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for educational and safety purposes
class, effects, and the receptor fingerprint, side by side; add up to four, then source the whole stack
Popular head-to-heads →AMPA receptorspositive modulator
Long-term potentiationfacilitates
NMDA (via AMPA co-activation)boosts calcium
AMPA receptor (ionotropic glutamate receptor GluA1-4; flip splice variants preferred)Positive allosteric modulator. Slows agonist-dependent desensitization and deactivation, increasing steady-state current and synaptic charge transfer. Partial (low-efficacy) modulator relative to cyclothiazide.
GluA2 (GRIA2) ligand-binding-domain dimer interface; the cyclothiazide/benzothiadiazide allosteric siteBinds within the LBD dimer interface and stabilises the agonist-bound dimer against dissociation. Hydrogen-bonds to Ser754, which underlies the partial selectivity of benzothiadiazides for the flip splice form.
NMDA receptor, GluN2B-preferring (GRIN1/GRIN2B)Negative modulator. Reduces whole-cell NMDA currents non-competitively and voltage-independently, shortens NMDA-mediated mEPSC decay, and is more effective at GluN1a/GluN2B than GluN1a/GluN2A. Effect is stronger at low glycine, suggesting interaction with the glycine site.
GABA-A receptorMixed and modest. Inhibits currents evoked by exogenous GABA while slightly prolonging autaptic GABAergic currents; net direction depends on the preparation.
NMDA glycine siteactivates
CaMKII / PKCastimulates downstream
AMPA receptors (indirect)facilitates
checking IDRA-21 and Sunifiram: no adverse interactions were flagged (1 compatible pair); the pairs read as compatible at the class level.
noted as a compatible pairing in IDRA-21's own profile; no adverse interaction flagged.
General educational info, not medical advice.
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