Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of Fasoracetam and Sunifiram — mechanism, side effects, legal status, and pricing.
Fasoracetam (NS-105, NFC-1) is a non-peptide racetam-class small molecule characterized as a metabotropic glutamate receptor (mGluR) activator that also modulates acetylcholine release and GABA-B signaling. A single Phase 1 trial in 30 adolescents with ADHD and mGluR-network gene variants showed clinical improvement on CGI scales, but broader development was discontinued and fasoracetam has never been approved in any jurisdiction. It is sold only as an unregulated research chemical/nootropic.
Sunifiram (DM-235) is a synthetic non-peptide piperazine derivative marketed online as an 'ampakine-like' cognitive enhancer. Despite common branding, primary research shows it acts indirectly via the glycine-binding site of the NMDA receptor to potentiate AMPA-receptor-mediated transmission, not as a direct AMPA agonist. No human clinical trials or toxicology studies have been conducted, and sunifiram is not approved for any human or veterinary use worldwide. It is sold on the gray market without regulatory vetting.
Fasoracetam
Sunifiram
Category
Legal Status
Mechanism
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
Fasoracetam
Sunifiram
COA corpus from Disclosed Labs — independently tested batches only.
Fasoracetam
1
COAs
99.7%
Avg purity
1
Labs
Sunifiram
1
COAs
99.5%
Avg purity
1
Labs
Human data exist but the compound is not approved anywhere. The best-sourced human study is a completed Phase 1 open-label single-dose PK/single-blind placebo-controlled dose-escalation trial of NFC-1 (fasoracetam) in 30 adolescents (age 12–17) with ADHD carrying mGluR-network gene variants (NCT02286817; Elia et al. 2018, Nature Communications). CGI-I improved from 3.79 to 2.33 and CGI-S from 4.83 to 3.86 from baseline to week 5 (both P<0.001) in this small, largely uncontrolled sample. In rats (Wistar), fasoracetam reversed memory disruption across scopolamine-, NBM-lesion-, AF64A-, cerebral-ischemia-, baclofen-, and ECS-induced amnesia models, increased cortical acetylcholine release, and enhanced high-affinity choline uptake in cortex and hippocampus (Shirayama et al., 1999).
No human data exist. In olfactory-bulbectomized mice given oral sunifiram 0.01–1.0 mg/kg daily for 7–12 days, spatial reference memory (Y-maze) and short-term recognition memory (novel object recognition) improved, and impaired hippocampal CA1 long-term potentiation was restored via NMDAR-glycine-site-dependent CaMKII/PKC signaling (blocked by gavestinel). In mouse hippocampal slices, sunifiram (1–1000 nM, peaking at 10 nM with a bell-shaped dose-response) potentiated CA1 LTP via the glycine-site/PKCα/CaMKII pathway. In passive-avoidance models, sunifiram reversed amnesia in mice and rats at doses roughly four orders of magnitude lower than piracetam. No toxicology studies or human clinical trials have been conducted as of 2016.
Fasoracetam and Sunifiram are both in the Cognitive category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Contraindications
Lab Testing
Disclosed Labs