Top Tweets for #InflarX
This is by far the most important part of your series. Must read.
$IFRX
Let's get the bridge study rolling.
#EverestMedicines $1952:HK shareholders, take note 😉, this is a match made in heaven. #InflaRx shareholders have a look too.
direct link to deck
https://t.co/8egA4awdhj
#InflaRx $IFRX 1 million irreplaceable filters per kidney. Many diseases. One convergence point. A $10 billion opportunity. https://t.co/HE9LzEXl07
#InflaRx $IFRX 1 million irreplaceable filters per kidney. Many diseases. One convergence point. A $10 billion opportunity. https://t.co/HE9LzEXl07
Biotech Surges as Big Money Backs High-Stakes Kidney Disease Push $IFRX #InflaRx #biotechstocks #microcaps #daytrading #investing #hotstocks https://t.co/q4dqrblAF9
#InflaRx $IFRX – A personal, well-researched, speculative look into the potential of C5a-C5aR1 signaling control biotech.
AAV, aHUS, FSGS, IgAN, LN, GN, CG, GS, RA, SLE, RF, TR, CIDP, CIPN, DM, BP, PASH, PAPASH, and CSU.
All claimed indications listed in a recent InflaRx patent, https://t.co/sQY6HrOhKX.
This subset makes the pipeline shortlist in my view: AAV, IgAN, LN, BP, and CSU (the first 4 covered in the no-brainer series). https://t.co/IK3WnrtrY7
RA (rheumatoid arthritis) is a contender: affects 18m people worldwide, is a $30b market shared by a dozen approved biologics and oral therapies, yet would present some study and market challenges.
This leads to a related, underserved, multibillion-dollar arthritic indication.
PsA (psoriatic arthritis): perfectly suited for study using the best-in-class oral C5aR1 inhibitor, izicopan. https://t.co/IxVxvxcTex
#InflaRx $IFRX #Alzheimers ➡️ Six patents. Two families. One signal the market hasn't read.
Full analysis: https://t.co/18PrK37DdZ
The market is pricing all of it – the platform, the pipeline, the patents, the race – at ~$65M.
The new filings reveal preclinical data in gout and kidney disease, IP claims across a dozen indications, and a systematic global IP build that goes far beyond what InflaRx discusses publicly.
But buried in the original patent family – preserved deliberately through every filing since 2019 – is a classification that points toward something bigger. A next-generation molecule designed to reach the brain, where Alzheimer's begins and where the existing drug cannot go.
Vanqua Bio – a company that knows this space intimately – just sold their peripheral program to Biogen for $70M upfront and up to $1.06 billion in milestones, and kept their brain-penetrant program for themselves, explicitly targeting Alzheimer's. You keep what you think is worth more.
The race to be first to market has started – Vanqua Bio is already running it, explicitly targeting Alzheimer's. And someone at InflaRx has been quietly keeping the option to join that race open since 2019 – for a disease affecting over 55 million people worldwide, projected to triple by 2050, costing the US alone an estimated $340 billion annually, and for which the best available drugs slow progression by roughly a third while leaving the neuroinflammatory engine that drives the remaining two-thirds completely unaddressed.
#InflaRx $IFRX Three misclassified patients may have killed a drug that works. The data on vilobelimab in pyoderma gangrenosum gets presented Saturday at AAD. Here's what to watch for. https://t.co/t97E5LN3QV
$IFRX #InflaRx #HS #PG #AAV
🔷Hidradenitis suppurativa🔷Pyoderma gangrenosum🔷ANCA vasculitis
We wrote the series. Links below. 👇
Three diseases most doctors can't spell.
Millions of patients. Years to diagnosis. Treatments that half-work at best.
Same broken biology underneath all three.
Same upstream fix that medicine keeps looking past.
If you know someone living with any of these, share this with them.
HS: https://t.co/rEEkGydY8w
PG: https://t.co/fWBEkqGthn
AAV: https://t.co/JItcc4ZD9L
$IFRX #InflaRx #izicopan
The Disease That Hides in Plain Sight - Hidradenitis suppurativa has been in the medical literature since 1854. In 2026, the average patient still waits seven years for a correct diagnosis — and the approved treatments don’t address its most destructive feature.
https://t.co/ZJliCudL6B
Fix the Tap, Don’t Mop the Flood
$IFRX The case for #InflaRx — and why one forgotten molecule could be the most important anti-inflammatory asset in biotech
https://t.co/PrZT0OU4OL
At the time of approval, avacopan-AAV peak sales in the US were estimated at around $2 billion. That’s worth #InflaRx $IFRX attention in this indication!
AAV is still a disease of hyperactive neutrophils, caused by a couple of abnormal surface presenting enzymes (PR3 and MPO) that invite autoreactive B cells to the party that in turn pump out a bunch of antibodies (ANCAs), activating neutrophils that go on to cause tissue damage (via ROS and NETs), priming C5a-C5aR1 signaling to really ramp up the tissue damaging feedback loop. Reducing that signaling is why avacopan shows efficacy in AAV; therefore best-in-class izicopan, already proven to reduce C5a/R signaling much faster and over a much longer efficacy window – and with a much better safety profile (no detected liver toxicity issues for example) – a great candidate in this indication.
The biology is not the problem. The study design of avacopan-AAV was and still is the problem, steroid rescue clouding drug efficacy. FDA raised study design concerns numerous times which ChemoCentryx ignored, all the details captured in this document, https://t.co/WHGKC80GG7, released just prior to the Adcom which ended in a 50/50 vote on approval. As I see it, FDA second guessing approval now because of ongoing legal battles. https://t.co/6Y03P6awNu and https://t.co/zlVXuJ4YxU
Makes that ongoing BDB1 (vilo) AAV p3 study, using a steroid placebo, all the more interesting. https://t.co/5sgM6nw6KQ
$IFRX #Inflarx Niels If research results cannot be brought to the market, then what's the use of blind confidence?
$IFRX #InflaRx #vilobelimab New paper out, coauthored by Dr. Ortega who has been (was?) treating the worst PG case ever identified, of a patient who hopes that $22k per month in donations will sustain his supply of anti-IL23 Tremfya, assumed to be that which is keeping him alive even though early p2 study of this drug in PG has stopped, presumably due to lack of efficacy, and no surprise there when considering the millions of years of established biological mammalian immune function. https://t.co/qnFZMnXjyc
The conclusion from the following fact-engine discussion: “PG is a C5a–C5aR1-driven neutrophilic dermatosis, secondarily amplified by Th17/Th1 cytokine networks.”
Let’s see that PG p3 topline. Let’s get on with it. Vilo please!
I write this with considerable frustration. Here’s why.
P1: I've heard ~100 billion neutrophils are released into the bloodstream every day and that each of these neutrophils has ~200 thousand C5aR1 receptors. Is that true?
“~100 billion neutrophils are indeed released daily. Each has roughly 200,000 C5aR1 receptors when resting. These receptors are dynamically regulated and can internalize within minutes after exposure to C5a. That turnover equates to an enormous receptor and signaling flux, explaining why C5a–C5aR1 blockade (e.g., vilobelimab, INF904) can profoundly dampen neutrophil-driven inflammation.”
P2: So we're talking 20 quadrillion C5aR1 receptors on these neutrophils per day. Sounds like a lot of zeros! How many?
“16 zeros. 20,000,000,000,000,000 C5aR1 receptors per day per person.”
P3: Wow. Isn't that around the same number of ants on this planet? How many ants we talking per person?
“Yes, it’s the same ballpark. ~2.4 million ants per person.”
P4: How about this for a big number: if 20 quadrillion C5aR1 per person per day, how many C5aR1 across the human population per day?
“~160 septillion receptors daily worldwide. 164,000,000,000,000,000,000,000,000”
P5: How many Milky Way galaxies are we talking about in terms of stars?
“About 1,640,000,000,000,000 Milky-Way-sized galaxies.”
P6: Ok, let's get serious. This noted paper acknowledges that PG is the result of neutrophil dysfunction, going on to claim that "PG is a Th17/Th1-driven neutrophilic dermatosis." 100 billion neutrophils per day start out in the bloodstream. So how do they end up in PG ulcers? I highly doubt it is because of Th17/Th1 involvement.
“In short: Th17/Th1 signals are real contributors, but most mechanistic and genetic evidence points to innate neutrophil priming/dysregulation and local triggers as the core of PG pathogenesis. The adaptive cytokines frequently amplify and sustain the neutrophil damage rather than being the single initiating cause in most patients.”
P7: You didn't answer the question as to how neutrophils primarily leave the bloodstream and get into PG ulcers to effect damage. Here are some hints for you: calcium, CD11b, and yeah, all the other stuff we were just talking about.
“Neutrophils exit the bloodstream at PG sites by a classic cascade: endothelial activation → selectin-mediated rolling → chemokine/C5a-triggered Ca²⁺ signaling → rapid CD11b mobilization and integrin activation → firm adhesion → PECAM/CD99-mediated transmigration → matrix degradation and tissue invasion — and because neutrophils in PG are often systemically primed, this cascade runs turbocharged and self-amplifying.”
P8: What is the primary trigger of CD11b surface expression on neutrophils?
“The primary trigger of neutrophil CD11b surface expression is a Ca²⁺ surge downstream of GPCR activation by C5a.
C5a → C5aR1 → Ca²⁺ influx → CD11b upregulation → adhesion & migration → PG ulcer formation”
P9: So considering how many C5aR1 receptors as previously discussed for C5a to bind to on neutrophils, primarily enabling these cells to leave the bloodstream, within the context of PG as a neutrophilic dermatosis, the statement in the noted paper, "PG is a Th17/Th1-driven neutrophilic dermatosis" is factually incorrect, absurdly so in fact considering its academic origins. Correctly stated: PG is a C5a-C5aR1-driven neutrophilic dermatosis. Yes?
$IFRX #InflaRx “expects to host a webcast/conference call accompanied by a slide presentation on Monday, November 10, 2025, at 8:00 AM EST / 2:00 PM CET to discuss the [HS and CSU] topline clinical data, and to also feature key opinion leader insight.” https://t.co/pVylN6GSpl
An opportunity now to review the fundamentals, stay ahead of the curve. All the best!
Updated link: https://t.co/smufhnbupZ
PDF link: https://t.co/MMneTXbk7t
Thank you #InflaRx $IFRX for organizing the recent R&D Event which detailed the exciting promise of oral C5aR inhibitor, #INF904. Both the presentation and a recording of the webcast are now available at https://t.co/Kl7YfrgMdh.
Some Highlights
▶️page 16: the C5a-C5aR signaling axis plays a significant role in many disease areas including cardiovascular, neurodegenerative, and autoimmune diseases.
▶️page 42: in Chronic Spontaneous Urticaria (CSU), higher histamine levels lead to more itchy hives; INF904 effectively blocks histamine release.
▶️page 65: in Hidradenitis Suppurativa (HS), draining tunnels have the highest negative impact on quality of life; C5a-C5aR signaling control shows significant reduction in these lesions.
▶️page 81: CSU and HS patients are currently underserved by available treatment options, resulting in significant market opportunities for INF904 sales: CSU exceeding $1B/yr; HS exceeding $1.5B/yr
#InflaRx $IFRX NETs were identified in 2004. Here’s the landmark paper: https://t.co/XOahPACrk1
No excessive neutrophil activation, no excessive NET formation, no NETosis.
C5a-C5aR1 signaling is primary to neutrophil activation. The implications in being able to safely and significantly control this signaling are profound. Game-changing biotech, fixing what’s broken.
Common sense healthcare.
NETs in ARDS: https://t.co/aXWxeLFvu1
NETs in PG: https://t.co/hgXlerxiA0
NETs in arterial thrombosis: https://t.co/PG9ZFnuot5
NETs in cancer: https://t.co/Q8l2J03qeM
100 billion neutrophils are released into the bloodstream every day. Where they go from there and how they get to a destination is key to understanding both the systemic dangers and key role of C5a-C5aR1 signaling.
This slide compares placebo response across some studies. It’s from an R&D event that #InflaRx organized back in the summer of 2024, https://t.co/smufhnbupZ (page 60).
A good presentation, plenty of technicals about INF904 in HS and CSU studies.
Vilo 800mg/wk had HiSCR at 50% by day 29 and hit 75% by day 50. I think even the lowest dose cohort, 60mg INF904, can hit those numbers, at least the same C5a/R signal stopping power as 800mg Vilo. Therefore the levels up, 90 and 120mg should be at least as good, though if already blocking >90% at the low dose during 4 week active dosing, not much more to be done even at higher dosing. However higher dosing should shine during 4 week observations, drug still active due to higher concentration levels). I see possibility of hitting > 80% HiSCR by day 50 in the higher dosed arms.
Then there are other measures such as IHS-4, avacopan hitting -26.7% change from baseline by week 4. That’ll be a comparative measure to INF904, and based on the same reasoning above, we should see at least double those measures with 904.
Most importantly is m-HiSCR, taking problematic HiSCR to the next level by actually expecting draining tunnel reduction, of the lesion that impacts QoL of HS patients the most. It took InflaRx months to finally get FDA approval to use this common-sense endpoint as primary. Only C5a/R signaling control biotech (Vilo, INF904) can put draining tunnel reduction as primary, after say 16 weeks of treatment, because only this biotech acts on the primary signaling that activates the effector cell that causes tissue damage, neutrophils. https://t.co/2fy60BeDS9
But tunnels take time to heal, so the question is if 4 weeks treatment is enough to get a signal. I think so, especially in high dose whereby therapeutic effect only takes a day; add to that the 4 week observation period following treatment, whereby drug concentrations have built up and therefore drug effect is still in play – so potentially 8 weeks of healing – a decent amount of tunnel reduction can take place, enough to get a healing signal at least.
@StreetCred2017 @3in5saved @medstudentinvst Highly recommend reading that post, and also the subsequent exchange between @3in5saved and you. $IFRX #InflaRx
@hannibalspeaks #InflaRx $IFRX Look mom, judgement without basis.
https://t.co/wleCXqIILe
https://t.co/BFGP21Ehrj
Endpoints on the INF904 HS/CSU p2a study are important to note.
Primary: Frequency, severity, and relatedness of treatment-emergent adverse events (TEAEs) and serious adverse events (SAEs) using MedDRA classification.
Secondary: <various INF904 plasma concentrations>
As to safety, here’s an InflaRx quote from a recent event: “We have 9 months tox study including in nonhuman primates…We have not seen a safety signal of concern. Small molecules like chemical inhibitors can sometimes inhibit certain enzymes in the liver. One that’s very much known is called CYP3A4/5, that’s an apparatus that’s detoxifying a lot of molecules including building down corticosteroids. That is a mechanism that is quite inhibited by the comparator [avacopan] in the market. We have shown in preclinical studies that we have a 36 fold lower engagement with that molecule. That’s important because liver tox is something you always worry about if binding strongly to that mechanism, and there have been signals of liver toxicity with [avacopan].”
Shouldn’t be any surprises as to the study missing those endpoints, free then to explore efficacy measures, of which there are many to consider.
I’m expecting there to be enough efficacy to continue study, especially HS, but also in that CSU high dose anti-IgE non-responders arm at least, noting that “despite availability of current treatment options such as anti-histamines and anti-IgE therapy, approximately 30-60% these patients are estimated to remain non-responsive or symptomatic.”
https://t.co/eqg6i3iDG0
![3in5saved's tweet photo. Endpoints on the INF904 HS/CSU p2a study are important to note.
Primary: Frequency, severity, and relatedness of treatment-emergent adverse events (TEAEs) and serious adverse events (SAEs) using MedDRA classification.
Secondary: <various INF904 plasma concentrations>
As to safety, here’s an InflaRx quote from a recent event: “We have 9 months tox study including in nonhuman primates…We have not seen a safety signal of concern. Small molecules like chemical inhibitors can sometimes inhibit certain enzymes in the liver. One that’s very much known is called CYP3A4/5, that’s an apparatus that’s detoxifying a lot of molecules including building down corticosteroids. That is a mechanism that is quite inhibited by the comparator [avacopan] in the market. We have shown in preclinical studies that we have a 36 fold lower engagement with that molecule. That’s important because liver tox is something you always worry about if binding strongly to that mechanism, and there have been signals of liver toxicity with [avacopan].”
Shouldn’t be any surprises as to the study missing those endpoints, free then to explore efficacy measures, of which there are many to consider.
I’m expecting there to be enough efficacy to continue study, especially HS, but also in that CSU high dose anti-IgE non-responders arm at least, noting that “despite availability of current treatment options such as anti-histamines and anti-IgE therapy, approximately 30-60% these patients are estimated to remain non-responsive or symptomatic.”
https://t.co/eqg6i3iDG0](https://pbs.twimg.com/media/G3zy9_BWQAAa5Av.jpg)
#InflaRx #HS #INF904 Now there’s a trigger, like a bunch of CD11b integrins called to action ;)
We don’t need AI to put this puzzle together.
Vilo-HS p2a dosing was 800mg/wk. Topline: “In the study, all twelve patients were categorized as Hurley Stage III and therefore most progressed diseased patients, demonstrating a mean duration of HS of 19.9 years. Nine out of the twelve patients had previously failed to respond to an anti-TNF-alpha antibody, the only approved biological treatment in this indication. The mean combined number of lesions (abscesses and inflammatory nodules) and draining tunnels at baseline was 6.4. and 11.2, respectively. Assessment of the HiSCR score demonstrated a response rate of 75% (nine out of twelve patients) at the end of the treatment period and 83% (ten out of twelve) at the end of the twelve week follow up period.”
Very promising results leading to high expectations in a larger Vilo-HS p2b study, though now looking at four dosing cohorts, high dose being 1200mg every two weeks (less than in p2a). Topline was mixed, the details noted in the referenced pub.
However, draining tunnel improvement stood out (even if arguably 1600mg dosing should have been used): 3 times the complete closure of these highest-QoL impacting lesions vs placebo. Whereas nodules and abscesses can spontaneously heal during a 16 week study (therefore HiSCR sensitive), tunnels do not: if significant reduction, it is because of the active drug. Fact.
So existing data testing C5a-C5aR1 signaling control – even in underdosed conditions – proves to statistical significance that what bothers HS patients the most, draining tunnels, can be effectively treated.
Why? Because the cells causing all this substantial tissue damage are neutrophils, originating from the bloodstream at the rate of 100 billion cells per day. So what, one might ask, draining tunnels are in tissue so what does that have to do with blood vessels? What a great question. Neutrophils go from fast flowing sentinels to vessel wall sticking attackers by the call to action primarily from C5a-C5aR1 signaling which activates “sticky” CD11b integrins that cause vessel wall adhesion and then guide these cells to the site of draining tunnels where further C5a signaling activates these cells even more leading to tissue damage.
Starts in the bloodstream, starts with C5a-C5aR1 signaling, starts with activation of those sticky CD11b integrins.
To that, INF904 30mg pills twice daily have shown the ability to significantly limit CD11b expression on neutrophils even under very high C5a loads of nearly 13nM, more than enough stopping power to address HS lesion severity. And just to homerun the INF904-HS study, InflaRx is dosing 60mg, 90mg, and 120mg BID.
Bye-bye draining tunnels, hello happy HS patients.
@BioValues It would be interesting if someone would put this exact study in ai and find out how INF904 would do instead of vilobelimab. Also pill vs not.
The timing of this 3 days ago likely not coincidence for Inflarx $IFRX
@3in5saved
https://t.co/M84Y2jU3K5
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