Replies to post #8007 on Algernon Pharmaceuticals Inc (AGNPF)

[lk52q]

As an investor my focus here Algernon has mega potential to be a runner since they has filed new intellectual property rights globally for Ifenprodil for the treatment of respiratory diseases. $AGNPF

[Flyerpf64]

Medchem, what are your thoughts on timeline? As in, when could this drug be manufactured in quantity to support positive results from the expected clinical trials.

[FatCatz]

Thanks for the informative reply medchem. You're right, the biopub videos are very good.

I read the Chinese H5N1 study and it appears that Ifenprodil may have reduced levels of several different cytokines, including some of the pro-inflammatory cytokines that are thought to be responsible for the covid19 cytokine storm!

Does anyone know of the status of the Oak Ridge Supercomputer's second analysis of the drugs with the new virus model?

[tcm55]

I am posting some research you made and this quote which implies that Ifeprodil affects the inflammation issues, described in the recent article I posted from the Lancet, that current IPF drugs do not address.
Your respected opinions would help refine this...

""And like I said before, HERE IS HOW OUR DRUG WORKS

Coronavirus infection induces increased production of proinflammatory cytokines and neuronal degeneration as a consequence of glutamate excitotoxicity. In physiological conditions, glutamate is mainly synthesized by neurons and released in the synaptic cleft as the primary excitatory neurotransmitter of the CNS that activates the ligand-dependant receptor AMPAr, which allows the entry of sodium ions and the passage of the nerve impulse in the post-synaptic neuron, leading to activation of the NMDA receptor (N-methyl-D-aspartate receptor) that allows the entry of calcium ions. During infection of neurons by coronavirus, cells detect the presence of virus and produce pro-inflammatory cytokines (TNF-alpha, IL-1 beta and IL-6) that down-regulate the astrocytic receptor GLT-1 (glutamate transporter 1) and prevent the efficient recapture of glutamate. This situation disturbs the regulation of glutamate homeostasis and theexcess of this neurotransmitter in the synaptic cleft leads to excitotoxicity associated with a massive entry of calcium which eventually leads to degeneration of and death of neuronal cells.""

Quote..." If antifibrotic therapy is to have a role, it is likely to take the form of inclusion in combination regimens, once effective anti-inflammatory treatments have been identified. Combination therapy could, in principle, address major anti-inflammatory and antifibrotic pathways while attenuating their fibrotic consequences."