@CloisterRes i mean jury summons doesn’t mean he will be selected to serve on a jury. odds are that even if he’s picked as a potential juror they let him go after knowing he’s ESL. just speaking anecdotally, i’ve had jury duty 3 times and every single time they let ESL speakers go home
something i've been cooking up. built a clinical trial ORR predictor based on pre-clin data. grounded in real data, but works across lines of disease and across molecular targets, with a couple of different modalities and 7 MoAs.
it's a bit better than "gork please tell me if the trial will succeed make no mistakes"
$TENX LEVEL reads out in August. Levosimendan already had a partial success in its phase 2 HELP trial, so I think people's thoughts on LEVEL largely depend on if you thought HELP was just a fluke. Here I'll compile some of my thoughts on common HELP critiques and levo in general.
The image below is presented as evidence IL17F inhibition is a theoretically superior strategy to IL17A inhibition. This matters because $ZURA ‘s tibulizumab targets IL17A, not F. So if this is true, it does not spell well for $ZURA . However, I believe this case for IL17A superiority is much stronger (thread)
New biotech blog by a Northwestern medicinal chemist -- debut post is a well-written, science-focused take on $CCCC. Check it out: https://t.co/4Pc5wUUKlO
long🧵on $SABS. full report on substack. this is a full-on bullish report. can you believe it? I've been long since $2 and $20m mc. now sitting at $4.50 and $200m mc I'm still very bullish, but it's a very high risk biotech (as they all are)
$TECX
If relaxin mimetic (TX45) decrease PVR by ↓PAP and ↓PAWP, TX45 is truly disease modifying (Pulmonary Artery Remodeling).
Instead, PVR declines by ↑CO (relaxin=↑stroke volume, PAP and PAWP declines via Frank-Starling Law - *NOT* from TX45 remodeling. Small PCWP△ indicates ↑CO drives ↓PVR. This is bad because:
Long term ↑CO exhausts the heart (akin to anabolic steroids, sympathetic stimulation). Hence, no efficacy in AZD3427, volenrexin, serelaxin. Yes, there's PK differences --> RASS compensation, but fundamental pathophysiology still drives lack of efficacy.
Short-term ↑CO is beneficial for HF. Hence, AZD5462 (oral relaxin) is progressing in heart-failure, while AZD3427 (FC-fusion similar to $TECX) is discontinued in PAH. TECX lower PK thesis likely fails (6mo+) from exhaustion.
Also, Relaxin stimulates Rennin increase (from kidney) independent of RASS activation/vasodilatation. Hence, background tx (ACE, ARNI, BB) will not prevent (see volenrexin, AZD3427). $TECX's lower PK = lower vasodilatation = lower Rennin thesis falls apart.
Re: anti-fibrotic, where's data showing relaxin receptors in pulmonary artery? There isn't.
Receptor's in the heart (↑CO).