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."
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