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Antibe Therapeutics Inc(Pre-Merger) ATBPF

Antibe Therapeutics Inc. is a clinical-stage biotechnology company. The Company is leveraging its hydrogen sulfide (H2S) platform to develop therapies to target inflammation arising from a range of medical conditions. The Company’s pipeline includes assets that seek to overcome the gastrointestinal ulcers and bleeding associated with nonsteroidal anti-inflammatory drugs (NSAIDs). Its lead drug, otenaproxesul, is in clinical development as an alternative to opioids and NSAIDs for acute pain. Its second pipeline drug, ATB-352, is being developed for a specialized pain indication. The Company also focuses on inflammatory bowel disease (IBD). Otenaproxesul combines a moiety that releases hydrogen sulfide with naproxen, a non-steroidal, anti-inflammatory drug. ATB-352 is an H2S-releasing derivative of ketoprofen, a potent NSAID commonly prescribed for acute pain. Its IBD candidates are being designed to maintain the efficacy, safety, and pharmacokinetic properties of ATB-429.


GREY:ATBPF - Post by User

Comment by MrMugsyon Aug 22, 2021 5:16pm
313 Views
Post# 33746549

RE:Can someone enlight me with transaminase mistery...

RE:Can someone enlight me with transaminase mistery...
Edou111 wrote:
I would like you enlight me with this please. During PH2 adjudication yields transaminase rates lower at an acceptable level.  Knowing that PH2 doses were higher than the AME trials, how could we logically explain such a failure at lower doses ?   And remember that transaminase thing is what made the stock retreat after PH2 results even after adjudication.   I am a bit confused to say the least...


I'm likely speaking out of my tush right now but ... 

Using Dan's analogy of the liver marinating in Naproxen ... this may be beyond the normal effect as seen by Naproxen alone and more attributable to the Naproxen/H2S combo over longer periods of time.

For all we know, this marinating effect (accompanied by a possible protective effect from H2S) may affect people in very different ways. 

As we age, we know the cell-to-cell H2S communications within the body usually become less efficient.  What happens if your H2S cell-to-cell communication is still pretty healthy and we further drive excess H2S at you?  Maybe something like that isn't easily measured by complicates what we see.

Who knows.

All I'm really saying is, there's likely a lot happening at the cell level that we can't explain effectively right now ... but ... maybe we'll get there.
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