Neeraj

@ipollit77 @RodLambertCPA @seedy19tron I read somewhere 25 mg isn't that effective for induction. What they can do is go for dual-dosing, 50 mg for 8 week induction, followed by 25mg for maintenance.

@RodLambertCPA @seedy19tron That's a good question! I'm no expert, but that sounds to me like a good way to get a clean label

***Free alpha*** $ABVX Part 3 Don't need to wait for mgmt Part 2 (will just confirm the below) but pooled all the relevant data to end the debate once and for all. 4 Snippets: 1. ALL the possible MoA related or drug related proof in one sheet tested against all metrics that Obe cannot and is not causing cancer (remember 2 pathways by which a drug causes cancer in humans) ^keep snippet 1 in mind when going over the below, because then you know the rest of the data is just filtering through statistical noise, but for the purpose of informing everyone completed the below 2. Pooled Malignancy analysis, w/ pt level data 3. LT EAIR. FDA methodology. ALL approved UC drugs except Velsipity and Skyrizi 180 mg have shown malignancy events in their Ph 3 maint trials. None carry malignancy specific boxed warnings outside the JAK class. Obe miR 124 moa is NOT in any kinase family no class to associate with 4. Apple to apple comp with other drugs - NMSC rate (separate clinical category, FDA convention) also note Obe pts had azathioprine/prior NMSC/JAK history. Conclusion NO BB! *Dysplasia is a UC surveillance finding, not cancer. UC patients have ~0.5-2% per year background dysplasia detection on surveillance.

@TonyFauci2 @fmuae11 Opposite! Obefazimod treats UC by suppressing pro-inflammatory TH17 cells, not by promoting them. $ABVX

@fmuae11 Good Question - one of $ABVX 's mechanisms of action is to increase TH17 cells which are anti inflammatory-great for UC but not always great for cancer as TH17's may convert To Tregs which make tumor microenvironment more conducive to growth. 1 possible reason for ⬆️ trial cancer

@medstudentinvst Great post. Prostate cancer (Stage 1) was detected during induction

I am a medical student whose primary areas of interest and research have nothing to do with oncology or dermatology and I would have known what Adam said about NMSC and colonic dysplasia a year into medical school. I am pretty sure Pathoma gives the definition of dysplasia vs cancer somewhere in the first few chapters. All to say, that Adam's statements about NMSC and colonic dysplasia are not niche, and not confined to experts deep in the weeds of a particular disease. Every medical student should know them, and this ubiquity of understanding is at least one explanation for why the company was not as careful in its messaging as it perhaps should have been. I would further add that you’ve got to tell an incredibly biologically implausible story to credit the prostate cancer case to obefazimod. Aside from being the most common cancer in men, prostate cancer is typically a very, very slow growing cancer. It takes millions of prostate cancer cells to detect its existence via a PSA test, imaging, or a prostate exam (biopsy is not being done unless the aforementioned tests give cause for concern). Best estimates would say that for a single cancer cell to yield the number of cancer cells required for detection it takes anywhere from 5 to 15+ years. Let’s say the prostate cancer case occurred at 311 days, which I believe was the latest time point post initiation at which cancer was detected in the trial if I recall the conference call correctly. Don’t know if that included induction so to be safe we could add the induction weeks to the 311 mark. In either scenario, if obefazimod caused the cancer (I’ll define this rather broadly as either caused an oncogenic mutation, created an immune environment that allowed for “breakthrough” of a pre-existing cancer cell, or created a cellular environment that drove an increase in a meaningful but decidedly undetectable burden of cancer cells - let’s say 500,000 cells) that would be an utterly unprecedented rate of growth for prostate cancer. Truly. I spent some time trying to find a case that might fit a profile of such rapid growth and couldn’t find a single one. Additionally, there is ample opportunity for $ABVX to demonstrate it is further implausible that obefazimod is the proximal cause of the prostate cancer, using patient data typically available in a prostate cancer case, at least at a major cancer center in the US. First, prostate cancer cases are rarely considered urgent and treatment is not immediate, especially in the early stages. Even if the patient goes for a prostatectomy or radiotherapy instead of watchful waiting, there’s usually a meaningful period of time that passes where further testing is done. As a consequence, there is typically a time sequence of PSA tests since the initial concerning test that can give a heuristic for the pace of cancer growth. If obefazimod caused or accelerated that prostate cancer case from say 500,000 cells, much less one (!!) cell, to a cancer cell burden that is detectable, that prostate cancer would have to be the Formula 1 of prostate cancers and there should me a concomitant unprecedented rate of growth in the PSA level that reflects such unprecedented cellular growth. If even 30 days passes from first concerning PSA test to a second PSA test, that would be ~10% of the 311 days that have passed and at the required rate of growth for obefazimod to have caused the cancer, that should be more than enough time to see a meaningful and stark jump in PSA. Typically, the repeat test is done anywhere from 4 to 12 weeks as per AUA guidelines. This line of argument would get even more bullet proof if the patient had prior PSA screening tests before a PSA test that was a source of concern, for we would be able to look at the rate of PSA growth before and after obefazimod initiation and see if the first derivative rapidly increases or not. This would particularly go a long way towards rebutting an argument that says something like, well there was already a burden of prostate cancer cells below the threshold of detection, and obefazimod accelerated their growth, tipping the patient passed the threshold for detection. As another important point, biopsy for the purposes of histologically characterizing the cancer is almost always done when the prostate cancer is a source of concern. Incidentally, if the cancer is not a source of concern, then we are right back to the reality that the cancer is too slow growing to have gone from one to tens of millions of cells in somewhere around 311 days, and too slow growing for any supposed obefazimod driven increase in the rate of growth to a baseline burden of a few million cancer cells to be clinically meaningful. A biopsy involves removing multiple samples (or cores, usually 10-12) of the prostate lesion(s), and looking at the cellular characteristics of the cells under the microscope. Based on those cellular characteristics, the cancer is then given a grade, which more or less gives a prediction for the aggressiveness of the cancer. If this patient was given a Gleason Grade 3+4, which would indicate the cancer is very slow growing, that’s histological evidence that is about as strong as it gets in biology against the notion that cancer cells were able to be so unprecedentedly transformed by obefazimod that they grew from one cell (or a few hundred thousand) to tens of millions (minimum) in the span of no more than 311 days, for this would require profound histological changes incompatible with such a score. Conversely, if the biopsy shows a very high Gleason score, that would reflect profound changes in cellular characteristics across multiple domains. Though, even the most rapid growing prostate cancer cell would almost certainly need more than 311 days to be detected if obefazimod was the proximal cause. However, even if such a black swan unprecedented growth event were to happen, the only way it could is if obefazimod engendered massive changes in a cell. This is a dynamic often missed in the lay understanding cancer. Prostate cancer with a high Gleason score requires the existence of a very large number of chances and mutations in a cell, with multiple mechanisms and pathways being effected. It's not going to occur with some kind of surgical snip or perturbation to a confined mechanism or pathway. It's going to reflects widespread destruction and perturbation across pathways. If obefazimod was capable of causing such widespread perturbations in cellular functioning, especially over such a short time frame, you would be highly, highly likely to see some other signal of that in preclinical and clinical data sets. So, the reality is if the prostate cancer patient did have a High Gleason score, this would really just be further evidence that it almost certainly has been growing for a very, very long time, well before obefazimod was initiated. Either way, High Gleason - aggressive - or Low Gleason - slow growing, it's quite implausible to put obefazimod as the proximal cause of the prostate cancer. Taken all together, I would say that $ABVX and any monitoring physicians have ample ability to make a statement that is pretty close to as definitive as it can get in biology that obefazimod did not cause the prostate cancer case. Breast cancer has different characteristics and can be more fast growing than prostate cancer. However, even still, it’s extremely unlikely there’s enough time between obefazimod initation and cancer detection for obefazimod to be causative, and there’s a whole host of staging / biopsy / genetic analysis (e.g. BRCA testing, biopsy for ER / PR / HER2 status, etc) that can be done which can further decrease the probability of obefazimod’s role, similar to what was described above with prostate cancer. It's also worth noting that I saw @seedy19tron say the breast cancer case emerged following the woman’s first mammogram. That cancer could have, and more than likely was given the timeframe of obefazimod initiation and clinical detection, growing for a long time. So to sum up, the most important point is that the “7 cases” are really two cases as Adam said, and we can further rule the prostate cancer out as related to obefazimod pretty definitively using the data we have and what is known about prostate cancer pathophysiology and prostate cancer diagnosis. That just leaves the breast cancer case, and there is likely ample ability to further diminish the possibility that the breast cancer case is related with more patient data around that case. Important context to start to understand why the company, independent monitors, KOLs, etc. feel comfortable saying the cases were not related and why it is probably unwise to think of those statements as based on little more than hope or fluff.

@aggregategains @DueDoctor x.com/Rajinvests/sta…

@DueDoctor Is unemon smoking per usual or is there a second data set for maintenance?

$ABVX $ABBV

@unemon1 @A_May_MD @seedy19tron

@unemon1 @A_May_MD @seedy19tron No I am not. But to dig further about the 1116 patients, I used AI. Here is what I found. Now I what Part 2 you are talking about.

$ABVX .. they have the data! Why waiting A conference in October? releasing clean Part 2 safety data (especially on the ~250 patients on 50 mg) would likely help alleviate market concerns substantially Yet, they are sitting on the data? have we to assume 50mg cancer incidence?

@unemon1 I don't know if such presentations of granular data needs elaborate preparations to ensure accuracy. Maybe it takes time to prepare, else management would have shared IMHO. I am sure Marc would do whatever it takes to stop this bloodbath $ABVX @A_May_MD @seedy19tron

@unemon1 By Part 2 data you mean the granular secondary data—such as deeper tissue biopsy details, histological clearance (HEMI) by patient sub-types, and comprehensive case studies of the malignancy patients which they will present at upcoming medical congress possibly UEG in OCT? $ABVX

@DuarteSatirico @unemon1 @biotech_jack So close to maintenance data release I doubt $ABVX will accept any CVR, has to be a cash deal. Had there been 6 months for the release then maybe acceptable. Only possibility of a CVR is for Crohns, that too at max 10% of the deal price IMHO.

@unemon1 @biotech_jack $ABVX The puzzle is complete. Stellar 96-wk data + May 4 capital raise anchored at ~€95. With the US long weekend here, a Buyout (BO) with a CVR structure by Monday/Tuesday makes perfect sense. 😉😁

$ABVX ... no need to put out those updates in the quarterly! ... Make $ABVX look a bit more de-risked ... ... makes u think if it was so that the Buyer could have a plausible excuse in the eye of its own investors ... for pulling the trigger ahead of real June data!

@seedy19tron Assuming that's (data +BO on Tue) true, why could they not have released the earnings along with data + BO announcement? Is there a regulation which stops them from doing that? $ABVX ER should have been a non-event, they have created needles anxiety by this scheduling 🫣

$abvx moved earnings from Monday to tomorrow.. they’re in quiet period…. I suppose it took them till 1 working day before to realise that Monday is Memorial Day ? Why not Tuesday? I have a feeling we either get data Tuesday or $vrtx x $apln esque buyout + data. BP will probably only want to get out that topline met , data to be presented at medical conference. Pure speculation! Don’t bet on it.

In defense of Indian 🇮🇳 democracy! During Prime Minister Narendra Modi most successful visit to Norway a minor incident happened. A Norwegian journalist demanded that the prime minister starts holding press conferences. She claimed that Indian democracy is in bad shape. May be its time to pause? May be its time to be a bit curious to the world’s largest democracy? Two weeks ago five Indian states and territories held elections. The turn out in the battlefield state of West Bengal was 94%. In the last local election in Norway it was 62%, in many European local elections turn out is below 50%. Can voting in massive numbers be a signal Indians trust their democratic process? In the same election BJP won big in Assam and West Bengal. It lost even bigger in Kerala and Tamil Nadu. Can this diversity be a signal that Indian democracy is reflecting the will of the people? The journalist referred to a democracy ranking putting India at 157 in the world, behind many dictatorships and deeply troubled states. When a ranking is so obviously contrary to common sense, why not ask critical questions to those making the ranking rather than demand that leaders shall comment on nonsense? I recommend Salvatore Babones book “Dharma democracy”. The book debunks convincingly the flawed methodology of these rankings. It was referred to a ranking claiming it’s very dangerous to be a journalist in India. Reality is that it is more dangerous to be journalist in the US and far more dangerous in the vast majority of other nations in the world. Let’s be real. India is not perfect. Of course there are incidents. India has a population the size of North America, South America and Europe combined. But India is much more peaceful than Europe or the Americas. That’s remarkable - given the ethnic, language and religious diversity of India and the many development challenges. Unless we consider democracy a form of government only suited for some very small, peaceful and homogeneous Western European nations, may be we should commend Indian democracy? India is the only major former UK colony which became and has remained a democracy. Its sometimes claimed that the Brits taught India democracy. If that was the case why isn’t Myanmar or Pakistan or the Gulf kingdoms democracies??? Reality is that Indian democracy is both homegrown and extraordinary successful.

@vijaypatil116 @capawanbothra Thanks, didn't know about that feature. Yes, I tried ICICI direct and HDFC Sec before the judgement announcement, both had barred buying. I don't get it why the brokers have to play parents.

@Rajinvests @capawanbothra There is an AI summary of the oral orders in the chat box. A few lines. I copied that to google AI which had the previous context of the phase. Unfortunately a lot of brokers have put a restriction on buying.

Judgment day on Monday, 4th May 2026, EMBDL case listed for judgement as seen in cause list (Serial No 3). Finally Light at the end of the tunnel. Hope for the best #embdl

@vijaypatil116 @capawanbothra How do you get the transcript of the judges oral pronouncement. I had attended the hearing online, the pronouncement was so brief, I could not understand whether the judgement was in favor or against :)

@capawanbothra AI read of the statement from the court today. Agreed with this @capawanbothra

@LnprCapital How is it different from the launch offer?

@RealTradingNick Haha! I know, its wishful thinking.

@Rajinvests It rarely works out like that, but that sounds like a good plan ;)

Hey $NKTR and $ABVX holders, what’s your approximate ratio? Mine is 1:2.2

$grce $xbi how many times can one get Muttoned in this thing? at least $abvx worked

Harsha Bhogle said "I am not excited about the #INDvsPAK match anymore coz it has become a tool for politics. The game is now filled with provocative statements & war like gestures,that's not cricket" Finally someone with a spine has spoken THE GOVT INTERFERENCE HAS RUINED IT