Important readout for $PMN too

$ZURA Summary against IL17F doesnt matter thesis: (1) Even though much less potent than IL17A (IL17AA>IL1717AF>IL17FF) Il17F is much more abundant in HS (and higher than in psoriasis) (2) Synergy between IL17FF and TNF/IL1b (both evidently important in HS and present in HS lesions) seems to bridge the gap in downstream potency vs IL17A (3) Part of the thesis is that Taltz was underdosed in psoriasis trials and at higher exposure regimen matched bime in psoriasis. BUT biology of psoriasis is very different (IL17F less important in psoriasis). + Anti-IL17A alone breaks a vicious cycle in psoriasis. So while it seems safe to assume Il17F has no/little additive benefit in psoriasis it is not safe to assume the same in HS. Nevertheless: (1) Even if Il17FF matters, clinical data suggest it doesn't add too much incremental benefit vs IL17AA/AF. (2) Seems safe to assume tibu will beat Concentyx (weaker AA and much weaker AF) based on just IL17 activity. And I believe tibu should come pretty close to bime based on just IL17A activity. (3) Market seems to ignore BAFF mechanism!! Pretty convincing evidence that targeting B cells works. Pathophysiology also suggests targeting BAFF should have additive benefit to targeting IL17A. So decent probability tibu matches (even beats?) bime (4) Even though 16w may be too short to capture the whole magnitude of benefit, prior anti-B cell studies suggest evident benefit within 16w The potency/size issues pointed by others seem minor to me based on pk/pd. Based on higher dose (accounting for higher size and accounting for BAFF sink) and half life tibu, should be able to a saturate IL17AA/IL17AF, at least at the 300mg dose Btw what is the bear thesis against SS with readout coming in 1H 2027? SSc indication alone should drive meamingful upside from here. So playing the HS binary seems like a free option (assuming SSc works) (I get why buying after HS readout makes sense if you believe it will fail though)? @A_May_MD @ElMonoGran42994 @Archimedes20311 @Andre_AGTC

$ZURA a paper against the IL17-FF doesnt matter thesis (although I believe BAFF mechanism will come to the rescue) @A_May_MD academic.oup.com/bjd/article…

$ZURA link to Cantor fireside chat for anyone interested cantor.zoom.us/rec/play/8Ukx…

$ZURA I finally read this pitch. Excellent read. Learnt a lot. I have a small position for the binary. What I particularly like about this pitch is that SS readout coming soon next. So even if HS readout dissapoints, price may recover eventually. PMR trial will be positive but seems like a long term bet. Main risk to the thesis is IL17FF (lots of it in HS lesions) actually mattering. Clinical data so far suggest otherwise but remains to be proven. Also remains to be seen if BAFF will have any additional benefit as add-on to anti-IL17A. Targeting B cells clearly works based on other trials in HS. But can never be sure whether this will add to anti-IL17A. I definitely recommend reading the pitch. Threads and post's like @A_May_MD 's is what I like about BioX

$GUTS restructuring gets them to Q1 12m topline + maybe eventuallt some non-dilutive cash for Rejuva (seems like a decent asset, albeit with no human data)

$EVAX good platform and melanoma data But who is going to fund a large, costly and risky melanoma ph3 trial given competition. Melanoma eas an easy indication to target but hard to partner.

$EYPT btw was the market expecting a succesful 2nd ph3 after the 1st (identical design) ph3 failed?? The difference in EYPT valuation yesterday vs today is crazy (yesterday overpriced, today oversold).

$EYPT Here is what went wrong in wAMD—and why DME is a different ballgame: ​(1) Vorolanib is a much weaker pure anti-VEGF than aflibercept. In wAMD, vorolanib kept 52–54% of eyes supplement-free, but couldn't stop breakthrough leakage in the more aggressive ~47% (who had to lose >5 letters + 75μm fluid before getting rescued). ​(2) wAMD pathology sits deep beneath the RPE in the choroid, behind the outer blood-retinal barrier. Aflibercept’s massive 2 mg bolus creates a steep concentration gradient to reach the sub-RPE space, and its large molecular size (115 kDa) slows clearance. Duravyu’s slow release creates a much smaller diffusion gradient across the retina/RPE, and once a small molecule reaches the high-flow choriocapillaris, it suffers rapid choroidal blood washout. ​Why DME (COMO/CAPRI) is different: • No RPE barrier or choroidal sink: DME leakage is in the inner retinal capillaries right next to the vitreous insert. • Multi-MOA actually matters in DME: DME is heavily driven by IL-6 inflammation. Vorolanib’s intracellular JAK1 (IL-6) inhibition provide incremental benefit—already proven in Phase 2 VERONA, where Duravyu + aflibercept beat aflibercept alone at Week 4 even when extracellular VEGF was 100% saturated in both arms. What am I missing?

$EYPT Not sure where the bottom is but seems silly cheap here. Cash per share >1$. May need to raise though to get to Q4 readout. Mechanism makes more sense in DME. ph3 DME program will be positive. Lots of competition but capturing just 5-10% of market should justify much upside from here

$EYPT Duravyu makes much more semse for DME than it did for AMD

$EYPT Overreaction?

$GUTS I think market overreacring. Shan overperformed because many restarted GLP1. Those are excluded. Those doing relatively well remained.

Dont know the field well but excelent analysis. Thanks for sharing. $ZURA

$CRBU I havent verified the numbers but current price seems to be at around the floor of a reverse merger scenario (zero value for assets and assuming assuming $13M lease termination). Doesnt mean it wont get cheaper though...

What if the answer is a resounding NO? Not good...

$CVKD pipeline has to be worth more than the current marker cap (which is $3.5M)... >$3B TAM. What are the chances this won't get pumped after announcing "strong" partnership interest and steatrgic alternatives