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Head-to-head comparison of Fasoracetam and Pramiracetam — 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.
Pramiracetam is a non-peptide synthetic racetam-class nootropic (2-oxopyrrolidone/pyrrolidinone acetamide derivative) with CAS 68497-62-1 and molecular formula C14H27N3O2. It was previously approved and marketed in Italy and some Eastern European countries under brand names Pramistar, Neupramir, and Remen for memory/attention deficits in aging-associated dementias; Italian authorization was revoked in 2020 at manufacturer request. It is not FDA-approved in the United States, where it is sold only as an unapproved gray-market research chemical. The related racetam phenylpiracetam is explicitly listed on the WADA Prohibited List as an S6 stimulant; pramiracetam itself is not explicitly named, leaving its status under WADA's 'similar structure/effect' catch-all unresolved.
Fasoracetam
Pramiracetam
Category
Legal Status
Mechanism
Side Effects
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Fasoracetam
Pramiracetam
No pricing data yet.
Check Pramiracetam prices →COA corpus from Disclosed Labs — independently tested batches only.
Fasoracetam
1
COAs
99.7%
Avg purity
1
Labs
Pramiracetam
2
COAs
99.9%
Avg purity
2
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).
Human data consist of a handful of small older trials (1985–1996): healthy-volunteer pharmacokinetic studies, a scopolamine-induced-amnesia challenge study, a placebo-controlled trial in young males with head-injury/anoxia-related memory deficits (400 mg TID improved delayed recall), and a small dose-finding trial in Alzheimer's disease that found no convincing benefit at doses up to 4,000 mg. A scopolamine-challenge study (600 mg BID × 10 days) showed partial mitigation of induced amnesia in healthy young and older male volunteers. No modern (post-2000) randomized controlled trials were located. Preclinical findings: in rats, 7.5 and 15 mg/kg/day × 7 weeks significantly improved reference (long-term) memory on a 16-arm radial maze but did not affect working memory; 300 mg/kg i.p. increased cortical nitric oxide synthase activity ~20% (synergistic ~40% increase with lithium pretreatment); moderate protection against hypobaric-hypoxia-induced deficits in immature rats.
Key references
Fasoracetam and Pramiracetam 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