Antibe Therapeutics Inc(Pre-Merger) ATBPF

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

[mstrmnd]

My take is it's on par with other NSAIDS.  In fact from an API perspective, it's less NSAID being ingested.

Why are LTE's occurring then?  H2S may be inhibiting cytochrome p450 enzymes responsible for NSAID metabolism therefore reduced clearance of metabolites through kidneys in long-term use.  

Since dose-dependence has been confirmed, the dose needs to be reduced to account for this reduced clearance for long-term use.  Otherwise circulating NSAID concentrations may be higher than traditional NSAIDS except without the GI risk but same LTE risk.  That's why in Phase 2a and 2b 150 mg daily x 14 days, LTE in keeping with NSAID rate is seen.  Don't forget, parent molecule is an NSAID (Naproxen) for Otenaproxesul, so LTE rate of about 5% is always expected.  The kicker is there's no GI bleeding and since this is a well-known potentially fatal outcome, even a slightly higher LTE rate may be tolerated in slow-metabolizers because of the mucosal healing + anti-inflammatory properties.

Hope that helps.

GLTA

Layth1990 wrote: Protect and yet we got thrown out of AME for having high LTE. The rate is higher than regular nsaids. If it is protective as what you are claiming we would have lower LTEs than other nsaids. Don'y give false hope to people