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Sunifiram (DM-235) is a synthetic pyrrolidinone-derived compound structurally distinct from the classical racetam family despite sharing a related core scaffold, investigated for proposed positive allosteric modulation of AMPA-type glutamate receptors.
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Ver resultados de laboratorio →Sunifiram (DM-235) is a synthetic pyrrolidinone-derived compound structurally distinct from the classical racetam family despite sharing a related core scaffold, investigated for proposed positive allosteric modulation of AMPA-type glutamate receptors. Research interest centers on its reported high in vitro potency relative to piracetam-class compounds at substantially lower concentrations.
Research applications include AMPA receptor potentiator pharmacology, glutamatergic signalling research, and structure-activity comparison within the pyrrolidinone-derivative compound series.
| Chemical Formula | C14H18N2O2 |
|---|---|
| Synonyms | DM-235 |
| Molar Mass | 246.304 g/mol |
| CAS Number | 314728-85-3 |
| PubChem CID | 4223812 |
| Total Compound Content | 10 grams |
| Shelf Life | 36 months |
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Sunifiram shares a pyrrolidinone-derived structural lineage conceptually related to the racetam family but is synthesized via a distinct chemical route and carries substituents not present in piracetam, oxiracetam, or other classical racetam-family compounds. This structural distinction is the basis for research comparing sunifiram's receptor-binding and functional potency profile against established racetam compounds, particularly given reports of substantially different potency ranges between the two groups in similar assay systems.
Patch-clamp electrophysiology in cultured neurons, brain slice preparations, or heterologous expression systems is the standard method for characterising sunifiram's effects on AMPA receptor-mediated currents, with key readouts including peak current amplitude, desensitization rate, and deactivation kinetics in the presence versus absence of the compound. These functional measurements are used alongside receptor-binding assays to determine whether sunifiram acts at an allosteric site distinct from the glutamate orthosteric binding site, consistent with a positive allosteric modulator mechanism.
Reports of sunifiram's in vitro activity describe substantially lower effective concentrations than those required for classical racetam-family compounds in comparable assay systems, prompting researchers to use nanomolar-to-low-micromolar concentration ranges when establishing dose-response curves for sunifiram, in contrast to the micromolar-to-millimolar ranges typically required for piracetam-class compounds. Researchers should empirically establish the relevant concentration range for their specific assay system and cell model rather than assuming direct potency transfer from other reported studies.
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