$TGTX one of the laggard of 2025, starting 2026 red. Briumvi sales growing with 84% YOY. Subcutaneous Briumvi trial enrolling. Topline data late 26/early 27. Recent 100M share buyback. Tailwind due to recent safety issue with competitor's BTK inhibitor oral pill.
Many are asking why is SpaceX, $SPCX, NOT trading yet?
Here's exactly how the IPO process works and when the shares will be available to trade (Bookmark this):
The IPO was quoted at 9:50 AM ET and was expected to begin trading at 10:00 AM ET, but that does NOT guarantee shares will trade at that time.
Before trading begins, Nasdaq must complete a price-discovery auction where buy and sell orders are collected and matched.
At around 9:50 AM ET, "first indications" came out which are essentially a "gauge" of where the stock will open.
The first indications on $SPCX came in at $175/share, or a ~30% premium to the $135/share IPO price.
During this process:
1. Orders are entered, but no trades occur yet
2. Nasdaq continuously updates the indicative opening price
3. The opening price is adjusted until supply and demand are balanced
4. Only then does the opening auction occur and the first trade print
For major IPOs, delays are common such as Google in 2004 and Meta in 2012 which saw their first trades over 2 hours after the US market opened.
We expect the SpaceX IPO to open for trading within the next 60 minutes.
Buckle up for a historic day.
$TGTX TG Therapeutics Announces Positive Topline Phase 1 Data for Subcutaneous BRIUMVI in Patients with Myasthenia Gravis and Initiation of Potential Registration Directed Randomized Phase 2 Trial | TG Therapeutics, Inc. https://t.co/QaoMN3F2kp
1/ Underappreciated $ABVX ABTECT maintenance data slide. Placebo 44-week completion was just 34.3% vs 78.8% (25mg) and 82.1% (50mg). Placebo fewer patient years = less surveillance = fewer chances to detect malignancy.
$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).
What an opportunity $ABVX was and still is IMO. I was able to increase my position by ~30% which already was a heavy position. I will start trimming some as it starts to move up but will hold onto the core position.
$TGTX So looks very likely indeed that every 3 month self-administered Briumvi via an autoinjector is going to work. They managed to get a high concentration of drug in a small volume (2ml) without it getting too viscous for an autoinjector - Ocrevus needed more than 10x that volume for their subq, which is why they required a pump.
So from a market perspective, they will have both an IV and subq where the patient can freely switch, and they will have only 4 injections per year instead of the Kesimpta 12 injections. Their IV with new dosing schedule will be way easier than Ocrevus for new patients. Their efficacy is likely a little better than both competitors.