort of all weather approach. PD i dont like gold, It drags down the return, long term It has a 0% real expected growth

Weary_Pirate_6737

If a stock has ever PD at any point in their chart, it’s forever a PD

Boatsssandhoesss

https://wendys-careers.com/job-search/?type=corporate&category=crew&site_numbers=9600%7C8220%7C1615&utm_source=Google(SEM)&utm_medium=Search&utm_campaign=D617710_columbus_crew&iis=Search&iisn=srm_google_sem&gad_source=1&gad_campaignid=14091563505&gbraid=0AAAAAB6ZQCdWWsYmqd-Ghpw0o05Uy3H-t&gclid=EAIaIQobChMI5Imm89u4kAMVlUT_AR0jjiEZEAAYASAEEgKQ5PD_BwE

Severe_Watercress875

Company has a game changing molecule and needs a partner. Molecule is called Leronlimab. It is effective in HiV and will be part of the cure of HIV one day during the Presidents term ( my opinion). Charlie Sheen was on it - it has a long hold placed on it which held it back. Cydy has a lot of debt and votes to authorize more shares in November. Company has gone through poor management but has an excellent CEO now who I believe has this company headed to greener pastures. The mechanism of action of Leronlimab is that it turns cold tumors to hot tumors. This allows for the destruction of the cancer cells and this has already saved lives. Metastatic Triple negative breast cancer patients alive with no disease after Leronlimab used. It’s currently in a colon cancer trial and obtaining more proof of its MOA. I’ve been in for 5 years. Alzheimer’s, any solid tumor that expresses PD-L1, HiV, fibrosis of the liver. It also saved lives of Covid patients but this use was derailed for various reasons. I’m a cydyholic and feel of all penny stocks out there Cydy has the real deal. .26 cents is a joke for what this molecule can do. Good luck

britash1229

THE PDL-1 up regulation discovery has sealed the fate of cytodyn and its trajectory‼️🙌🏼 The checkpoint inhibitor companies (MERCK , ROCHE,ect) only been able to treat 15% of solid tumors, which are PD 1 positive , will now be able to treat the remaining 85% that a PDL1 negative‼️ We are talking about over 30 types of solid tumors ‼️😆This Is mind boggling. The five women that are still alive from the compassionate you study ,from five years ago ,that received Leronlimab + checkpoint inhibitors are disease free. THERE BRAIN METS ARE GONE‼️. DR. JAY HAD DINNER WITH ONE OF THEM AND WAS SO EMOTIONAL.

britash1229

THE PDL-1 up regulation discovery has sealed the fate of cytodyn and its trajectory‼️🙌🏼 The checkpoint inhibitor companies (MERCK , ROCHE,ect) only been able to treat 15% of solid tumors, which are PD 1 positive , will now be able to treat the remaining 85% that a PDL1 negative‼️ We are talking about over 30 types of solid tumors ‼️😆This Is mind boggling. The five women that are still alive from the compassionate you study ,from five years ago ,that received Leronlimab + checkpoint inhibitors are disease free. THERE BRAIN METS ARE GONE‼️. DR. JAY HAD DINNER WITH ONE OF THEM AND WAS SO EMOTIONAL.

darlenesapira

Best Results from CYDY (Leronlimab) Trials – Summary HIV (Combination Therapy & Monotherapy) 1) Achieved primary endpoint in Phase 3 trial for treatment-experienced patients. 2) Some patients on monotherapy maintained viral suppression for years. COVID-19 (Severe/Critical Cases) 1) Phase 3 data showed reduced mortality and faster hospital discharge in critical patients vs. placebo. NASH/MASH (Liver Disease) 1) Phase 2 (open-label):  50% of patients showed ≥80ms reduction in cT1, a key marker of liver disease severity. Preclinical data showed reversal of fibrosis and liver fat reduction. Metastatic Triple-Negative Breast Cancer (mTNBC) 1) In small subgroup, 15/17 patients on ≥525 mg dose showed increased PD-L1 expression (potential synergy with immunotherapy). 2) Some long-term survivors (up to 4 years with no evidence of disease). Metastatic Colorectal Cancer (MSS, CCR5+) 1) FDA cleared Phase 2 trial design combining leronlimab with TAS-102 + bevacizumab. Trial to assess ORR and safety. Promising. Something for the longs to feel hopeful in seeing.

britash1229

Leronlimab is a game-changing in the fight against HIV and ALL SOLID TUMORS, and it’s finally getting the attention it deserves. For years, many believe its potential has been overlooked or even suppressed by big pharmaceutical interests. Now, recent findings suggest leronlimab upregulates PD-L1, which could dramatically improve the effectiveness of existing immunotherapies for cancer — potentially helping the 85% of patients who previously didn’t respond. This shift could turn what was once seen as competition into collaboration, with major pharma companies standing to benefit as well.

twinter11

Thank God for snap judgements. All the reasons typically quoted for why to avoid something It allowed me to buy a lot of shares before it becomes obvious whats gonna happen. But when there is a good chance to cure (I know, strong word ) possibly some large percentage of currently non treatable cancers with the addition of ICI's, and data coming in slowly is supporting its going to be reality. It becomes obvious with 30 minutes of research focusing the relevant released data, that there is virtually zero risk investing at this price I think. Heres an article with a quick synopsis that says it better than me. [https://talkmarkets.com/content/stocks--equities/cydy-this-penny-stock-keeps-looking-better-coming-into-summer?post=500795](https://talkmarkets.com/content/stocks--equities/cydy-this-penny-stock-keeps-looking-better-coming-into-summer?post=500795) And a previous article from the same guy. Its a super deep dive with TAM's and financials and company history etc. That mostly becomes irrelevant once they upregulate PD-L1 in all solid tumor ccr5+ cancers and qualifying them be be treated with ICI's. [https://talkmarkets.com/content/stocks--equities/when-penny-stocks-can-become-compelling-a-long-term-buy-with-cydy?post=489422](https://talkmarkets.com/content/stocks--equities/when-penny-stocks-can-become-compelling-a-long-term-buy-with-cydy?post=489422)

twinter11

I did a quick scroll through some posts on another board. this guy knows quite a bit about everything known about ccr5 agonist. here is how he described it. but I'm sure its more complicated than I can explain. "A mistaken impression I've seen here several times. Tumors are considered hot because they have a high immune response in other words a very high levels of M1 killer macrophages and natural killer T-cells. PD-L1 doesn't exist in cold tumors because PD-L1 is a response to a high level of killer macrophages and NKT cells. PD-L1 may be considered a marker of a hot tumor but only because the killer macrophages induce PD-L1 proliferation. Ideally a hot tumor would not upregulate PD-L1 which protects the tumor, but that's not how it works because the immune system is trying to balance out the over-representation of killer cells. When leronlimab increases the M1 macrophage phenotype it results in an increased level of PD-L1 which must be knocked down for the killer cells to do their work most effectively."

Acceptable_Ad_4193

“Finally, I am happy to share a very promising announcement as it relates to a patient who prospectively upregulated PD-L1 after having obtained access to leronlimab through an eIND application submitted by her treating physician. In early 2025, we received a compassionate access request for a patient with mTNBC who was previously unresponsive to treatment with Keytruda. This particular patient had two prior tissue biopsies, both of which were PD-L1 negative. In April, the patient started treatment with leronlimab, and in July blood tests confirmed an increase in PD-L1 levels. Our past clinical observations have shown that upregulating PD-L1 is the first step towards prolonged survival in this patient population and we are encouraged by this readout, which supports our working theory. This is the first of hopefully many PD-L1 upregulation readouts across our CRC and TNBC trial(s) in the coming year. I continue to have high hopes for our upcoming Phase II trials, as well as our expanded access program, as we look to reshape treatment paradigms in solid tumor oncology.”

twinter11

I linked the recent abstract. it's pretty brief. Abstract B019: CCR5 inhibition with leronlimab is associated with enhanced PD-L1 expression, ICI response, and long-term survival in metastatic TNBC. | Cancer Immunology Research | American Association for Cancer Research [https://share.google/8UaIrAve4hzZJ0qBE](https://share.google/8UaIrAve4hzZJ0qBE)

PruneReady7081

Im an immunologist, and I follow this with quite some interest. Just to note that ive no positions in this company at all, and ive no intention on taking up any. This comment is purely on a scientific perspective, and i’ve no idea how that translates to share prices. Ive never heard of this idea in converting a cold to hot tumor by promoting the activation of the very axis (PD1-PDL1) that is central in causing the coldness to begin with. I’m skeptical, but find this strategy very interesting and will follow these trials with keen interest. I think the efficacy of the drug will be fairly dependent on the immunological context of the drug to begin with. Since the cancer is metastatic and TNBC, i would suspect that any PD-L1 expression in the tumor would be the case of active immune suppression by the tumor, and not the upregulation of the axis by immune cells upon exhaustion post immune stimulation. In this context, i wonder if ‘helping’ the tumor upregulate PD-L1 would be a good idea. Of course, the propf is in the pudding and i’d be happy to have my skepticism disproved! Some other things im curious about. They note 42% reduction in combination with endocrine therapy. TNBCs are, by definition, refractory to eendocrine therapy since they lack the expression of hormone receptors (hence, triple negative). Are they suggesting their drug is also re-activating endocrine pathways? That would be interesting, and would need more clarity. I am also very curious about their data on CTCs. There’s this seed and soil hypothesis with CTCs, which suggest that CTCs are crucial in seeding distant metastatic organs with the appropriate factors to make it favorable for metastasis. So how good of an idea is it to be targeting CTCs after metastasis has occured? Could the CTCs maybe also have important roles in sustaining the metastatic tumor, making them a good therapeutic target? Or perhaps, this drug is highly effective in early TNBC? I’m not too sure, but given the aggressive nature of TNBC, any drug in this space must consider the limited amount of time available to suppress the cancer, and I would hope the strategy that targets CTCs would not be a case of showing up to the fire after the house has burned down. Overall, I think its an interesting case, and im excited from a scientific perspective to see if the hypothesis behind this drugs mechanisms of action will bear fruit. Of course, an obligatory, this is not financial advice. Im just nerding.

Ok-Recording4145

chemo drugs are very hard to classify this early-- although it does something good (PD-L1 upregulation) it's really anyone's guess what it does systemically otherwise. Less than 10% of chemo drugs go from Phase I to market for a reason. I would take a flier on it since it's so low but keep in mind the Phase II results could be very disappointing.

Simple-Knowledge-411

On the 15th, IBKR raises the margin on leveraged ETFs. If the leverage says x2 and the margin is 25%, they raise it to 50% based on the 2 x 25 rule. I hope I don't get a margin call on the 15th. Aside from the fact that it's a shitty broker that didn't allow me to trade, AND I could have made 200% in 2 days. PD: UNNISTALL BRO

C3POmeetsR2D2

Iovance Biotherapeutics is a biopharmaceutical company specializing in cell-based immunotherapies for cancer, particularly tumor-infiltrating lymphocyte (TIL) therapies. Here are the key points about what Iovance produces/develops: What is TIL therapy? Tumor-infiltrating lymphocytes are immune cells (T cells) that are found in tumors and have the potential to recognize and attack cancer cells. In this therapy, such cells are removed from a patient's tumor, multiplied ex vivo, "reinvigorated," or activated, and then reinjected into the patient. [iovance.com](http://iovance.com) This usually includes preparatory chemotherapy (lymphodepleting) and, if necessary, additional interleukin-2 (IL-2) to support the effect of the T cells. Products and Pipeline Amtagvi® (active ingredient: lifileucel) is Iovance's lead product. It is a TIL therapy for the treatment of adults with unresectable or metastatic melanoma when previous treatments with PD-1 inhibitors (and, if relevant, with BRAF inhibitors for BRAF-mutated tumors) have failed. BeyondSPX They also have Proleukin, a product with IL-2 that is used as an adjunct in therapy. [Investing.com](http://Investing.com) Other programs in the pipeline: IOV-4001: genetically modified TIL in which, for example, the checkpoint protein PD-1 is deactivated (using TALEN technology). The goal is a more effective TIL therapy for solid tumors. [iovance.com](http://iovance.com) IOV-3001: an IL-2 analog/antibody cytokine construct licensed from Novartis to enhance the IL-2 component of the regimen. [https://www.wsj.com/market-data/quotes/IOVA/research-ratings](https://www.wsj.com/market-data/quotes/IOVA/research-ratings)

robbur88

So I see these sometimes and it throws me off. Same description but, in this case, very different stock prices GPUS vs GPUS/PD?

2MuchSend

Alright boys and girls, weekend is here. Alcohol is great until it isn't. Drinking and driving is a big no-no. Best case scenario, you look like an ass hole. Worst case scenario, you get in a head on with a family driving home from a nice dinner and create a few orphans and then get to enjoy the rest of your life with your new friends Bubba and d-boi. I know that you know that if you've got the cash to yolo on 0DTEs then you can afford the Uber. Look out for yourself and look out for others. Homie got the nose beers? Test that shit. Imagine the local PD having to tell your family that you OD'd on bad booger sugar. Don't add to the population. Don't subtract from the population. Avoid confrontation, be cool, de-escalate, only fight if you have to and if you have to win and get the fuck out. Every one knows something these days, nerdiest guy in the back office probably has a blue belt and if he doesn't, he probably has a piece. Hope to see you all on Monday.

TheSoarsCode

Is it just me or did ATCH just blink from .63 to .65? 

CertainFan7743

The monthly dividend stock of GPUS is a preferred issue GPUS-PD trading above $23 a share

bubbasnub

He's about to have enough to just buy the PD outright

Brilliant_Law2545

I didn’t say they aren’t successful. Most folks here looks for a growth engine and PD ain’t it.

megadalon

PD just shitting itself last few days

naked_space_chimp

Alright ASSHOLES! You wanna make some money! Here are my plays: * $ASAN 🐻 | 20 Sep ATM PUT @≈$12–$14 — play the 85% IV crush on this SaaS dumpster fire. * $NIO 🐂 | 13 Sep ATM CALL @≈$7–$9 — bet on the EV hype train derailing post-earnings. * $LULU 🐻 | 20 Sep 190 PUT @≈$8–$10 — actual downside play from $202 spot, retail puke incoming. * $PD 🐻 | 20 Sep ATM PUT @≈$6–$8 — SaaS turd ready to dump and vaporize IV. **Exit at +100% or -50%.** These are pure **volatility** plays, GTFO from the trades, don't fall in love with direction.

No-Western-9331

It is profitable if you catch it in time. I actually bought more at low price to avoid out better. And now waiting for pump. What does a PD pattern look like?

No-Western-9331

I was scammed in last PD cycle via wats app group. Came out early or would have lost 50k. Looking and its last 3 PD cycles im hoping it may pump again so I can exit with some profit. I have 6000 @1.9. Any ideas or suggestions how to predict a pump?

No-Contribution1070

I mean, the individual national guard member is technically also a citizen. If a citizen breaks a law in chicago, the can be arrested by local PD. It's interesting for sure.

saryiahan

So does that mean we would see local PD arresting national guard members?

Harooooouuld

ZS, PD, GTLB are probably the best bets for next week but early September could start with some red. FIGMA is either going to launch higher to screw any put holders or be a theta play. I say that even with a high PUT/CALL ratio because this seems to always happen with new IPOS. They move down more outside earnings weeks.

Spankynpetey

You must not be paying attention, top Republicans have already introduced a bill to regain authority over tariffs and remove those powers granted to the executive by prior congressional actions and the same is pending before the US Appellate Court because the Federal ICC found the current tariffs exceed the authority of the executive and constitute unconstitutional acts. The only hope Trump has of avoiding impeachment is complete and total martial law which is why he tested the military with occupation around the federal courthouse in LA and is now supplanting the District of Columbia PD. These are the steps he thinks will gain him complete totalitarian authority, but the strands of power have begun to unravel and he knows it. News channels walk a tightrope afraid to cover it in fear of retribution but the wheels are turning, the cogs of his downfall are in motion. Nobody is beyond reach…

DumplinButt

You have to remember there are limits in insurance. So if he has 10k of PD limits then the insurance company will only pay a maximum of 10k for the damage to the rivian and the insured is on the hook for the rest. Same with Bodily Injury limits, there are maximums for those as well.

Specialist_Jelly888

You really think the local PD is going to be of any assistance on something like this? Seriously?

Key_Ad7977

What's your avg $RAYA? Sure, it can go. Every ticker can go no matter the circumstances. Ok very fast check $RAYA havr better cash position, they get in more then they spend, $CHSN seems like had debts. But was probably because of that they did the dilution, but it's over now. BUT $RAYA have RS coming which don't attract investors like you probably already know, else you need to change interest or learn more. $CHSN DON'T have any RS coming, no planned shareholders vote meeting planned to decide about RS (that's known about. I would definitely say $CHSN it's in a much better position for a well either PD up to 0.20-22.5, or a mice squeeze up to 0.50. No matter what THIS is not a financial advise!

DiskAlternative9854

China 🇨🇳 classic PD

DiskAlternative9854

Hopefully not PD today, expect $2.5 then I am out.

Practical-Tennis-508

If NuCana is currently in Phase 1, has a catalyst date in August 2026, and met with the FDA in June 2025, it is likely that the company is planning or has recently completed discussions with the FDA regarding the regulatory pathway and pivotal trial design for its Phase 1/2 candidate—specifically NUC-7738 in combination with pembrolizumab for PD-1 inhibitor-resistant melanoma. Based on NuCana's recent communications, the June 2025 FDA meeting was expected to provide regulatory guidance for a pivotal registration trial of NUC-7738[3](https://www.nucana.com/downloads/NuCana02JUNE2025.pdf). The August 2026 catalyst likely refers to the anticipated timing of either a major clinical trial readout (such as final data from the expansion or pivotal trial) or a key FDA regulatory milestone like the acceptance of a New Drug Application (NDA), subject to successful clinical results and further guidance from the FDA. Essential context: * NuCana's press release from June 2025 stated its goal to "obtain regulatory guidance from the U.S. Food and Drug Administration on pivotal study design for NUC-7738 in melanoma," with final data from ongoing studies expected within 2026. * The drug remains in Phase 1/2 as of mid-2025, with expansion trials underway and no pivotal trial initiated yet. * The "catalyst date" in August 2026 could thus represent (depending on FDA feedback and clinical progress): the start of a pivotal Phase 2/3 study, a data readout from a key expansion cohort, or submission of a regulatory filing (NDA/BLA) if accelerated pathways are pursued. Regulatory and developmental progress will depend on outcomes of ongoing studies, FDA feedback, and successful patient enrollment. The August 2026 date marks a critical value-creating milestone for investors tracking NuCana's clinical and regulatory trajectory.

manomus

this the entire market a PD

Straight-Annual8687

multicam hawaii livestreams with PD and fire dispatch in background (unsure which agency/island the dispatch is for). So far, meh as you'd expect [https://www.youtube.com/live/TfpuAwCQmGQ](https://www.youtube.com/live/TfpuAwCQmGQ)

Spidyyellowfish

I thought so too! Saw this as a chance to ride the momentum of the evil corporate overlords while pressuring their margins and championing PD

Virtual-Bid-1728

Man, u hit the nail right on the head! Seen the same thing go down at a few places I worked. They swoop in, squeeze out every last penny, leave the place a ghost town. TBH, it sounds like PD's exactly their type. Got a sinking feeling in my gut, but hey maybe we can make them sweat a lil', right? Upvote from me dude, this needs visibility!

Spidyyellowfish

Pagerduty is in a similiar boat with talks of a sale catalyzing a squeeze. Two good ones. PD is going pretty unnoticed also

figlu

issue is that they tested the drug (PD-L1 silence) in cSCC which rarely metastasize and the treatment of choice is local resection. Metastatic disease is treated w/ PD-L1 antibodies. Where will this drug be used?

SlackBytes

Why is $PD up?

cat1254

Based on the latest data, **$NCNA** is shaping up to be a **high-risk, high-reward play** with explosive upside potential, especially heading into **August 8.**   **📈 Short squeeze score**: **97.92/100**, one of the highest in the market **🔥 Technical Setup** * **Float shrinking** from \~381M to **\~1.9M shares** post-split * **Short interest >100% of float**, with borrow fees still above 21% * **Fails-to-Deliver (FTDs)** from July 9’s 1.81B volume day are likely being forced to settle now **🧬 Clinical Momentum** * **NUC-7738**: 75% disease control rate in PD-1 resistant melanoma * **NUC-3373**: Tumor reductions in solid tumors and lung cancer * **FDA engagement** expected later this year **🧠 My Take** If the reverse split executes cleanly and clinical data continues to impress, $NCNA could become one of the most dramatic biotech turnarounds of 2025. But it’s not for the faint of heart - volatility will be extreme, and timing is everything.

Fate916

Never too late we’re waiting for these news to drop in any days; Regulatory approvals for Amtagvi "expected" in the UK, EU, and Canada in 2025. Regulatory submissions remain "on track" for Australia in the first half of 2025 and Switzerland in the second half of 2025. Patient enrollment in TILVANCE-301, Phase 3, continues. Additional data for IOV-LUN-202 post-anti-PD-1 NSCLC "on track" for 2nd half 2025. "Initial results" for IOV-END-201 endometrial cancer "expected" 2nd half 2025.

yellowLantern

I worked in oncology for mid-size and big pharma. This data is not as compelling as you think it is. 1. This is Ph1b data with very small sample size. It's not registrational, many things can go wrong before the drug is approved. 2. The outcomes you point out are the weakest surrogate outcomes for oncology (ORR-objective response rate). Company released some data for mPFS and mOS, and they seem okay for a post-PD1/PDL1 setting but again the small sample size makes the data unconvincing. 3. You need to think about the population being treated and thus the potential revenue. The studies are post PD1/PDL1 metastatic melanoma, which cuts down on the eligible patient population. Uveal melanoma is a nothingburger, it's about 5% of metastatic melanoma and maybe 1-2k cases a year are diagnosed in the USA. 4. Melanoma trials are long. It can take years for the Ph3 to read out and be approved. I'm not sure if I saw this company has an accelerated approval strategy. 5. Approval is only the first large barrier, the second is getting utilization and reimbursement from the insurance payers or adoption by the clinical guidelines/pathways that guide access. Without these revenue will falter. As such, there's still a long lead up time to both approval and profitability. A lot can happen (both good and bad) in between then.

SlackBytes

Pagerduty $PD. It’s only $1.4B market cap. It’s a tech company and they have no competition. They specialize in paging systems. And well I guess every company needs some users with it and they’ll eventually adapt Pagerduty.

Nusanss

they're actually showing slightly better numbers than the current standard. Casdozokitug combo is showing 38% overall response rate with 17% complete responses in liver cancer. Keytruda + Avastin (current standard) shows \~36% response with \~12% complete responses. So marginally better, but here's the real play: They're attacking different mechanisms. Keytruda blocks PD-1 (removes the brakes on immune cells). Casdozokitug blocks IL-27 (removes the tumor's "invisibility cloak"). CHS-114 kills regulatory T-cells that protect the tumor. Think of it like this - Keytruda is a sledgehammer that works great for some patients. Coherus is building targeted tools for the 60%+ who don't respond to Keytruda. The smart money isn't on beating Keytruda head-to-head. It's about capturing the patients where Keytruda fails. Even 10% of the liver cancer market = massive returns at current valuation. Plus if that 17% complete response rate holds in larger trials, Big Pharma will come shopping. Different mechanism + better complete response rate = acquisition bait. TL;DR: Not trying to replace Keytruda, trying to fix what it can't. At negative enterprise value, they don't need to win the whole market to print tendies 🚀

richbeezy

Shitty stocks that rose today for the sole reason of being heavily shorted. Ones that you could and should buy puts on: -ANGI -REAL -GEO -RUM -PD

jorge-emilio

I'll answer your question using the four points that I established in one of the yellow notes. The four points are the following: 1. Macro trend (is it clearly bullish or bearish?). 2. Macro PD Array (are there one or more PD Arrays that align with the macro trend?). 3. Micro signal / Mathematical logic (this would be your personal entry technique on whatever timeframe you use). 4. Trade the momentum that favors the macro trend (go with the macro trend, not against it). These are the criteria that I look/wait for in order make a high-probability decision. \*\*\* This is not financial advice and should not be used or considered as financial advice.

En_CHILL_ada

https://youtu.be/PD5gtM1A990?si=pHsdOLr7PzU6yRb3

Ikeelu

I also some one slow down for a deer crossing the street today and slow down to cautiously pass PD. The deer didn't show up on camera though which was surprising it still slowed down not registering it as an object on screen.

richbeezy

Here's the kicker, when markets get overbought (which they are getting close to), you keep your shares in high growth "Chad" stocks - but also buy lots of puts on SHITTY companies like BMBL, LUMN, REAL, GEO, RUM, PD, etc). Shitty stocks that are in a 5 year downtrend. Therefore, if the market keeps going higher - these shitty stocks will still struggle in comparison. Then when the market truly turns, these puts will print. The ones I have are out to 10/17, plenty of time for a correction between now and then and markets tend to trough in early/mid October. Yes, I've been doing this for a long time (almost 26 years now).

Possible_Cheek_4114

https://www.businesswire.com/news/home/20250618276691/en/FDAs-Approval-of-Keytruda-for-PD-L1-Positive-Head-and-Neck-Cancer-Patients-Signals-a-Clear-Pathway-for-CEL-SCIs-Multikine-to-Address-a-Major-Unmet-Need-in-PD-L1-Negative-Cancer-Patients

smutmybutt

I would say that example just proves that the Baltimore PD is fucking stupid. Any ineffective system can recommend people to arrest. I think Musk and Thiel are capable people who have compromised their own capability by falling so deeply into their ideology, self-absorbed echo chamber, and worst instincts (although Elon has the most publicly available evidence to back up this claim). In the case of Elon he has a long-term addiction to drugs that are negatively impacting his brain. There was also evidence of Elon being a bad manager in his “golden years.” His main talent was being a bully with VC money. By most accounts he was basically kicked out of PayPal. If Elon was smart he wouldn’t have needed to support the anti-EV party in order to avoid SEC trouble. If he was smart he wouldn’t have alienated his main customer base for Tesla, running the only EV brand with declining sales. If he was smart his multi-year head start producing cars in China would lead to his vehicles beating out BYD and other Chinese competition (companies run by smart people like Apple have no problem maintaining their first mover advantage in China).

North_Ad_4609

Just a PD my guy

richbeezy

Give me a few shitty stocks to buy puts on (out to 10/17). I already have 2 good ones (BMBL & PD). I am looking for weak stocks with little future growth. Not an over-valued tech play, as they still have nice growth.

No_Feeling920

Just in time for this regarded bean counter leadership kicking in. Like it ended well the last time INTC tried it. Truly regarded... [https://www.digitimes.com/news/a20250609PD227/intel-gross-margin-profit-policy-business.html](https://www.digitimes.com/news/a20250609PD227/intel-gross-margin-profit-policy-business.html) They will be wishing to have kept Gelsinger a couple years down the road.

Same-Brilliant2014

Live PD is already back

Danyzinho29

Voyager Therapeutics, a clinical-stage biotech developing treatments for serious neurological diseases, including Alzheimer’s disease and Friedreich’s ataxia – both of which have limited therapeutic options. Voyager’s lead clinical candidate is VY7523, a monoclonal antibody designed to target pathological tau (pTAU), a protein closely associated with the progression of Alzheimer’s disease. Intended for early-stage intervention, the therapy has shown encouraging preclinical results. In mouse models, its murine surrogate demonstrated high selectivity for abnormal tau while sparing healthy tau and delivered strong efficacy in the P301S seeding model, a benchmark in Alzheimer’s research. Voyager recently completed a Phase 1 single ascending dose (SAD) trial in healthy volunteers and has since launched a multiple ascending dose (MAD) trial in patients with early-stage AD. Topline SAD results were positive, showing that VY7523 was well tolerated across dose levels and achieved expected central nervous system exposure. Alongside its antibody-based approach, Voyager is also advancing a gene therapy pipeline powered by its proprietary TRACER capsid technology. These engineered capsids are designed to deliver therapeutic payloads directly to brain cells while minimizing off-target exposure in tissues such as the liver. Among these programs is VY1706, a tau-silencing gene therapy intended to suppress pTAU production in neurons for the treatment of Alzheimer’s. At the 2025 AD/PD conference, Voyager presented encouraging non-human primate data showing that a single intravenous dose of VY1706 achieved dose-dependent, robust reductions in MAPT mRNA and tau protein across critical brain regions. An Investigational New Drug (IND) filing remains on track for 2026. The promise of Voyager’s TRACER platform has attracted major pharmaceutical partners. Through deals with Neurocrine Biosciences, Novartis, and Alexion (a subsidiary of AstraZeneca), the company could earn up to $7.4 billion in milestone payments. The Neurocrine collaboration is already advancing gene therapy programs for Friedreich’s ataxia and GBA1-related disorders, with IND filings expected in 2025 and clinical trials slated to begin in 2026. Voyager could receive up to $35 million in milestone payments tied to these near-term milestones. Source: TipRanks

the_whole_arsenal

By waiting in the wings, you mean 3-4 years before it reaches its next-generation phase design, 5-6 years before it is on the wing of a plane, and 8 years before it is certified outside China, right? From what was said about it at the Dubai Airshow in 2024, the first-generation engine has serious power deficiency issues. It needs 28,000 lbf to make the c919 airborne, and testing has it in the 25,000 to 26,000 range. The LEAP engine produces 30.8k to 31.6k lbf in thrust depending on the model. The CJ-1000A is closer in architecture to the CFM-56-5 (an engine designed 38 years ago) than the LEAP with an 8.5x bypass ratio and suggests it would be limited to ~27,000 max thrust. China would honestly be better off contacting United Engine Corp (Russian) and offering a boatload of cash for a turnkey design to build the Aviadvigatel PD-14 under contract. It is 6-8 years more mature in design than the CJ-1000A, but I'm sure I'll hear a lot about both next week in Paris.

Formal-Industry-5243

I recently came across a relatively small biotech company called Faron Pharmaceuticals (FARN on AIM, FARON on Nasdaq Helsinki), and I wanted to share some thoughts and hear opinions from others who follow the biotech space. Faron is a Finnish biotech company developing immunotherapies for the treatment of aggressive cancers and inflammatory conditions. Their lead candidate, bexmarilimab, is a macrophage-targeting antibody (anti-Clever-1) currently in clinical trials for several types of solid tumors, including NSCLC, HNSCC, and melanoma. The early data from the BEXMAB trial (combination with anti-PD-1/L1 therapies) shows some promising responses in difficult-to-treat cancers. Here are a few points I found interesting: • Unique Mechanism: Bexmarilimab aims to reprogram tumor-associated macrophages (TAMs), potentially enhancing the patient’s immune response against cancer. • Small Cap: The company is still quite under-the-radar, with a market cap under €200M, which leaves room for volatility but also upside. • Funding: Like many small biotechs, they face financing risks. They’ve had a few rounds of fundraising, and dilution is a concern. • Upcoming Catalysts: More clinical readouts expected in 2025 – could be make-or-break depending on data. I’m curious: • Has anyone here been following Faron? • Thoughts on the BEXMAB trial or the TAM-targeting approach? • Is this a potential hidden gem or just another risky small-cap biotech? Would love to hear others’ DD or bear/bull theses!