Maybe interesting to look at competition, not sure how their trials will go, but possibility of some red flags.
AI....
DISC's Bitopertin with NDA submission next month, and trial data end 2026 possible approval 2027.
By inhibiting GlyT1, Bitopertin increases ambient glycine, which can enhance NMDAR activation.
This mechanism was the basis for Bitopertin’s original development in schizophrenia—aiming to correct NMDAR hypofunction thought to
underlie negative symptoms.
While boosting NMDAR activity can be therapeutic, it also carries risks:
Overactivation of NMDARs can lead to excitotoxicity, especially in neurodegenerative conditions or stroke.
Cognitive and behavioral modulation:
GlyT1 inhibition may alter learning, memory, and emotional processing—effects that are subtle but clinically relevant.
Voltage-dependent effects:
GlyT1 can act as a glycine source via reversed uptake or heteroexchange, which may affect NMDAR activation differently depending on membrane potential.
These dynamics are not relevant in EPP, where GlyT1 inhibition targets erythroid cells—not neurons.
But they’re important in long-term safety modeling, especially if Bitopertin is used in younger patients or off-label CNS contexts.
END.
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