Antibe Therapeutics Inc(Pre-Merger) ATBPF

RE:RE:RE:RE:RE:RE:RE:RE:RE:RE:RE:RE:Time to Market for H2S Pipeline

[MrMugsy]

Well said Pez.

Fact is ... company has some figuring out to do.
In the meantime ... we're adding acute pain.
We wait for more information.

Some of the boys here are at least chatting it up and having a conversation.
That's what this place was supposed to be.

Stockings ... you're being a downer man.

Inthepez wrote: I see. you need a binary answer for your binary thinking. Best for you to message the company or even health Canada regarding their regulations and report back instead of complaining. 

StockingUp21 wrote:

So they can resume trial. if this is simple they would respond to questions and not be hiding.

 

Inthepez wrote: The infomartion from MB and mstrmnd matches up perfectly with the "adverse events" slide at the of the corporate presentation.

https://antibethera.com/wp-content/uploads/2021/09/Antibe-Corporate-Presentation-September-2021.pdf

Any other FUD you want to spread? 
 

 

StockingUp21 wrote:

you guys now spreading false info. If everything was this easy we should restart AME trial instead of initiate chronic baghold program

 

themagicbox wrote: I agree with Pez. If you're out, then be an adult and leave without spreading false info.

But since a few people have laid eyes on your false claim, I'll quickly debunk it. 

In this publication, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160634/, it demonstrated the hepatotoxicity of drugs in general with a section dedicated to NSAIDs. The hepatoxicity of other NSAIDs are in fact on par if not worse than what we have seen in this AME trial. Yet all of them are on the market.

Non-steroidal Anti-inflammatory Drugs

Due to their extensive use, non-steroidal anti-inflammatory drugs (NSAIDs) are also an important cause of hepatotoxicity.55,56 Diclofenac, the most studied in this class, is glucuronylated and also subjected to cytochrome p450-mediated reactions that result in bioactive products.57,58 Both reactive metabolites and immune mechanisms mediate toxicity. Decreased prostaglandin synthesis due to cyclooxygenase (COX) inhibition may also enhance injury. Chronic diclofenac administration may result in elevated ALT levels in the first four–six months of therapy, but severe toxicity has also been reported.59

Clearly with NSAIDs (NOT H2S), the actual mechanism of clinical benefit (COX inhibition) may contribute to DILI.

Therefore:

1- this is just literally a side effect of how all NSAIDs work to reduce inflammation

2- likely is directly correlated with efficacy, which I think is a good thing in that if the drug really is "too potent" or too long-lived via half life, reduction in dose should still be effective

Keep in mind, you dont draw conclusions from one study, but this has been reproduced time and time again. Naproxen is actually one of the worst NSAIDs in terms of GI safety. H2S solves that problem. There is no evidence to implicate the H2S is responsible for the LTEs and ALTs given the overwhelming information on hepotoxicity we have from this class of drug.

Perfection is the enemy of good, at our current point we are still strategically well placed. We solved the NSAID GI problem, this will always guarantee that the platform is worth owning. Every other issue can be managed, similar to the other drugs currently on the market.

The problem with this company is the management, especially how they execute and how they phrase their NRs. Retail market are always looking for the quick money. Make decisions on foundation not retail market senitment.  
 

 

Layth1990 wrote:

We got withdrawn but the company said it nicely. If we have same lte like other naaids. The AME would be resumed. I got out with 80% loss and wont be a sheep and believe what dan rights