Sunifram 15mg – 60 capsules

Sunifram (DM-235) 15 mg — 60 oral research capsules. Sunifram (DM-235) is a piperazine-class ampakine-like nootropic and one of the most potent memory-enhancing tool compounds in the entire research literature — approximately 1,000-fold more potent than piracetam on a per-milligram basis in standardized rodent memory paradigms. Developed in the laboratory of Carla Ghelardini at the University of Florence, Sunifram operates through positive modulation of the AMPA-receptor glycine site and downstream BDNF release, producing dose-dependent enhancement of working memory, recognition memory and amnesia rescue at sub-milligram-per-kilogram oral doses — placing it firmly in the same potency tier as the most refined contemporary AMPA-PAMs.

Research Overview

Sunifram (DM-235) is a 1,4-disubstituted piperazine derivative developed at the University of Florence by the Ghelardini and Bartolini groups in the late 1990s as part of a structure-activity program around novel cognition-enhancing molecules [1]. The compound is structurally unrelated to the racetam scaffold but produces a similar — and substantially more potent — pro-cognitive phenotype. In passive-avoidance and amnesia-rescue rodent paradigms, Sunifiram is approximately 1,000-fold more potent than piracetam on a per-milligram basis, with active doses in the 0.1 mg/kg oral range [1,2]. Mechanistically, Sunifram modulates the AMPA-receptor glycine site, enhancing receptor sensitivity to endogenous glutamate, and produces downstream upregulation of BDNF release — the same mechanistic axis that underlies the most refined contemporary ampakines [2,3]. The compound also exhibits NMDA-receptor co-agonist activity at the glycine binding site, and lacks the convulsant liability of high-efficacy AMPA agonists. Sunifram has emerged as one of the most pharmacologically efficient nootropic research tool compounds in the published literature.

Primary Research Areas

• AMPA-receptor glycine-site modulation — an unusual and pharmacologically distinctive mechanism among nootropics; complements the canonical ampakine-binding-site PAMs [2].
• Memory and amnesia-rescue research — approximately 1,000-fold more potent than piracetam in passive-avoidance and amnesia-rescue paradigms, at sub-mg/kg oral doses [1,2].
• BDNF release and synaptic plasticity — induces activity-dependent BDNF release and enhances hippocampal LTP at low concentrations [2,3].
• NMDA-receptor glycine-site co-agonism — the secondary mechanism, providing a clean dual-pathway probe of glutamatergic plasticity [3].
• Comparator compound for AMPA-PAM research — a useful structural and pharmacological alternative to the benzothiadiazide ampakines (IDRA-21) and racetams in side-by-side studies [1].

References

1. Ghelardini C, Galeotti N, Gualtieri F, et al. DM235 (sunifiram): a novel nootropic with potential as a cognitive enhancer. Naunyn Schmiedebergs Arch Pharmacol. 2002;365(6):419–426.
2. Galeotti N, Ghelardini C, Pittaluga A, et al. AMPA-receptor activation is involved in the antiamnesic effect of DM 232 (unifiram) and DM 235 (sunifram). Naunyn Schmiedebergs Arch Pharmacol. 2003;368(6):538–545.
3. Romanelli MN, Galeotti N, Ghelardini C, et al. Pharmacological characterization of DM232 (unifiram) and DM235 (sunifram), new potent cognition enhancers. CNS Drug Rev. 2006;12(1):39–52.