GT

stocktadercryptobro

Wen Eleanor GT500?

one

The thesis is coherent, the sizing is... committed. The Supreme Court catalyst is a legitimate wildcard that most aren't pricing. **The GT3RS scenario:** NVDA needs to hit roughly $210-220 by 3/20 for this to be life-changing money. That's a 15-20% move in 5 weeks. Aggressive, but: * Earnings beat + raised guidance to $70B+ * SCOTUS strikes down IEEPA tariffs same week * Algos pile in, short covering accelerates It's not impossible. It's just needs everything to hit. **The Wendy's scenario:** Stock flat-to-down post earnings, calls expire worthless or near it, you're sitting on shares underwater and short puts getting tested. Your main risk is timing/structure: concentrated short-dated calls + earnings vol crush + binary SCOTUS timing. If you're genuinely comfortable with the downside, respect. If not, you could always convert some of your long calls into vertical spreads to reduce risk and theta decay. But GT3RS requires moon mission and spreads won't get you there. Godspeed.

CEOofBeanz

Mustang GT is inferior to German sports cars, I’ll still buy to support the factory and engineers

Correct_Proposal_409

Correct. And I think it is safe to say that David Einhorn is aware of what is going on with Gain and GT-02287. Michael J Fox Foundation is definitely aware. Listen to Gene Mack speak at the Sach's Forum on January 11th, mentioning how MJFF has been a great resource to them. Also not that Gene is sitting right next to Gaia Skibinski, Director of Discovery and Translation at MJFF. (Start at around 52 minutes): [https://www.youtube.com/watch?v=Hvsllm583Vc](https://www.youtube.com/watch?v=Hvsllm583Vc)

Correct_Proposal_409

Nothing has changed fundamentally about the science and the data except that it has gotten better. I'm as disappointed in the share price as anyone, but the potential is giant here. The data from the extension will keep coming in, and by the sound of company statements, it is very positive. If you want more info, there is active discussion over at Stocktwits. I've been adding as the price has fallen, and I've never owned more than I have now. I still believe strongly that GT-02287 is the most promising disease-modifying therapy being developed.

tedontwo

I found the Select and Premium to be a little bouncy, the GT is firm but more planted. Horses for courses, glad you like yours!

tedontwo

I really prefer the MagnaRide suspension and big brakes on the GT. The ride is firm but I found the lower trims a little bouncy. Plus it's a big girl, the big brakes are handy for spirited driving. If it's a daily that never sees performance driving I'd agree, the Selects and Premiums are pretty solid.

tedontwo

The original comment was in reference to a Mach-E 👍 they come in a GT trim.

Amaeyth

Sorry I should've clarified, I meant a 2015-2020 GT350. But yes the new ones are also absurdly marked up when dealers do special order them from Shelby American. Ive seen ADMs on RTRs and Shelby American variants in excess of $30k. I was on a lot last year remarking on one in mystichrome saying plainly, 'thats a nice car, but Im absolutely not paying 150k for that'. The sales rep said 'for this one you would'. My response was a simple, 'no way this is still a Mustang.'

nomaam05

GT owner here, I wouldn't bother with the GT unless you can't find a Premium for less.

Patient_Commentary

We got a premium. We test drove the GT and didn’t like that the suspension was tighter. It was just so bumper. But other than that, they are all amazing! Similar to the other guy, best car I’ve ever owned.

sinovesting

You must be thinking of the GT500. GT350s are no longer sold new but they can be had in good condition for sub $50k easily.

notevenapro

In 2006 my wife and bought two brand new GT's, 27k each, 0% financing.

ShallWeGiveItAFix

I feel bad it’s failing but I snagged a Mach E GT motor for next to nothing. The thing is major!!!

RaggaDruida

And about enthusiast cars, they only make the mustang. They had some history, iconic vehicles like the Escort RS Cosworth, Capri, GT, etc but as far as I know they don't make anything similar any more. Add to that the shrinking market and the negative image that usa products have outside of their own national market...

CelebrationNo5541

That Coyote engine is no joke. Just got a new base GT Mustang simply because of the engine and its ability to take a beating on a race track.  Last Coyote I had was a drag car and you are spot on with the boost. I ran it with stock oil pump gears at 1khp to the ground for over a year before it blew up. 

The_Zenki

Ignorant to them, didnt know if GT meant about gas coupes or the machE, but now I know MachE can get GT badging/trim

tedontwo

The key part is that it really is only a few extra hundred to go from a base model Select to a loaded GT. The value is unmatched at the moment. Although they can be said for a lot of EVs at the moment if a different model fits your needs better.

The_Zenki

Mach E GT?

fasurf

Awesome to hear. GT is worth the extra couple of bucks? Can find one under 30.

tedontwo

I bought a used GT with 38k on it for $29k and it's the best car I've ever owned.

Amaeyth

That's just one example Im most familiar with, but the sentiment of overcharging is present in the entirety of their vehicle line. 60k XLT F150s, anyone? Hell, a GT premium with a handful of options is $67k or more. You can't swing a dead cat around a Ford dealership without hitting something marked at least $10k above where it should be for it to be attainable for an average consumer. All that said, Dark Horses are hardly limited or niche. Its just an upbadged GT with a twin throttle body. It is quite literally just a Mach 1.

deletersdelete

I’ve been unable to contain my excitement for 48,000 Mustang GT models with cloth seat out of a Fiesta. Or $82,000 dark horse models. Ford. Smh.

pmotiveforce

Woot. Good for me, may pick up a Mach E GT Rally for on the cheap.

SchwiftySchwifferson

NOOOOO GT missed 😭

Ok-Bullfrog-2243

GT Resources (GT) and World Copper (WCU)

Ok-Bullfrog-2243

GT Resources (GT) and World Copper (WCU)

ArsonOfTheErdtree

I hold around 5k of GT ($), love the company it's a solid pick

franker555

Im thinking im gonna buy shares on GT and UPWK before earnings today. Convince me which ones better or not to do one

DryEntertainment8270

I was a big mountain biker - a super expensive bike use to top at at 4 to 5 grand.  Now, you can spend almost $20k on a top end bike.  WTF.  What's even scarier is how many people are still buying them. Old Porsches are also insane.  A 1996 911 could be had for 40k.  That's now over a 6 figure car. New GT models are being sold for a $100k dealer markup with most being bought by speculators, further increasing prices.  It's truly insane how that market has shot through the roof in the past 3 years.  It's scary because they will lose their asses at some point. I have also seen a record number of $10 mill+ houses in one area of where I live.  All completely vacant.  I'm talking dozens of 10,000 sqft homes.  Finally, private equity companies have now invaded every industry.  It's how ultra wealthy buy up businesses, pump them up by spending a few mill of investment and 3 yrs later ask for 10x return by selling to the next private equity who will do it again.  I've now dealt with 3 PE firms at 3 companies and they have eventually destroyed ALL of them.  All solid businesses with +10% growth, but the PEs wanted 20x.  So they trim the balance sheet, eliminate paid vacation (for the "as much as you want" crap that doesn't get approved and that people don't take) move things around to become a software company so they can ask for stupid returns, sell for their stupid inflated amount and then do it all again. PE will destroy the mid market enterprise in this country.

ByahhByahh

In completely unrelated news a million GT3RSs have hit the market.

ilikeag

Boo boo, someone’s mad they didn’t get to buy in at $85/share. I did 😎 And you can check my profile, I know the Model Y is the better car but I got a Mach E GT just for the looks and the blue

gettinLearnt92

https://preview.redd.it/avqfzsssoygg1.jpeg?width=1242&format=pjpg&auto=webp&s=ac58b99769acd50ce396a3c00f5a28b363217439 GT RESOURCES

Rocket089

AND IT WAS GLORBIOUS. ALL PRAISE MY NEW PORSCHE GT2RS :kekdab:

Wide_Load_7075

Almost had a GT3 RS…almost…

Just-Here2-Learn

People always talk about a crash, my grandfather always said, I'll never sell until I'm starving or homeless. Why stress it unless you just need the money. Same with the Fire Community always talk about the what-ifs and I'm over here like you can always go back to work in tough times. I've sold investments three times in my life and all three times I lost future growth and regretted it. 1967 Shelby GT500 bought for 40k sold for 85k now they sell for 225k and up Sold a 10 year collection of gold and silver 3 years ago now look at the value Sold 688 shares of BRK B when it was 400 a share, before April crash it went to 530 a Share Did all that when I didn't even need the money.

Correct_Proposal_409

I did see that. Mack's quote is great because it very succinctly described how GT-02287 is superior than the other Gcase drugs, and also why (IMO) it is superior to the other treatments being developed which work around the edges by focusing on one cellular process or another. “Rather than simply trying to boost enzyme activity in the lysosome, GT-02287 stabilizes GCase folding and trafficking throughout the cell, restoring function across multiple compartments, including those critical to mitochondrial health,” Mack explained. “That matters because Parkinson’s can be seen as a disease of cellular stress, impaired waste clearance, and energy failure.” I could see a future where GT-02287 is a foundational treatment for many/most PD cases (and other diseases), while other downstream or peripheral treatments like the other ones mentioned are used in conjunction based on specific patient phenotypes or stage of progression.

Kalspiewak

Systematic releases of the same IPs every 12 months, buggy launches, weak post support, has plagued them for years and now they are paying the price. Gamers are very different from the Cinephile. Movie goers will focus on the director, but gamers pay attention to who develops and publishes the games they buy. Ubisoft isn’t going to magically get better. I've noticed at the start or end of every console generation, a major publisher usually either goes bust or gets swallowed up. I see it as the change agent as we enter a new generation. GT Interactive - PS1/N64/Saturn (1999) Acclaim Entertainment - PS2/Xbox/GameCub (2004) Midway & THQ (2009-2012) - PS3/360/Wii PS4/XboxOne/Wii-U closures happened, but nothing to that scale And now we have arrived to today PS5/Xbox Series/Switch 2 Generation: Ubisoft (2026/2027) - I think they will get liquidated and their IPs sold to the other big publishers. Which is a shame because despite the issues with their games, they do have very compitent developers on their roster. It just seems like the upper management doesn't give them the time lines and support to allow the games to flourish

Icy-Bullfrog1891

Really looking forward to the data we get in March, and news on how Phase 2 will be funded. I wish I had more cash to buy at these prices, but I’m all out. Despite the share price drop from December, it’s relatively easy to ignore the noise if you focus on the data. It’s going to be a big year. And data like the one seen the opening post, just strengthens the disease modifying possibility in GT-02287.

Correct_Proposal_409

With the GBA1 subpopulation, which alone is giant, it appears that you will be able to screen early, and if these individuals are able to take GT-02287, which corrects the very Gcase dysfunction that their mutation causes, it is unlikely that the disease starts in the first place.

eje0100

AMD Calls = 997 GT3

MediumSinger8088

I am "hoping" (I hate that word, really; hope makes you believe things that just aren't true, but nonetheless) that GT-02287 keeps working. But here, objectively, where it stands: One expects MDS-UPDRS Part 3 (the semi- objective clinical evaluation) to increase by 2.5 points in on year for the patients in the Phase 1 study (assumptions: Early stage patients receiving drug from the levadopa "on" state). Divide that by 4, you get +0.63 points every 90 days. So expected +0.6 at 90 days, we've got -2.5, for a difference of -3.1. The minimum signal is about 3 points, some say 4 points. So time marches on and the ONLY question is this, in my opinion: Will the difference between the expected MDS-UPDRS Part 3 and the observed value grow, stay the same, or shrink as the continuation data trickles in? For those who want to play at home, here's the table to fill in. Numbers are rounded to the nearest tenth. KEEP IN MIND the scale is 132 points so a -3.1 is still only a 2.3% difference; minimum signal/noise. Repeated measures at equal time intervals can improve confidence because if the results of any one time point may be due to chance alone, but all-time intervals show the same effect, the probability of chance effect decreases multiplicatively. Time (days) Expected median change Observed median change Delta 0 0 0 0 90 0.6 -2.5 -3.1 180 1.3 ? ? 240 1.8 ? ? 360 2.5 ? ?

Sorry-Point-999

Already did...bought a Xiaomi phone last year (15 Ultra + camera kit) and ditched iPhone. Bought a Huawei watch recently (GT6 Pro). Both products are brilliant and far ahead of stagnant American tech. Will be putting my name down for one of the EVs that are heading here to Canada soon as well.

pmotiveforce

Sweet. Then I could beat you in a used 2024 Mustang Mach E GT that I bought for 30k.

OpeDefinitely

While we're throwing out dream cars, somebody buy me a 2013 Shelby Mustang GT500

ChuckOfTheIrish

Years late but ran back across this reflecting on the experience I had. Apple absolutely used toxic contracts to bankrupt the company, but company leadership for GTAT was either extremely incompetent or direct frauds. What was announced is sapphire glass would be used for the camera glass and potentially for the screens as it was wildly durable (significantly higher test ratings than gorilla glass), Apple investing was just what investors needed to believe it had selling power beyond just proof of concept. Turns out Apple included very high loans for the glass ovens used and added fine print for various penalty classes and that they could collect at any time, they decided to collect just after GTAT burned all this money on a mass production facility and ovens, bankrupting GT and allowing Apple to acquire on pennies to the dollar. Lawsuit was filed and a pretty decent payout was given to investors, I didn't get a ton, but wasn't that heavily invested (IIRC I got around 15% of my losses back which is good for class action payouts). While GTAT leadership clearly failed legal due diligence or were in on the scam, Apple and some other giants are very well known for intentionally bankrupting small partners with toxic contracts.

Correct_Proposal_409

Completely disconnected with the data, the science, the de-risking, and the potential. 7 analysts have an average target of $8/share, and this is after applying a standard risk discount of getting to FDA approval, which I believe does not take into account the extent to which GT-02287 has been de-risked. In other words, analysts will generally apply the same phase-based discount to to all drugs in phase 1, no matter how much more compelling the biology of one drug is vs another in the same phase. So the price targets do not fully capture this de-risking. I added yesterday, and will add more if it drops further. The silver lining here is that the most promising disease-modifying Parkinson's treatment being developed is at a giant discount.

pmotiveforce

I'm looking at used 2024 generally. Audi q8 (q6 seems to have issues). Got my eyes on a 24 Mach E GT Rally. Optiq and Lyriq other good options. A bit more but the 2024 BMW IX is fucking nice, if I can find one with drivers assistance pro and air suspension for under 50k id buy one.

Correct_Proposal_409

Theoretically, since GT-02287 is an oral drug which gets absorbed into the blood and then crosses the blood-brain-barrier (enabling it to address Gcase dysfunction the brain), it should also work for Gaucher’s, which mainly affects cells in the body. I’m sure Gain has blood plasma levels of GluSph. If they are anywhere close to what they showed in the brain, I’d expect that would make it relevant for Gaucher’s, and especially for the small percentage of cases that include neurodegeneration. Whether GT-02287 could be better than the current therapies remains to be seen, but a 81% reduction in 90 days, if similar in the peripheral cells, would be a bigger impact than current therapies remains. But there are other considerations, and they’d of course need to have proper clinical trials.

Outside_Reserve_2407

I think an example of Ford “coming full circle” would be when it sold exclusive hand-built cars like the GT40.

FUBOSOFI

Idk man everyone thinks they’re pretty lame. Unless it’s a Shelby GT

Correct_Proposal_409

No, and this is one of the things that is so remarkable. Of the 13 patients in the slide above, 7 turned out to have elevated levels of GluSph, and 4 of those 7 were idiopathic, 1 was GBA1, and 2 were "pending". In fact, only one of the patients who *didn't* have elevated levels of GluSph was confirmed to be idiopathic. There were 3 who were "pending" who did not have elevated baseline levels, so maybe there were more. Yes, this is a small sample, but it is completely fair to say that many idiopathic patients have elevated GluSph. This is not controversial. This a giant market. My understanding is that it is thought that GBA1 are more likely to have elevated GluSph than other genotypes, but it looks to be common in idiopathic cases as well. This also does not mean that the patients who did *not* have elevated levels at baseline will not develop elevated levels as their disease progresses. These patients who did not have elevated GluSph at baseline had what is considered to be mild baseline UPDRS pt. 3 scores, although most of the patients who had elevated baseline GluSph also fell into the mild category of pt. 3 UPDRS at baseline. They did not screen for patients who had elevated GluSph in order to enter the trial, so if we are to take this sample of patients as representative of Parkinson's populations, then about 50% of mostly mild cases have elevated GluSph levels. Maybe that number is higher if you include more advanced cases. There were 21 patients who entered the trial only 3 confirmed GBA1 patients. This jives with the estimate that 10-15% of Parkinson's cases are GBA1. This greatly de-risks phase 2 if they can screen for elevated GluSph, or if they can simply pre-specify a sub-group in the study of those with elevated GluSph. This is a huge number. And, importantly, it does NOT mean that GT-02287 cannot be helpful to patients who do not have elevated GluSph. Maybe it takes longer to show benefits, maybe it helps some patients in their mitochondria, and maybe it simply prevents levels of GluSph from elevating int he first place, and results in stable or slowed progression of UPDRS scores, which is disease-modification.

Correct_Proposal_409

You can find the patient demographics and baseline characteristics [here](https://gaintherapeutics.com/wp-content/uploads/2025/10/MDS-2025-Interim-Phase-1b-Data.pdf) for Gain's 1b. You are misinterpreting the Bial data. What they showed was an increase in Gcase activity, but it did not actually *improve* anything (in fact, GluCer *increased--* wrong direction*)*. Read MediumSinger's comment below. Peter Lansbury, who was one of the KOL's today in the Gain event, was involved in the development of Bial's drug, which did not show efficacy. This is why Lansbury was so impressed by the results for GT-02287. Here is a key distinction. It doesn't really matter if Gcase is increased 30% or 90% if it doesn't actually reduce lysosomal dysfunction (or mitochondrial function for that matter). Bial's activates Gcase already in the lysosome. But if there is limited Gcase in the lysosme, or if the lysosome is already dysfunctional, those limited "activated" Gcase may not be able to get the job done. That seems like it could be the issue there with Bial's drug. GT-02287 MOA is different in that it corrects folding in the ER and traffic functional Gcase to where it needs to go, including the lysosome and mitochondria. The GluSph reduction is proof that GT-02287 is working in the lysosome. BTW, GT-02287 also activates other Gcase that is already in the lysosome. A drug that increases Gcase by (just for example) 30%, but reduces GluSph by 80% is much more beneficial and efficient than a drug which activates Gcase by 100% (for example), but fails to decrease GluSph. ANd that's just the lysosome. Bial's drug theoretically should not be able to activate Gcase in the mitochondria, whereas GT-02287 has shown in patient-derived fibroblasts that it completely restored Complex I since it is able to traffic (and activate) Gace to the mitochondria. For the phase 1b, Gain did not screen for patients who had elevated levels of GluSph. Of the 13 patients in the slide above, 7 turned out to have elevated levels of GluSph, and 4 of those 7 were idiopathic. In fact, only one of the patients who *didn't* have elevated levels of GluSph was confirmed to be idiopathic. There were 3 who were "pending", so maybe there were more. Yes, this is a small sample, but it is completely fair to say that many idiopathic patients have elevated GluSph. This is not controversial. This a giant market.

Cautious_Room1910

Forgive me, can you tell me where you read in the publication that only 1 of the participants with a reduction in GluSph is a GBA1 case, 4 are idiopathic, and 2 are other cases? I can’t find this information. First of all, I would like to talk about BIAL: if I’m not mistaken, it is precisely in the PubMed article linked by the other person in the conversation that they show a 2x increase in GCase activity in patients with GBA1 Parkinson’s after 28 days, whereas, although different in the way and consequences, in the case of another drug and phase 1a, GCase activity increased by about 50% with GT. So in sick patients, the BIAL molecule reaches the right tissues and correctly activates GCase (I cannot speculate on whether this results in more or less effect than GT, despite the excellent numbers). This is an extremely promising data point regarding what the drug is precisely trying to achieve (i.e., not preclinical studies in animals that do not have a chronic disease course like in humans and cannot or should not influence proper financial decisions!). Regarding the concern raised by the other user about the transient increase in GluCer with BIAL’s drug, I would not worry, because, as also stated directly in the PDF published by Gain on January 6: page 20, "Reducing GluCer levels has no clinical effect in GBA-PD." In any case, just a few more months to see who will be right regarding the release of the data, noting that, being a private company in an already delicate sector, they are not absolutely required to release biomarker information to the public, and so far this has been the case. Furthermore, their phase 1 study was very short, so if this did not allow presenting useful data, we should at least keep the door open. Now, if it is true that Gain’s data show significant decreases in GluSph even in idiopathic Parkinson’s (I could not find this information), this could slightly change the company’s operational window. However, it is still incorrect to say, as you did, that there is a suggestion from these data that a large number of idiopathic Parkinson’s cases have lysosomal lipid degradation failure as a primary or co-factor… I see only 4 cases, not the majority of the 10+ million Parkinson’s cases recorded worldwide, and therefore, if you cite these as exceptional data, forgive me if I did the same with what I reported above. In conclusion, if GT does not show concrete potential for idiopathic Parkinson’s, it will then have to test its cards on GBA1. BIAL will present phase 2 data in about 3 months, allowing us to conclude the chain, connecting—or not—the increases in GCase functionality to improvement in lysosomal repair function. One cannot invest in BIAL, but are you sure you want to invest in a drug that in 3 months could have a competitor with the same functionalities but 2 years ahead?

Correct_Proposal_409

Well, I think they've gone a long ways already towards de-risking, but :de-risked" is never absolute. As more data comes in from the extension patients, assuming the scores remain stable or improve, this is further de-risking. I think the big question is at what point will a big pharma make a fair offer for buyout or partnership. I think Gain has already received offers, just not reasonable ones. Maybe there's one one the table or will be soon, or maybe potential partners are waiting for the 6-month UPDRS scores. I don't know. The only thing I can say with confidence is that with the GluSph reductions and what looks like a clear translation to UPDRS improvements, the GT-02287 alone is worth much more than what the current market cap. Not saying there are no risks, but I really like the risk/reward here. BTW, the more institutions wake up and are able to take positions here, the less volatile the share price becomes.

Correct_Proposal_409

A couple of things. First, what is interesting about the above slide is that only 1 of the 7 patients who showed a big drop in GluSph is GBA1. 4 of them were idiopathic, and 2 were "other". So this suggest that a large number of idiopathic cases feature lysosomal lipid stress as a primary or contributing factor. Second, GT-02287 is not simply “stabilizing GCase”. The human data now show functional lysosomal repair (large GluSph reductions) with patient-level concordance to clinical improvement. That’s very different from prior GCase approaches that increased protein or activity without correcting toxic lipid accumulation or showing a clear clinical correlation. Regarding BIAL’s program: it is restricted to GBA1-PD, targets a narrower downstream mechanism, and has not shown GluSph reduction or a biomarker-to-clinical linkage like this. Being further along in development doesn’t help if the biology isn’t hitting a disease-relevant bottleneck. Many PD programs have reached Phase 2+ without demonstrating disease modification. Maybe I'm missing this promising data, but from what I've seen, even pre-clinically, it has not shown improvement in mitochondrial function, reduction in a-syn aggregation, reduced neuroinflammation, reduced ER stress. All of these were shown pre-clinically by GT-02287, and now this reduction in GluSph, along with linking it to UPDRS improvements, goes a long way towards validating these pre-clinical findings. Do you have a link to this promising Bial data?

Cautious_Room1910

It has been observed numerous times in the scientific literature, as well as in the data presented at the most recent Gain event, that GCase activity can be relatively functional and GluSph levels relatively low, while a patient still fully suffers from idiopathic Parkinson’s disease. Of course, one could argue that if GT improves GCase stability, this would ultimately lead to a healthier cellular environment and more functional lysosomes, which would help prevent the formation of Lewy bodies. However, how much of Parkinson’s pathology truly derives from this additional GCase instability, rather than from mechanisms that are more intrinsic to idiopathic Parkinson’s disease itself? This is especially relevant if it is true that, in idiopathic Parkinson’s disease, the disease actually progresses at full speed despite stable GluSph levels and functional GCase-->the problem is somewhere else. GT appears to be a good molecule for cases of GBA1 mutation–associated Parkinson’s disease because, at the very least—if it performs as suggested by current data—it would slow the mutated disease course to regression timelines more similar to those of idiopathic Parkinson’s disease: this would partially eliminate the problem of a cellular environment with poorly active GCase, while leaving largely intact the fundamental pathological mechanisms of Parkinson’s disease. But In mutation cases, it could be possible that the factors driving idiopathic Parkinson’s disease act as a trigger that ignites alongside the problems caused by the GBA1 mutation, or alternatively that these are cases of full-blown idiopathic Parkinson’s disease that are exacerbated by the mutation; one scenario or the other will change the effect of GT for better or worse on the mutated disease, neutralizing a component that may or may not—depending on the aforementioned hypothesis—represent a fundamental bottleneck of the disease. In any case, why bet on Gain Therapeutics when the pharmaceutical company BIAL has a molecule with a similar mechanism of action to GT that exclusively targets Parkinson’s disease with GBA1 mutation, with extremely promising data and already in advanced Phase 2—thus 1–2 years ahead of GT?

Beneficial_Weight766

I dont know... They just had a webinar today to talk about the results and stuff. [Gain Therapeutics Highlights Biomarker Evidence Supporting Disease-Modifying Potential of GT-02287 | Markets Insider](https://markets.businessinsider.com/news/stocks/gain-therapeutics-highlights-biomarker-evidence-supporting-disease-modifying-potential-of-gt-02287-1035686118)

CEOofBeanz

I’ve been a racist since I was a child. I love Formula 1, IMSA, British GT, all kinds of racing.

TheVariantView

Thanks! I do agree it’s an improbable outcome, but it is a bullish one in the case where the administration does move into Venezuela. This post is just a special update for $GT on the macro events.

TheVariantView

Read the previous DD... Again, this is an update on a bullish potential outcome of the current events. If the US secures Venezuela and provides property rights whilst removing sanctions and bringing private companies back in (as they are doing with oil) to their respective plants, I can assure you these companies wont be vulnerable to attacks by gangs. The bullish case on the Venezuela capture is the above happening. The base case is cheaper oil for US $GT facilities, and the bear case is inexistent.

the_Q_spice

>Analyze outcomes Basically all of your “analysis” rests on the US securing Venezuela and basically giving handouts to private companies. You know *nothing* about Venezuelas government or society. It isn’t going to be a fast or clean transition and it’s increasingly clear by now that the US wasn’t invited. You give the *best possible outcome* for GT. The worst? They go through with this frankly hairbrained scheme, get attacked by [Colectivos](https://en.wikipedia.org/wiki/Colectivo_(Venezuela)), *actually* lose everything, and also get sanctioned in the process.

TheVariantView

This is an update on my previous DD, highlighting potential effects Venezuela has on $GT. US control vs Opposition’s control could lead to the same outcome with similar probabilities. I’m not buying $GT off the news, but saying it is bullish for the company given they can reclaim their Venezuelan factory & resume operations without sanctions.

dicktoballratio9000

Sub is full of liberals, what do you expect? Hope you get your GT3… just got my 4S a couple months and I also am on the road to a GT3 😂

microcapreturns

Gaucher was the original target and they did a lot of preclinical work. When they figured out it works for all Parkinsons patients they targeted the much larger market. GT-02287 could be a $50b a year Parkinsons and Alzheimer's preventative medicine.

HowLongCanIMakeACock

Lugano Blue GT3

Correct_Proposal_409

Phase 1 trials are to make sure that a drug is safe and shows target engagement. Phase 2 trials test efficacy in a controlled setting, and when phase 2 trials fail, it is usually because: * there is insufficient CNS exposure * the target turns out not to be central to the actual disease biology, * they don’t have the right patients. The drug may work for a particular subset of patients, but the trial has been diluted by too many patients who have a different disease biology. Parkinson’s Disease is often called Parkinson’s Disease**s** because there are multiple different points of initial failure which ultimately turns into Parkinson’s. Different genetic mutations, and some might start with lysosomal dysfunction, while others might start with mitochondrial dysfunction. Or maybe neuroinflammation. This is still being researched. * they are measuring the wrong endpoints, * they don’t have the timing right (i.e., trial not long enough to show efficacy, or the initial benefits don’t sustain for the length of the trial). * the biomarkers move, but they don’t translate to clinical benefits Gain’s 1b trial, along with the extension, gives them a lot of valuable information which goes a long way towards derisking the phase 2. Many phase 1 trials do not go nearly as far as Gain went since the 1b measured many biomarkers, along with clinical symptoms. This is unusual. The first major hurdle towards proving efficacy was reducing GluSph, since it is both a direct measure of lysosomal dysfunction and also a driver of further dysfunction and cellular stress. By reducing it in such a short time period (90 days) means not only that there was sufficient CNS exposure. It also strongly suggests that the lysosme has regained lost functionality and that the cellular stress burden has been reduced. And based on what we know about Gaucher’s disease, this GluSph reduction is a central marker for disease control, and the parallel lysosomal recovery is the key driver for disease-modification. So the most important biomarker for efficacy is already there. And the UPDRS score improvements that they’ve already released suddenly look more credible. We should know more about further scores and biomarkers shortly, but it follows that if GluSph was reduced so thoroughly in such a short time, other important biomarkers which take longer to affect should show signs of improvement even by 90 days, and if there is broad biomarker improvement, this reliably predicts clinical improvements since they are so well-correlated. The other big advantage of the data they know have is that they can use that to inform the phase 2 set-up. They’ve already narrowed the focus for their phase 2, tightening inclusionary and exclusionary criteria for enrolling patients, and they can further adjust as data comes in from the extension. Same with outcome measures. [Here is their current phase 2 registration](https://clinicaltrials.gov/study/NCT07280299?tab=table) (which can be updated). One inclusionary criteria that stands out is “Positive SAA in CSF at Baseline” and another exclusionary criteria is “PD-associated LRRK2 pathogenic variant or other PD-associated genetic mutations other than GBA1.”  They now know that GT-02287 is more likely to move the needle from a biomarker perspective by screening this way, so this increases the likelihood of success. So to answer your question, based on what we now know, I think the chances for success in phase 2 are high. And if we get more biomarkers (like Complex I, Miro1, aggregated a-Syn, NFL) that are beginning to show improvements, and if the UPDRS scores that are not worsening-- and I think Gain will show this data between the KOL and the AD/PD conference in March-- then I think the chances for phase 2 success will be extremely high.

HowLongCanIMakeACock

Just cold started the GT3

Brilliant_Goose7265

Curl the mostly heavily shorted. Tru and GT have more loyal followings to buy the dips.

Correct_Proposal_409

Yes. I'm not saying that there are no more risks to market. There are many risks from the beginning of a drug's development all the way through until approval by FDA. But GT-02287 has cleared the most significant of the risks. They first did extensive pre-clinical studies that showed that the drug *should* work in humans. They basically showed that GT-02287 reversed Parkinon's in animals. Then they passed a significant test in the phase 1a with healthy volunteers showing that the drug was safe, crossed the blood brain barrier, and achieved its target (Gcase) as predicted by the pre-clinical models. Many drugs fail in one or more of these steps. Most recently, in the phase 1b, safety was further established, and it took a big step towards showing efficacy by reducing GluSph by 75-95%, which had never been done in Parkinson's patients. The improvements in the UPDRS motor scores that showed in October suddenly look like they weren't just random increases. This reduction in GluSph also makes it likely that further downstream, slower-moving biomarkers should also show improvement,,, and clinical symptoms as well. So through the lens of likelihood of a successful phase 2 study, and also through the lens of large pharamas looking to partner, GT-02287 has been derisked to where the answer is "yes". I also think that the drug is even further derisked if you narrow the patient target to GBA1 Parkinson's (\~10% of Parkinson's cases), which is originally what they were targeting-- dysfunctional Gcase caused by a genetic mutation. They've since realized that improving functional Gcase is also important in idiopathic cases as well, which represent the vast majority of PD cases. This is why I think the asymmetry is so rare here. The risk is now low for failure, especially in GBA1 cases, but the upside is enormous.

Correct_Proposal_409

This assumes that GT-02287 doesn’t become known as the most promising disease modifying drug for Parkinson’s, and it also assumes that Gain doesn’t become one of the many companies with early phase treatments that gets acquired or partners with a large pharma that understands the potential and wants the drug in their pipeline. I’m confident that partnership or acquisition will happen by mid-2026, likely sooner. They’ve been in discussions with a handful for a long time now, and are currently under CDA’s with at least two!of them.

microcapreturns

GT-02287 boosts enzyme activity in Parkinson’s brain: Trial data Developer Gain Therapeutics to review results in January webinar https://parkinsonsnewstoday.com/news/gt-02287-boosts-enzyme-activity-parkinsons-brain-trial-data/

TickTockTaudit

Porsche Cayman GT4

No_Bus_9534

I’m trading away my c63 and was considering an m4 but just didn’t like it. About to purchase a GT C in few days. God Speed Brother

Correct_Proposal_409

Not sure I'm following you. I do believe they painted themselves into a corner in that they promised data by the end of the 4th quarter and also signed CDA's/embargos. But the GluSph biomarker was the big one all along, and they provided topline for that. You can find that this biomarker was [**pre-specified here**](https://gaintherapeutics.com/wp-content/uploads/2025/04/ADPD-2025-Phase-1b-Design.pdf). We also now know from the [**Roth report**](https://gaintherapeutics.wordpress.com/2025/12/19/gain-therapeuticsganx-roth-mkm-thought-on-phase-1b-data-raising-price-target-to-10/) that GluSph levels were reduced 75%-95% from baseline. That's a big deal. I think the company assumed that this alone would be big news and enough to lift the share price, but they obviously misread what this would mean for the average investor who has no idea what the implications of this biomarker means. In the PR, they did link the KOL event that had already been planned, and in which it states "The event will also review biomarker results from the Phase 1b clinical study of GT-02287, demonstrating disease modifying potential in Parkinson’s disease patients with or without a GBA1 mutation." In retrospect, they should have included this up top in the PR as one of the bullet points (instead of being relatively hidden in the link), something like "additional supporting data will be reviewed during our KOL event on Jan. 6th," To your statement on them raising-- they made it clear that they have enough cash to last through 2026, although this does not include phase 2. That's where partnership comes in, though. Lastly, yesterday's trading volume and price movement was very interesting. Nearly double the volume from the day before, which was the PR and big sell-off day, which was the biggest volume day in the company's history prior to yesterday. That's unusual. Usually it's the big sell-off day that is the high water mark for volume. Again, yesterday, where the share price recovered by finishing up 28%, the volume was nearly double from the day before (sell-off/news day). And there was also a record amount of after-marker volume. This tells me that there was some new buying coming in. Maybe life-science funds. And it would make sense. They are the ones who would understand the implications of what was shared in the PR from the day before.

Correct_Proposal_409

Thanks for this. From what understand, Landsbury is very excited about GT-02287 and these results.

MediumSinger8088

Deep dive- Peter Landsbury, the KOL advising Gain, was the CSO of Lysosomal Therapeutics around 2018. That company had a compound LTI-291 that allosterically activates GCase, theoretically similar (but different from) GT-02287 which chaperones folding of the enzyme. Lysosomal and LTI-291 got acquired by BIAL, which is sponsoring a phase 2 trial of the drug now called BIA 28-6156 (pariceract) called the ACTIVATE study in PD. Last patient due to visit clinic in April 2026 and topline data expected Q2. Published data that LTI-291 (28 days, 40 patients) did not change GluCer in CSF or plasma but paradoxically increased the analyte in peripheral monocytes. No effect on MDS-UPDRS in this study. Take aways: IMO BIA 28-6156 is the closest competitor to GT-02287 but there are key differences and results from ACTIVATE may affect Gain price in ways that are illogical due to Mr. Market confusing the MOAs. Also GT-02287 seems to have done something unique in decreasing CSF GluSph. Note there is no data arguing glycosylsphingosine is a biomarker for PD progression but is a marker of target engagement which WILL bring some big pharma players into a conversation at least. There is some evidence that PD patients with elevated GluCer / SM are more prone to cognitive decline over 3 years, which indirectly speaks to cholinergic pathways involved in AD (there's that AD connection). It will take a long time to see this all play out. Years. Invest accordingly. And circling back: Listen to what Landsbury says in the KOL talk. He's probably the most informed guy in the world about this topic.

Correct_Proposal_409

Very unfortunate market reaction to positive news which goes a long ways towards confirming that the drug is working. The PR was to conservative, and they are holding back additional data (possibly due to CDA with a pharma partner, or the are holding data for the KOL event and the AD/PD conference, not sure). Regarding the KOL event, it sounds like they will be reviewing additional data: “The event will also review biomarker results from the Phase 1b clinical study of GT-02287, demonstrating disease modifying potential in Parkinson’s disease patients with or without a GBA1 mutation.” I just wish they had put that as one of the top bullet points for the PR. I’m holding for buyout/partnership, which I think is more likely now. BTW, the BTIG analyst just came out with this note, and he agrees: “Readout Suggests GT-02287 is Activating GCase in the CNS. Additional Steps to Confirm it a PD Drug, but the Gain Approach Works. WHAT YOU SHOULD KNOW: We see the findings today serving as definitive evidence supporting GT-02287's ability to activate GCase in the brain. As a result, we see validation for the Gain approach and increased likelihood others will agree and look to partner other novel applications where allosteric modulation of enzyme deficiencies might benefit patients. The readout today measured the levels of GCase substrate, glucosylsphingosine (GluSph) in the CSF. The observed GluSph reductions in every patient that had elevated levels of this GCase substrate at trial start make it clear: GT-02287 increases the activity of its target enzyme. After 90 days of GT-02287 treatment, all individuals with elevated CSF GluSph experienced significant decreases.”

Accomplished_Bath940

 Man made 50% profit when the market falling apart

OutlandishnessUsed24


Correct_Proposal_409

Okay. fair comment, since elevated liver enzymes are common with early oral small-molecule trials. But there was only one case of transient elevated liver enzymes in the 1b trial, and they withheld dosing, then reduced the dose and the enzymes normalized and stayed in normal range. And the only other case (of 77 people) was in the 1a trial and it was a mild increase: "One subject had a transient, mild increase in AST and ALT after receiving a single dose of GT-02287". No SAE's.

benjamin_noah

Sure. As I also said before, I am concerned that the trials have shown that GT-02287 causes elevated liver enzymes (ALT, AST, and alkaline phosphatase). Which, for what would be a long-term medication, could be problematic. But I believe there's also some evidence those levels could normalize over time. So, that feels like a normal biotech risk. I don't like that I've never seen either of you address that in your posts.

Ye_Olde_Basilisk

We bought a very expensive completely custom 2025 Mustang GT Premium last year. When I was talking to the sales guy, he said they had dozens of Lightnings they couldn’t sell. They can’t even get anyone to look at them. I was like, shit, my truck is 11 years old. Let’s see what kind of deal we can make. The dude said there is no wiggle room or negotiation on those prices. 

magicjohnson89


Correct_Proposal_409

Absolutely. If they prove GT-02287 in idiopathic Parkinson's cases, and early data says that this is likely, it opens up Alzheimer's and other neurodegenerative diseases. At the very least, I think this drug will work for GBA1 cases, so that's my base case, and that's multiples higher than current share price level.

strudel_investing

https://youtu.be/Rv7GT9HsJZc?si=SS5T-tDnRVYEVLSL

stupidber

Why can't I bring a GT Racer to the ski slopes?

Correct_Proposal_409

You are right about biotechs. But in my post, I addressed why this has been derisked and why I believe this is not a binary event. I also gave recent examples of where stocks have skyrocketed off of data, often on data that is much less compelling that what we already know about GT-02287. And the examples of these huge upside moves are endless.

Correct_Proposal_409

Anyone interested in looking a little closer into the science, here's a post that touches on GT-02287 and importance of mitochondria in Parkinson's: [https://www.reddit.com/r/pennystocks/comments/1pex0jz/gt02287\_addresses\_multiple\_potential\_sources\_of/?utm\_source=share&utm\_medium=web3x&utm\_name=web3xcss&utm\_term=1&utm\_content=share\_button](https://www.reddit.com/r/pennystocks/comments/1pex0jz/gt02287_addresses_multiple_potential_sources_of/?utm_source=share&utm_medium=web3x&utm_name=web3xcss&utm_term=1&utm_content=share_button)

ColdComplaint8

thanks - i'm acutely watching the MMM's predictions for $GT lately i'm honestly hoping for $9.25-$9.50 before they expire and I'll be cashing out a decent chunk of change

Beginning-Tap-95

GT too the moon let’s go! 

PhysicsViking0901

Interesting, I am actually a medical physicist working in radiation oncology. We have implanted several patients with what looks to be a competitor: GammaTile from GT medical. I'll have to look more into this.

_hiddenscout

Interesting write up.  However, you’re missing actual research into the company itself. I can look at their numbers in quickfs and tell it’s going to be a pretty bad investment in like 5 minutes.  https://quickfs.net/company/GT:US Just look at the QoQ numbers, it’s not a great story. Like over the past year, they are seeing negative revenue growth.  On top of they have terrible ROIC.  To each their own, just can’t picture this a good investment other than hoping for a buyout.  Elliot even tried to add activits to the board like two years ago and it’s still not working.  https://www.reuters.com/business/autos-transportation/goodyear-tire-add-three-directors-settle-with-elliott-2023-07-25/

Swearwolfofwallst

[How can Standard and Poors help you?](https://youtu.be/mwdo17GT6sg?t=154)

Correct_Proposal_409

The main point of the post is that it seems that there are two or more conditions that need to be present for Parkinson's disease, or at least particular cases of Parkinson's (and other neurodegenerative diseases), but that inflammation is a constant. I'm not claiming it is the cause in all cases or even most cases. Gene mutations for example could create a susceptibility for which systemic inflammation is the trigger. In others, it could be something else. The point is that we don't know, but neuroinflammation is a constant in all cases of Parkinson's. The second point of the post is to point out that GT-02287 has the key bases covered. It doesn't target neuroinflammation per se, since its primary role is to increase Gcase activity and effectiveness by stabilizing its intermediate folding state and restoring trafficking to the lysosome and mitochondria, which in turn addresses the dysfunction driving neuroinflammation.

microcapreturns

Yes the misfolding that Gains GT-02287 corrects is likely the start of the chain and makes it obvious why it works. Thanks for pointing that out.

microcapreturns

There was an article written by a short and they had not even looked at the data. Lol. Parkinson’s studies in the last 30 years that showed placebo affect showed it improving right after start but then heading back up very quickly. We are the opposite. GT-02287 is modifying the trajectory of Parkinson’s. Amazing. https://preview.redd.it/nbpgwlj6ys5g1.jpeg?width=1600&format=pjpg&auto=webp&s=abae53607209c13ec7af40d76e89932806884812

microcapreturns

This comment by the analyst on the three unique models that all show Gains GT-02287 works in Parkinson's is worth reading. Very important. Gain Therapeutics(GANX): H.C. Wainwright $8 PT 12/1/25 Three Month Data Imminent https://gaintherapeutics.wordpress.com/2025/12/01/gain-therapeuticsganx-h-c-wainwright-8-pt-12-1-25-three-month-data-imminent/ 

microcapreturns

Placebo affect goes out the door when patients show improvement after the first 30 days. If placebo affect was going to happen it happens right away. The data shows GT-02287 is working. That will be huge news for the world in the next few weeks. A $200m market cap and it should be $5b if it works.Huge change to their slide wording right before data release. https://preview.redd.it/smx8ovwyrs5g1.png?width=1052&format=png&auto=webp&s=8e49875b4fb1c018c6aad5a61dec3de9c0b37f00

Outrageous_West_1564

Yeah I know this interview. I heard it multiple times and my rigidy and fatigue got better the more I was reading about GT-02287. I feel better overall. Would I say my smell got better if someone got me a fructose pill at exactly the same time and told me "this maybe can cure Parkinsonism"? Probably.  And exactly that's the point for my initial Post. I know it first hand what hope and a good mood makes to people with Parkinson. An normal investor doesn't. You "just" see the data and compare it to other trials for other diseases and that's a big mistake when it comes to Parkinson trials.