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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 TriumphSpitSixon Oct 14, 2021 6:03pm
340 Views
Post# 34007144

RE:RE:RE:Otenaproxesul pulled as Arthritis drug.

RE:RE:RE:Otenaproxesul pulled as Arthritis drug. ATB-346 has been given to at least 700 people since 2014, the vast majority of whom did not experience elevated LTEs. Who is the "subset" with hypersensitive livers that ruined this trial?

Why didn't this issue arise when we were dosing 250mg? If it's "dose dependent" we should have seen crazy LTEs at 250mg when it happened in people at 100mg and even one in the 75mg cohort. It still doesn't make sense.

How can there be LTEs "exceeding five times the upper limit of normal" in the 100mg and 75mg groups but not a single one in over 600 patients in the 200mg and 250mg groups from Ph2? Shouldn't there have been 2x more LTEs at minimum, assuming a representative patient sample similar to those in the AME study?

Why now and not then?

Why at these very low doses but not higher?

One could reasonably have expected Ph1 trial participants' livers to just explode when they were dosed at 750mg and 1500mg knowing what we allegedly know now! Yes, we know these doses were way too much, hence the Ph1 halt, but in their follow-up did they find LTEs exceeding seventy-five times the upper limit of normal, given the 15X higher dose?

(15 x "5 times the upper limit" = 75X the upper limit)

I cannot believe they didn't see these same kinds of results in the previous trials at doses 2x to 3X higher than the AME doses if the issue is "dose dependent."
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