Thomas Moroder 👁️^👁️=e^(-🥟/2) @ThomasMoroder

@lorenz_swen @Premski_SGP Hehe, no time for the beach this year, just the mountains 🏔️

Summer reading thx to @Premski_SGP & @lorenz_swen

@finance_schmidt Evtl. Capital Gain Steuern sind nicht zu unterschätzen ;-)

Does $USOU still exist, @calvinfroedge ?

Quiver Quantitative @QuiverQuant

2 weeks ago

BREAKING: We just caught a wild trade. Representative Dan Crenshaw just filed a purchase of a triple-leveraged oil ETF, $USOU. He sits on the House Energy Committee and the House Intelligence Committee. Why on earth is a congressman trading a leveraged oil ETF right now?

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@whirlybard @Premski_SGP The reason for that is that those were not microcaps some time ago 😂

@reverentia_vp @AlexejGanin @ZeeContrarian1 That might be true*, but you'd have to then adjust EBITDA accordingly (for EV/EBITDA comparisons). Still calculating what values were used or would make sense. Current lease liabilities $1,074.0M + non-current $4,320.7M = $5,394.7M total; net debt $2,933M.

@Premski_SGP @Jam_invest Will they be able to collect?

And you must size (extremely) small if you want to be in the game for the long run

Premski_ @Premski_SGP

3 weeks ago

Making money on shorts:

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@Merridew__ They rely heavily on simulation, but aren't we doing the same ;-)

@agnostoxxx Your meme-game = Golden Goose (Masa) level - and I mean that as a compliment.

@silberschmelzer @SilbergleitJr PTF_THETA is negative - realistically it's just ~zero - Time Value shows ~$28 of extrinsic left across all three positions. Nothing left to collect at −0.95 delta - these options trade at intrinsic!?

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Aristidis Alafouzos @Aristidis

a month ago

Suez and Vs about to jump a lot higher. $ECO $OET TWs is an excellent contra!!

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@Simi_2210_ 18 I can see ;-)

@SebKrog @evfcfaddict $TIG.L divestiture of Domain segment could bring in $160m; remain-co trading at ~5x EBITDA/EV and assymetric optionality from antitrust litigation and no net debt; London liquidity 😜 Can send research via DM if you want

@Premski_SGP Good run!

@__paleologo attracted by gradient.. descent 🤭 Sorry couldn’t resist

Unreal $META

@calvinfroedge Ticker typo Calvin!? $CPB vs $CBP

$ABVX As a follow-up to a few posts that I saw regarding the perceived elevated rates of NMSC and malignancies in the 50 mg arm specifically in the phase 3: A few thoughts: 1) The phase 3 50 mg dose is actually a small minority of the patient years of safety data acquired -- the much larger dataset for that dose comes from the phase 2b long-term open label follow-up, which can be reasonably pooled with the phase 3 results given the same dose and detection protocols (Note, we have seen some analyses that pool 25 mg and 50 mg arms. We would NOT recommend doing this as it is not fair to claim that the risk of developing cancer in the 25 mg arm is known to be the same as the 50 mg arm). Pooling 50 mg phase 2b and 50 mg phase 3 data sets yields a much lower rate of events across the board. (I suspect it was just a bit of bad luck on the smaller phase 3 dataset for the 50 mg dose in isolation, see below chart for what we've been working off of after integrating these phase 2 data -- note there are some assumptions that go into this but the variability should be pretty de minimis); 2) Two ways things generally cause cancer: DNA damage from some oxidative/radiation/something else source that damages DNA or inhibits DNA repair mechanisms at their core OR substantial or highly targeted immunosuppression. Because both of these events are total exposure related, typically events accelerate over time. The phase 2 had the much longer follow-up with fewer patients whereas the phase 3 had more patients followed up for less time. The phase 2 had a very low number of events, and the phase 3 50mg dose was the only arm that had an elevated set. A priori, if the drug was a carcinogen, we would have expected the opposite: that the phase 2 would have a higher incidence/100 PY than the phase 3 given the individual patient exposures on a cumulative basis to such carcinogens are much higher in the phase 2 than the phase 3 in addition to the idea that there is a delay between when the carcinogen can cause the malignancy to when it can be detected (and T=0 is always the first instance in which that timer could start). Also, if the drug was as immunosuppressive as would be needed to cause cancer, you would expect to see a boatload of opportunistic infection before you'd see the cancer signal -- we see none.; 3) Pre-clinical testing confirmed that the drug is actually an anti-proliferative -- we would have expected the drug to be protective against tumor growth, not stimulating it; 4) No consistency or clustering for any cancer type at any time point; 5) NMSC carries a much different (lower) risk profile than other types of malignancies since they are caught very easily and have a low rate of metastases, and are seen at a massively disproportionately high case numbers relative to other types of malignancies (also included in the bottom table following pooling of the 50 mg arm), so FDA is less concerned about it than non-NMSC; 6) To warrant a black box, the FDA usually requires, at a minimum, consistency of preclinical and/or striking clinical datapoints such that careful consideration must be made to determine if the benefit/risk profile inverts in a subset of all patients that may receive the drug. In this case, we not only have completely disparate and conflicting datapoints, but we even have one data point relating to the MoA and pre-clinical data findings that suggest the drug should have the opposite effect. In addition, black box decisions are not made in isolation. They are heavily debated back and forth between the company, internally, require a lot of internal consensus on establishing causal link, and are not made in a vacuum to unmet need and efficacy; 7) UC patients have an elevated rate of inflammation (by definition) and, in turn, elevated rates of cancer compared to healthy individuals (~+.5 events/100PY vs non-UC). Obefazimod is now a proven highly effective therapy that leads to robust endoscopic remissions and attenuation of much of this inflammatory effect. I would hypothesize if you ran a large enough study and followed patients for long enough, you would find that there would be a cancer benefit from the drug secondary to the disease control that it would afford. The weight of this potential benefit (which makes sense given the pathophysiology) must be considered against the risk of the agent itself causing cancer (for which we have no reason to believe it actually should cause cancer).