TraderNick (@RealTradingNick) profile picture

starting from ~120k my goal is to hit 1M by 2028 latest. until then I will invest aggressively and take considerable risk. plan is to ~2x my portfolio each year

Joined August 2025
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TraderNick retweeted
What concerns me most about this market is that the S&P 500 is almost at an all-time high, yet so many individual stocks have already suffered massive sell-offs. Look at what’s happened to the neoclouds and other AI stocks. Even semiconductors have been hit hard. If this much damage has happened while the index has barely dropped, what happens if the broader market starts selling off? We could see some of these high-beta stocks fall another 20–30%. That’s what worries me. A lot of retail investors could struggle to recover from that. Especially those who’ve borrowed money or keep buying the dip in companies simply because they’ve fallen a lot. The main thing I’m watching is oil. Brent touched $110 last week because of the situation in the Middle East. The longer this war in Iran continues, the longer we risk keeping oil prices and inflation high. That’s what creates more uncertainty around interest rates. So investors are reacting to every negative headline. You can have a company doing everything right, but its shares still get sold off because of something happening on the other side of the world. Then we have two elections coming up. One in Israel and the midterms in America. Let’s be real, both governments want something they can point to as a win before people vote. I think that’s a sad reflection of the world we live in. People are struggling to afford the basics, but so much of politics seems to revolve around how to win the next election. My fear is what happens after the midterms. Trump won’t have another presidential election to fight. He’ll still have limits on what he can do, but I worry about what decisions he might make over those final two years without that same election pressure. Meanwhile, the companies are still delivering. Meta just grew revenue 26%. SpaceX reported revenue growth of 161%. Those results helped their shares, but they haven’t removed the uncertainty hanging over the rest of the market. I expect more strong earnings this season, but earnings alone can’t settle what’s happening in Iran or where interest rates go next. Honestly, if I were a new investor starting today, I’d probably be tempted to wait this out. Every day feels like another disaster is about to happen. But we’ve been through a lot this year, and we’ve managed to recover before. I believe we’ll recover again. I just don’t know how long it will take. It may take longer than usual. Long term, the amount of money that’s going to be spent on AI is astronomical. We’re talking about trillions of dollars. McKinsey estimates $5.2 trillion of investment in data centres by 2030 just to meet AI demand. This is one of the biggest infrastructure investments we’ve ever seen. We’re in a transition period. I believe AI is going to replace a huge amount of the work people do today, and the impact could be bigger than the internet. Just look at how quickly ChatGPT and Claude are advancing. Anthropic says that by May, Claude was already writing over 80% of the code being added to its production codebase. Before Claude Code launched in February last year, that figure was in the low single digits. Think about how much has changed in that short space of time. That’s why my long-term view on my AI investments hasn’t changed. Short term, though, I’m very concerned. But I’ve never been able to time the market consistently. I could sell today and end up buying back higher while still worrying about the same headlines. So I’m going to stay invested. I still believe in the companies I own, even if holding them through this market is exhausting.
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TraderNick retweeted
Obefazimod in UC: the phase 3 maintenance data, from two talks @my_ueg 580 people with moderate to severe ulcerative colitis who responded to 8 weeks of obefazimod, a once-daily oral medicine, were re-randomised for 44 more weeks. Placebo here meant stopping a drug that had just worked. It works. Clinical remission at week 52 was 39 percentage points higher than placebo on 25 mg and 40 points higher on 50 mg. It works across the secondary endpoints too. On endoscopic improvement, endoscopic remission (Mayo 0), histo-endoscopic mucosal improvement, steroid-free remission, sustained remission, clinical response and symptomatic remission, the delta over placebo ran from 31 to 53 points, every one at p<0.0001. It works with and without prior advanced-therapy (AT) failure. In AT-naive patients the delta in clinical remission was 45-48%; after AT failure it was 28-33%; smaller, but still large. And it was well tolerated. Serious adverse events were within 2 points of placebo on either dose, fewer people stopped for an adverse event on drug than on placebo, and there were no deaths. Two cancers outside the skin, both on 50 mg, were judged unlikely to be related. What next: @Abivax_ plans to file in the US by the end of 2026, and the full phase 3 paper(s) are still to come. The first Crohn's data, from the phase 2b ENHANCE-CD trial, are due in mid-2027.
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TraderNick retweeted
448 days since my last pitch ($ABVX), it’s now finally time for my next one: $ZURA (Zura Bio). Like with the $NKTR and $ABVX pitches before this, I will post a general outline of my research on $ZURA as a thread here. However, for those looking to really get into the weeds, there is a Google Doc link to the full length pitch attached below. Let’s dig in. docs.google.com/document/d/1…
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Donald Trump hat gerade verkündet, dass Russland 300.000 Tonnen Diesel an die USA liefern wird. Der Rest der Welt setzt im Energiebereich gnadenlos Deals und eigene Interessen durch. Deutschland geht einen anderen Weg. Wir haben uns für Atomausstieg, Kohleausstieg, feministische Außenpolitik und Moral entschieden. Die Zeche zahlen die Menschen. An der Zapfsäule. Im Supermarkt. Und wenn ihre energieintensiven Arbeitgeber für immer die Türen schließen.
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TraderNick retweeted
H.C. Wainwright keeps a Buy rating and $185 PT on $NKTR after the Co. presented AA data at #EADV2026 and hosted a conference call to review the data. $QTTB $NBI H.C. Wainwright said in its note: Of the eight patients who achieved SALT ≤20 after 52 weeks of rezpeg treatment, 75% (6/8) maintained the response at four months and 63% (5/8) at six months off treatment (NRI, with all patients available for assessment), versus an estimated 30% and 20% for low-dose baricitinib (2 mg) after the same 52 weeks of treatment (cross-trial comparison, Exhibit 1). Response was also independent of current episode duration, a key prognostic factor in AA: among patients who entered the 16-week treatment extension, 29% with a current episode of <4 years and 30% with an episode of 24 years achieved SALT ≤20 at Week 52, whereas baricitinib 2 mg response fell from an estimated 28% to 11% across the same cut (Exhibit 2). Most notably, responses kept deepening without drug. During the six-month off-treatment period, 41% of the 27 patients in the 52-week treatment cohort achieved a deeper best response than on treatment and another 22% maintained their regrowth (Exhibit 3), while SALT ≤10 rose from 7% at Week 52 to 19% (Exhibit 4) and one patient reached SALT 0. Despite these results, NKTR shares fell 22.4% to $46.99 on October 1, versus a 2.1% decline in the Nasdaq Biotechnology Index (NBI). We view the move as unjustified and believe the stock is oversold. We maintain our Buy rating on NKTR and a 12-month price target of $185 per share.
Canaccord Genuity🏁 $NKTR Buy-$153 and said in its initiation report that the Ph3 program for lead asset rezpegaldesleukin in atopic dermatitis has commenced and a Ph3 program in alopecia areata is expected following an end-of-Phase 2 meeting with the FDA—expects rezpeg's unique mechanism of action to appeal to patients and physicians alike, if approved. Rezpeg has two big advantages in the dermatology space, namely its potential for disease modification and safety.
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A year ago, I wrote about uniQure's ($QURE) 3 year readout of AMT-130, their gene therapy for Huntington's disease (HD), and said we should wait for the longer follow up. Today, the company released data on another timepoint, the 4 year readout, which now reinforces my earlier argument for the need for further follow up to know if the treatment is really working. At 4 years, the primary end point, cUHDRS, showed 44% slowing of disease progression in the high dose group (n=12) compared to external controls, down from 75% at 3 years. It was not statistically significant this time (p=0.144), compared to p=0.003 at 3 years. The secondary end point, total functional capacity (TFC), held up better, with 61% slowing (p=0.008), about the same as the 60% at 3 years (p=0.033). Some context: after the 3 year readout, FDA first said the data was not enough, then in June this year said it was enough, and the company filed for accelerated approval based on the 3 year data. Today's results were not part of that filing, but they change the lens through which one would look at the 3 year data. The company's explanation for the weaker 4 year result is dropout in the external controls. 53% of the matched controls had no data at 4 years, and those who stayed longer in the study were slower decliners compared to the dropouts. Fair argument. But for that argument to hold, the dropouts one needs to look at are the ones who left the study between year 3 and year 4. According to the company's own slides, the controls with data went from 690 at 3 years to 625 at 4 years, which is a loss of only about 65 people (~9%). So, whatever bias the dropouts caused was already present in the year 3 comparison, which showed 80% slowing in the updated analysis. Ignoring the controls and looking at the treated patients only, the high dose patients (n=12) had lost 0.38 cUHDRS points at 3 years, and another 0.52 by year 4. That looks like disease progression picking up pace. In the adjusted numbers, TFC stayed flat between year 3 and 4. But TFC is a coarse scale (0 to 13) that barely moves in early HD, which is why cUHDRS was chosen as the primary end point in the first place. Also, TFC is part of cUHDRS, which points to continuing decline in motor and cognition. One argument in the treatment's favor is the comparison between the high dose and low dose groups. At 4 years, the high dose group declined by 0.91 on cUHDRS and the low dose group by 1.94, which is about 53% slowing. The low dose group declined similarly to untreated controls from the older ENROLL-HD dataset (also 1.94), so it behaves like a natural control that went through the same surgery and trial visits (though the two doses were not randomized against each other). The between dose difference is similar to the high dose vs control (older control) difference. CSF NfL, a marker of neuronal damage, went from 11% below baseline at 2 years to 4% above baseline at 4 years. NfL is noisy over short periods, so I wouldn't read too much into it, either in favor of or against the treatment. So, different ways of looking at the data all land around ~50% slowing at 4 years, not the 75-80% seen at 3 years. It's difficult to say whether the 4 year data indicates regression to the mean in a small group, the treatment effect wearing off, or the patients just entering the fast phase of the disease. The 5 year data, likely around this time next year, will be the one to watch. uniqure.com/investors-media/…
Today, UniQure ( $QURE ) announced the 3 yr readout findings of their gene therapy trial for Huntington's disease (HD). At the bottom line, the company reports a statistically significant reduction of disease progression (~75%) compared to an external, propensity matched controls. Apparently, everyone is excited about the results, as can be seen from the >250% increase in $QURE stock price today. Understandably, a first positive trial news in a long time for a devastating disease with no cure has excited the scientific community and increased the hopes of patients. I am seeing headlines like "Huntington's disease successfully treated for the first time" and claims like scientists' have found a cure for HD. I am not sure if the findings are that groundbreaking to warrant such claims. It might be the case that treatment really is working, but I am not sure if the current findings are strong enough to be too confident on the treatment effect. There are many uncertainties around the results. Below are my some of my thoughts. HD is caused by a triplet repeat mutation HTT gene that somatically expand over time and cause neurodegeneration. The repeat mutation in HTT gene gets translated to polyglutamine repeats in the HTT protein, which is believed to be neurotoxic (though we don't know exactly what's killing the neurons). Past treatments have largely focussed on knocking down HTT gene using different approaches, none of which translated to clinical benefits. Most notable among them, is tominersen (developed by Roche and Ionis Pharmaceutials), an antisense oligonucleotides (ASO) drug that lowered the production of HTT protein in the brain (both the mutant and normal copies). Although, tominersen successfully reduced the HTT levels in the brain, it failed to treat HD. All past failed efforts on treating HD by reducing HTT production, led to many critical questions, such as - Is it safe to blindly knockdown HTT in the brain, as normal versions of the protein might play some important functions ? - How early one should intervene to make clinically meaningful impact on disease progression? Even though the clinical symptoms appear late in the disease course, the neuronal damage itself seem to start very early in the disease course. - At what level does the toxicity originates, protein or RNA or DNA? how much of the existing neuronal damage is reversible? There are many more unanswered questions. Recently, the therapeutic focus have shifted to reducing the somatic expansion of HTT mutation rather than reducing the HTT expression (refer to this article for more details on this, nature.com/articles/d41586-0…). With this background, here we have a new gene therapy--AMT-130--developed by UniQure that is trying to treat HD by reducing HTT production using a viral vector based genetic drug surgically injected directly into the brain striatum (key brain region affected in HD). The idea is to permanently reprogram the neurons to produce microRNAs that reduce production of HTT proteins (both mutant and normal copies). It's challenging to have true controls for such trials, so scientists used external controls (in large numbers, n>100) that matched closely to the trial participants with regard to clinical characteristics. There were two groups. One (n=9) received the high dose injection and the other, low dose (n=12) The primary end point is a composite score called composite unified Huntington's disease rating scale (cUHDRS) calculated from multiple clinical scores measuring motor, cognitive and other functioning capacities of the patients. Additionally, neurofilament light chain, a CSF biomarker of neuronal death, is also measured. At 24 months follow up (July 2024), the press release reported a statistically significant reduction (~80%) in the cUHDRS decline in high dose group (n=12) vs external controls. But there was no significant effect in the low dose group (n=12). With regard to CSF Nfl, the report showed a slight decrease in trial participants (n=21) compared to baseline, both high and low dose pooled together the CSF. No data on this from individual groups. Now (Sep 2025), at 36 months follow up, the press release reports a statistically significant reduction (~75%) in the cUHDRS decline in high dose group (n=12) vs external controls. But there is no significant effect in the low dose group (n=12). With regard to CSF Nfl, the report shows average reduction in CSF Nfl in both low and high dose groups individually compared to baseline. No mention of P values. From the data, the reductions are likely not statistically significant from either baseline or between the high dose and low dose groups. Reviewing the data, I see two major concerns: small case sample size (paired with unusually large controls) and short follow up period for a noisy outcome measure such as cUHDRS. Firstly, there are only 12 individuals in each case arm (with 36 months data) and 568 individuals in control arm. The control sample is disproportionately larger than case sample size. It's difficult to confidently assess a different between these two groups. The variations in the control group would be smaller due to large N, but the variations in the case group would be bigger with mere chance pushing the average to extremely higher or lower levels. Currently, individual data points are not reported. It's possible that even one or two patients with extreme scores would have pushed the average of trial participants higher favoring a statistical significance. If the number of controls is reduced to, let's say, n<100, it's possible the P value becomes bigger, even to non-significant level (P>0.05). One might get excited about the large effect size, 80%, but effect estimates are meaningless for extremely small sample size. Secondly, the 3 year follow up is short for tracking HD's disease course. HD has a really long latent period and the disease progression happens slowly until very late stages when things escalate quickly. Also, the neuronal damage happens asynchronously. The disease course can differ wildly between patients with some staying stable for many years while other worsening quickly. Given this complexity, interpreting a 3 year readout based on n=12 individuals is challenging. My other major concern is the low dose group, in which there is no meaningful effects either at 24 months or at 36 months. Even worse, with regard to some measures they seem perform poorly compared to controls. This is worrying, as it suggests there is no dose dependent effect. But we don't know for sure. Much longer follow up is needed. Adding to the concern, the press release avoided mentioning anything about low dose group, and focussed only on high dose group. Of course, even a remote possibility that this gene therapy works and may give back years of quality life to HD patients should excite anyone in the field. I am excited too. But at the same time, one should be also cautious in interpreting the results and raising hopes for patients and families. For now, I'd say we should be cautiously optimistic about this readout and wait for longer follow up results. Of course, it's possible the drug clear regulatory approval and gets rolled out to many patients. But it's gonna take a long time before we really know if it's truly working. uniqure.com/investors-media/…
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TraderNick retweeted
$ABVX A frustrated shareholder can leave in a click, but a patient in durable remission will stay for years. These UEG data have me thinking about what that difference is worth. From my view, Obe is essentially the convenience of Otezla and the benefit/risk of Dupi smashed into a once-daily pill. I think this idea of it being "just another therapy" is not fully capturing the dynamics of how IBD can change going forward with the totality of characteristics obe seems to possess. This is a repeatable inefficiency I've seen particularly in I&I, where the lack of hard market "comps" makes it difficult for investors to underwrite a precise expectation of sales, but then miss the signal of practice-changing potential through the noise of a desire to seek false precision. There are elements of Obe's clinical profile that seem to mirror Dupixent. While dupi launched into a less competitive market, the combination of generally reliable efficacy that could conveniently throw patients into a low or no disease state with a "prescribe and forget" safety profile, outside of some conjunctivitis or psoriasis popping up, led to physicians moving quickly from "give this to the most severe patients" to "why bother with anything else upfront?" Some patients are needle averse, but many accepted that tradeoff for benefit/risk. During the initial dupi launch, sell-side had ~$1.5 - $3.0 bn in peak sales estimates. Dupi currently does ~$18bn growing 38% yoy, of which ~$10bn are AtD growing at what we estimate to be ~20% yoy. That's the power of changing clinical practice. I think the assumption that obe will be used after IL-23 in most/all cases may not turn out to be true eventually. Physician behavior can depend heavily on first impression use and burden on the staff to not only prescribe, but also manage, the patient follow-up period. You know what is a low burden on the office staff? A happy patient in durable remission, which these data continue to show. And there's a whole bunch of patients who are in the current prevalence pool who may not be in remission and want to try to achieve that when obe hits the market. The steroid-free remission is an underappreciated element of these data too -- patients and physicians generally try to limit steroid use when they can for their patients, especially high doses over long periods of time, due to QoL burden and risk of Cushings. Otezla, despite having a quite weak efficacy profile, grossed >$2Bn at peak across indications because it was a convenient "prescribe and forget" option. For a market that is driven by community physicians who are less resourced than tertiary centers, this low administrative burden really matters, and approximately 2/3rds of IBD patients are seen in the community, not the academic, setting (academic.oup.com/ibdjournal/…). So far, the totality of data from obe suggests to me that you get the best of both of these worlds, seemingly without any meaningful tradeoffs thus far that I can tell. Transient Advil for some patients in induction, but likely no burdensome extra labs, monitoring, or tail risk safety event. Happy to take a third bite at this apple if those with less patience don't want to wait for that potential large upside. programme.ueg.eu/2026/week/d…
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Dieses Video ist ein must-watch. Unfassbar, dass Jens Spahn nach diesen Vorgängen noch im Bundestag sitzt und sein Gehalt von Steuerzahlern bekommt. Wie kann die @CDU das hinnehmen?
Sollte Spahn damit wirklich davonkommen, darf sich niemand über Politikverdrossenheit wundern.
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The Best Investment Strategy in the World There are a hundred ways to make money in the stock market. You can diversify, concentrate, buy and hold, day trade, trade options, buy junk bonds, follow momentum or search for tiny companies nobody has heard of. People have become extraordinarily rich doing almost all of them, so what exactly is the best way to invest? I don’t think there is a best investment strategy. There is only a best investment strategy for each person. What works brilliantly for one investor could be a disaster for another. Investing cannot be separated from the person doing the investing. Your age, wealth, income, family, goals, knowledge, temperament and the way you react to losing money should influence how you invest. A 28 year old with $50,000 is playing a completely different game from a 68 year old with $10 million, yet we talk about the “best strategy” as though the person executing it barely matters. This is why I think Wall Street’s definition of risk is incomplete. We measure volatility and drawdowns, but what about the probability that you panic, become bored or abandon a perfectly good strategy after three terrible years? Some of the greatest risks in investing exist inside the investor, not the investment. Envy may be one of the biggest. The market gives us a daily scoreboard of everything we should have owned instead, and somewhere someone will always be getting richer faster than you. If you compound at 15% while somebody on X makes 80% trading options, it becomes surprisingly easy to feel unsuccessful while doing something objectively extraordinary. That is how investors get pulled into games they were never supposed to play. A long term investor becomes a trader, a conservative investor starts speculating and someone who spent twenty years studying businesses suddenly decides they need to trade options. Their abilities didn’t change. They simply became distracted by somebody else’s success. One of the great breakthroughs in investing happens when you stop asking what everyone else is doing and decide what game you are actually playing. You don’t need to master every corner of the market or participate in every opportunity. Find an approach that matches who you are and become exceptionally good at it. This is where the circle of competence becomes much more interesting. It isn’t only knowing what you understand. It is also knowing what you can safely ignore. If your goal is to own $MELI for the next decade because you believe MercadoLibre can become dramatically larger, does it really matter what $NVDA reports tonight? Do you need an opinion about $CRWD, Bitcoin, oil and the next Fed meeting? Unless those things change your thesis, much of it is probably noise disguised as knowledge. We have access to more financial information than any generation of investors in history, yet that doesn’t necessarily make us better investors. Information tells you what happened, knowledge helps you understand why it happened, and wisdom tells you whether you need to do anything about it. I think the last part is where much of the money is made. This is also why copying great investors is so difficult. You can copy someone’s portfolio in five minutes, but you cannot copy the twenty years of experience that produced it. You don’t inherit their temperament, pattern recognition, financial circumstances or ability to sit through a 50% decline. Eventually investing becomes a very personal exercise. In the beginning you study stocks, accounting, valuation, business models and famous investors. If you are paying attention, eventually you begin studying yourself. 🌹
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🚨🚨🚨 CARDIO-TTRansform data presented at @escardio #ESCCongress and simultaneously published in @NEJM. The (very surprising!) topline data was released last month – now we get the full data release. Much to break down – it’s all here in the 🧵 below. (1/25) nejm.org/doi/full/10.1056/NE…
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Replying to @BAMBossie81
KOL‘s are always something between payed puppets and legitimate experts with an honest professional opinion
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$TENX tenax axed
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TraderNick retweeted
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✅ News $ABVX : Morgan Stanley raises PT from 132$ To 180$ , citing KOL feedback following ABTECT maintenance and Part 2 data has come in incrementally positive #Abivax $XBI
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Replying to @ezmoneymonty
You are reading this wrong. You cannot just hit pause and wait until a buyer shows up. Every day lost until patent expiration is millions lost. Someone needs to execute and get everything set-up. A few millions for some experienced experts are a good investment regardless on the path forward. A buyer will appreciate knowing that they don’t have to immediately start working, but can have a smooth transition. In addition, these guys have friends and former colleagues at all potential buyers so you get some visibility for free ($AMGN $MRK $BMY $ABBV $TAK $LLY $ABT)
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Neue Slack-Chats der „Proximal Origin“ Autoren freigegeben! Darin zeigen die in 🇩🇪 "Qualitätsmedien" oft als verlässliche Quellen zitierten Virologen ihr wahres Gesicht: krasse Beleidigungen, klare Widersprüche zu eigenen öffentlichen Statements zum Coronaursprung und krasse Eingeständnisse zu früheren tödlichen Ausbrüchen. Ein 🧵 teapawt.net/SenRandPaul/status/208… 1/
🚨New documents show NIH hid public comments about Wuhan Institute of Virology and Ivermectin on social media, calling them “off topic.” NEW DOCS: paul.senate.gov/readingroom?…
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Heute hat uns das fünfte Paar aus dem engeren Freundeskreis erzählt, dass sie auswandern wollen: Alle fünf Familien haben kleine Kinder, alle sind unternehmerisch tätig, alle verdienen sehr viel Geld. Drei nach Mallorca, zwei nach Portugal. Es ist Wahnsinn. Am Ende wird Deutschland zum Land der Beamten, Rentner und Grundsicherungsempfänger.
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Ok ladies and gentlemen, it’s truly over now. Ffs $xbi
Cramer says biotech is the hottest sector in the market. The setup is definitely improving: M&A is back, capital is flowing, and Big Pharma still needs pipeline. Just don’t confuse a bull market with easier drug development. In biotech, the data always wins. thestreet.com/investing/stoc…
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