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@AnnaFlorcia Would've hoped he had it tee'd up and ready to hit send shortly after the ruling. My guess was before the wknd, but that might be a little aspirational. $LQDA

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@Paperboy2009

4 days ago

HIKMA reversed. Judge Andrews is hopefully now free to relase his judgement for $LQDA in the next few days, hopefully. This was the only thing that made sense regarding the delay. Bring it on, Judge!

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@Paperboy2009

4 days ago

@avidresearch @semodough @Maximus_Holla @Archimedes20311 If a potential sale was soon-ish, why raise? $MLYS

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deathTouch

@deathtouch2k

4 days ago

Passing on $ABVX at this valuation is equivalent to passing on buying it at $55 in the post-market following the induction data readout. The market is getting a second chance at the same mistake. Here is the question the market will answer over time: what is the right value for what may be the best UC drug ever developed? Obefazimod appears to be a safe, once-daily oral therapy with no pre-prescribing burden, no meaningful ongoing monitoring burden, a unique mechanism of action, and exposure to what should become a ~$20B IBD TAM? The answer is likely more than ~$7B. Let’s put this in perspective: ~$7B is roughly what Pfizer paid for etrasimod before the Phase 3 UC data read out, which was a second-in-class S1P modulator behind ozanimod, with weaker efficacy, QT-related considerations, ECG screening, monitoring burden, and a less differentiated commercial profile. So what is capping the stock today? Outside of the cancer debate, based on conversations with market participants, the current pushback appears to be that there is “no catalyst.” They appear to have missed there is a major safety update expected by the end of this month that should nearly double the total patient-years of obefazimod safety exposure. I know pods have short-term thinking, but three weeks does not seem that far away when the next dataset has the potential to directly address the central bear case. That matters because the current bear case is safety. If the upcoming dataset continues to show that the malignancy rate is in line with UC background risk and non-JAK UC comparators, it should materially reduce the central sentiment overhang on the stock. That is the broader setup. The market appears to be treating the June 1 safety update as a structural impairment. That interpretation is wrong. These data now establish obefazimod as a potential frontline “prescribe and forget” oral therapy in UC which is a profile often hoped for and talked about in IBD and I&I more broadly, but rarely realized. The concern around non-NMSC events reported on June 1 is overblown. The June 1 data update should strengthen, not weaken, the core $ABVX thesis. The 50 mg safety concern is best understood as a red herring when evaluated against pooled exposure, the elevated baseline cancer risk of a refractory UC population, and malignancy rates observed with other UC therapies that do not carry black box warnings. The more important signal is efficacy. The 50 mg dose remains highly effective, with potentially best-in-disease endoscopic remission data, while the 25 mg dose provides meaningful flexibility for chronic maintenance, labeling, and physician adoption. The market reaction materially over-discounted safety-related risk, underappreciated the commercial significance of 25 mg / 50 mg dose flexibility, and failed to appreciate that the strength of the endoscopic remission data supports potential earlier-line use in UC while materially increasing the probability of success in Crohn’s disease. UC supports the base case. Crohn’s is the key upside driver for valuation. The reported 50 mg obefazimod malignancy data should be evaluated in totality by combining the pooled 96-week Phase 2b dataset, which used the same dose and similar NMSC surveillance, with ABTECT Maintenance Part 1. The right question is not whether there were headline malignancy events. The right question is whether the rate looks out of line for a refractory UC population that is already at elevated risk of cancer, and whether it looks out of line versus other UC therapies that do not have black box warnings. On the totality of the data, it does not. By construction, per regulatory convention, and consistent with standard practice in clinical IBD trials, dysplasia should not be counted as a non-NMSC malignancy event. Dysplasia is pre-malignant and, by definition, is not cancer. Such findings are also not uncommon against the background risk of longstanding ulcerative colitis. Including dysplasia as cancer distorts the safety interpretation and makes the 50 mg dose look worse than the data support. There were two non-NMSC events reported in ABTECT Phase 3 Maintenance Part 1. There was one non-NMSC event reported in the ongoing Phase 2 series of trials. It is unclear whether this event occurred during the 96-week portion of the Phase 2 series, but conservatively counting it against obefazimod still yields an event rate of approximately 0.58/100 patient-years. This places obefazimod in the middle of the range across UC comparators, including ustekinumab, vedolizumab, etrasimod, ozanimod, and mirikizumab, none of which carry black box warnings for malignancy, and ahead of black-boxed JAK inhibitors, including upadacitinib and tofacitinib. That is not what a broken 50 mg safety profile looks like. The safety debate is distracting from what should be the dominant interpretation of the update: the efficacy data are exceptional. Obefazimod has produced what may be the most impressive endoscopic remission dataset observed in ulcerative colitis, particularly after adjusting for how refractory the ABTECT population was. This was not an easy-to-treat biologic-naive UC trial. The study included substantial advanced-therapy inadequate responders and prior JAK inhibitor inadequate responders, yet the 50 mg dose still delivered a level of mucosal efficacy that appears best-in-disease or near-best-in-disease on a refractory-adjusted basis. That is the point the market appears to be missing. RINVOQ likely remains the stronger acute induction/rescue benchmark, but upadacitinib’s pivotal UC trials did not face the same degree of prior JAK-exposed disease biology. For chronic maintenance, obefazimod appears highly competitive and potentially superior when adjusted for baseline severity, with particularly strong endoscopic remission and corticosteroid-free remission performance. A non-JAK oral drug delivering this level of mucosal efficacy in this population is not just “strong data.” It is a potential frontline-enabling efficacy profile. This is what creates the frontline “prescribe and forget” opportunity. Community GIs manage many moderate UC patients before they become severe or refractory. A clean 50 mg profile would offer a rare combination: enough efficacy to keep moderate UC patients controlled, and enough safety comfort that physicians do not feel burdened managing the drug. Oral dosing, strong efficacy, no infusion logistics, no JAK-label discomfort, and minimal incremental workflow burden create a practical profile that community physicians can use earlier. The larger opportunity is not merely post-biologic / pre-JAK positioning; it is post-generics / pre-biologics use by physicians who want an effective, low-friction oral option. The 25 mg dose further strengthens this profile. It is not a rescue thesis; it is a strategic advantage. It provides flexibility for chronic maintenance, labeling, and physician adoption, while preserving 50 mg for induction, higher-need patients, or flex-up dosing. A commercially viable regimen could mirror the established IBD treatment paradigm used with RINVOQ: higher-intensity induction followed by lower-dose chronic maintenance. In practice, patients could receive 50 mg obefazimod induction or JAK induction followed by 25 mg obefazimod maintenance, with the ability to flex back to 50 mg in selected patients who require additional disease control. This preserves the key commercial attributes of the asset: potent induction optionality, a lower-exposure 25 mg maintenance backbone, oral dosing, dose flexibility, and strong mucosal efficacy. A potential 50 mg chronic-label limitation should therefore be viewed as a manageable dosing/labeling issue rather than a thesis-breaking safety problem. If the practical regulatory choice were between preserving broad 50 mg chronic dosing at the cost of a black box warning versus adopting a cleaner regimen of 50 mg induction and/or selective flex-up with 25 mg maintenance, the rational commercial strategy would be to prioritize the label that maximizes broad chronic use, physician comfort, and adoption. Even if, for the sake of argument, obefazimod ultimately received a black box warning, the asset would still not be broken. RINVOQ is black-boxed and still represents a multi-billion-dollar IBD product. That creates a reasonable downside commercial anchor for obefazimod: constrained label, not zero. In that scenario, obefazimod could still have a role in the post-biologic / pre-JAK setting, and potentially as maintenance after RINVOQ induction or after 25 mg / 50 mg obefazimod induction. If obefazimod is viewed as safer and more effective in maintenance, it could still be used ahead of RINVOQ for chronic disease control in selected patients. But the Crohn’s readthrough is the major upside driver, and the headline of the maintenance data should have been "Crohn's now appears largely de-risked". Can anyone think of a therapy that produced this degree of mucosal efficacy in UC and then failed to work in Crohn’s? Tofacitinib is the closest example, but it is not a close comp: inferior mucosal healing, a much easier-to-treat UC population, and a JAK mechanism with a very different safety and commercial profile. The point is not that UC success guarantees Crohn’s success. It does not. The point is that a non-JAK oral drug producing this degree of mucosal efficacy in a hard-to-treat UC population should materially increase the prior probability of CD success. Above a coin flip certainly seems reasonable given prior UC to CD translational examples, and we would venture should be closer to 75%, but regardless, meaningfully above where the market appears to be underwriting it today. That makes Crohn’s a real valuation driver today, not a free option worth zero. Global peak obefazimod sales can be reasonably framed at approximately $3.5–5.0B in ulcerative colitis alone, with upside to $6.0–10.0B if Crohn’s disease is successful. On a risk-adjusted basis, assuming a high probability of UC approval and a 66% probability of success in Crohn’s disease, a reasonable underwriting range could be approximately $4.5–6.5B in global risk-adjusted peak sales across IBD. There is additional upside approaching or exceeding $10B globally if the safety profile remains benign and the drug moves into frontline or earlier-line UC/Crohn’s use. The UC-only case is supported by a differentiated profile: oral once-daily dosing, strong maintenance efficacy, robust endoscopic remission, potentially cleaner chronic safety, 25 mg / 50 mg dose flexibility, and a refractory-adjusted efficacy dataset that compares favorably with leading advanced therapies. The base case is that obefazimod remains a multi-billion-dollar IBD asset. The downside case is a narrower 50 mg maintenance label, a 25 mg-centered chronic-use strategy, or even a constrained/black-box label, which remains commercially manageable and still anchored by a RINVOQ-like IBD revenue framework rather than zero. The upside case is a clean label, earlier-line UC positioning, community-GI adoption in the post-generics / pre-biologics setting, and successful Crohn’s development, which could support global peak sales toward the high end of a $6–10B range. To sum it all up: The risk/reward appears highly attractive because the market is focused on a worst-case interpretation of the 50 mg safety signal while failing to credit the durability, mucosal efficacy, Crohn’s readthrough, and commercial flexibility of the 25 mg / 50 mg profile. Layered on top of that is fast short money arguing there is “no catalyst,” despite a major safety update expected before the end of the month that should add a truckload of patient-years and directly address the only real bear case. If that dataset is clean, the debate should quickly shift from “is 50 mg impaired?” to “why was a potential best-in-disease oral IBD drug, now post-pivotal UC data, ever valued below inferior IBD assets acquired before their Phase 3 readouts?” Disclosure: May hold or trade securities mentioned, including $ABVX, and views/positions may change without notice. Not investment advice.

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@Paperboy2009

4 days ago

@jfais20 Hopefully it will be a slow grind up once we’re clear of the offering. The data was great, and I think the stock will be higher months from now. PDUFA next month too. $CELC

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@Paperboy2009

5 days ago

@EuroEule @JPZaragoza1 Since that's the new timeline, I don't think they'd wait for that data to consummate a deal. YE is one thing, but mid-27 makes it more likely they won't wait, and would go the CVR route. Just my thought on it. $ABVX

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@Paperboy2009

5 days ago

@ScribblesTay @seedy19tron There is the scientific side of the biz, in which they excelled, but there is also the public-facing IR side. There they didn't handle messaging well. I certainly don't have the same faith in them handling things IR-wise like I did last week $ABVX

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@Paperboy2009

5 days ago

@Biohazard3737 Someone is going to get a good deal now around $200-230/sh for the company $ABVX

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@Paperboy2009

6 days ago

@Biohazard3737 How do you feel about the mgmt, how they presented the data, and has your opinon of the company / drug changed at all over the last 24 hours? $ABVX

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@Paperboy2009

6 days ago

Big bullish bet today on $AUPH with >10K Jan 15 puts SOLD to open

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@Paperboy2009

6 days ago

@HulkCapitalPro While there’s a good chance for an eventual raise, I did buy more on the dip. This will be the standard of care, eventually $ABVX

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Adam May

@A_May_MD

6 days ago

Always sharp @drug_smolecules making the case here that $ABVX doesn't even get a black box warning by comparing malignancy rates to Sotyktu, which was under a huge microscope for safety because its target (TYK2) is a member of the JAK family. Sotyktu did NOT get a black box warning despite huge regulatory attention that came with technically being a JAK inhibitor only by a different name. Our friend DRUGS calculates $ABVX's per year malignancy risk as 0.48, versus 0.46 for Sotyktu with its ***CLEAN*** label. So there you go - FDA precedent says no black box, right? 0.48 is basically equivalent to the 0.46 rate of the drug that got zero labeling for malignancy... But there's more! DRUGS here is actually missing a key, very big nuance - He's including only the *2nd* extension of the phase 2 trial and not the first. So he is missing 2-4 years of EXTRA squeaky clean safety for all 130 patients. This is essentially and entire extra *Phase 3* worth of patient-year safety data... So let's redo the math with the full P2 dataset (using his initial numbers): ➡️357.5 patient-years from the 2nd P2 extension ➡️310 patient-years from the P3 (80% of 388 patients were completers at 52 weeks -not 44 weeks-) ➡️Now the extra 2-4 years of P2 at 50mg dosing that was inadvertently excluded...let's say the average time on therapy was only 2.25 years to account for dropouts. 2.25x130 = 292.5 more patient-years from the initial 2-4 years of P2 he missed. Adding that in, the grand total becomes 960 patient years (instead of 619). Much of it at 50mg as well! That takes the "malignancies excluding NMSC" rate to 3/960 = 0.31 👈👈👈 0.31...Lower than the 0.48 he initially roughly calculated and SIGNIFICANTLY lower than the 0.46 that Sotyktu showed WITOUT getting a black box warning DESPITE hitting one of the 4 JAK-family receptors. 0.46 with no black box versus 0.31...what are we to determine from that? To me, that very clearly reads as..."no black box". Biotech is absolutely notorious for DRAMATIC and IRRATIONAL price swings after hours on new data. Anyone in this business can tell you a dozen times something opened WAY up or WAY down and ended up going completely the other direction over the next week. IMO this is going to be one of those cases. I understand the market's knee jerk reaction, as this was a highly watched catalyst with a lot on the line, and any time you hear CANCER RISK you freak out. But the market does not appreciate the nuances of such safety risks right away, and it certainly doesn't make calculations like what I laid out above on a dime. The market freaked out. It saw the "C word" and sold. IMO the market got this totally wrong and cooler heads will prevail tomorrow...the math says so. Will some people stay freaked out despite the objective math above...sure...I mean, a rate of 0.31/year for $ABVX vs 0.46/year for a drug with no black box warning...come on. I can't tell you why people will look at that and still freak out but lets assume they do: How much does that wash out with the fact that ABVX just showed the most unbelievably strong efficacy that has ever been seen with any drug for UC EVER (by a WIDE margin on endoscopic remission - like, it actually even crushed the *JAKs* on that)? Objective MATH says no black box warning. And if that's what the market actually believed, with this efficacy, $ABVX would currently be $200+. Back to $98 AH. The smart money will do the same math I just did above overnight, and in my opinion most will come to the same conclusion. Tomorrow, the "truth" -i.e. the price- will (in my opinion) end up somewhere in between. Would I be shocked to see $ABVX green tomorrow? Far less shocked than I am at the absolutely INSANE efficacy they just showed. It would be neither the first nor last time the market got the initial reaction completely wrong.

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