Phenylpiracetam

Phenylpiracetam is a synthetic racetam. Its chemical name is 2-(2-oxo-4-phenylpyrrolidin-1-yl)acetamide. It is piracetam with a phenyl group on ring carbon 4. Its International Nonproprietary Name is fonturacetam. It is also called carphedon and 4-phenylpiracetam (PubChem CID 132441). A 1983 Russian paper called it a new phenyl analog of piracetam (Bobkov et al., 1983). A 2010 review called it more potent than piracetam (Malykh and Sadaie, 2010).

In Russia, clinical papers call it Phenotropil.

So are the format and storage. PubChem CID 132441 matches the CAS number, formula and weight. It also supplies the synonyms and structure. It does not state the stereochemistry.

Published work on phenylpiracetam falls into six areas. Each summary states its model.

What the phenyl group changes

In the 1983 report, 4-phenylpiracetam activated operant behavior more strongly than piracetam. It countered diazepam's depressant effects. It also prevented retrograde amnesia. Unlike piracetam, it was anticonvulsant. At high amounts, it was itself depressant (Bobkov et al., 1983). Neither compound changed ligand binding at AMPA, NMDA or metabotropic glutamate receptors in rat brain tissue. This held from 0.1 nanomolar to 100 micromolar (Firstova et al., 2011). Models: mice, rats, guinea pigs and rat brain tissue.

R- and S-enantiomers

Phenotropil is used clinically as the racemate. In mice, single exposures raised open-field locomotor activity. This was seen at 10 and 50 mg/kg of the R-form and 50 mg/kg of the S-form. Both forms had antidepressant-like effects in the forced swim test. Only the R-form changed passive avoidance. It raised retention at 1 mg/kg. Yet brain levels of the two forms were similar (Zvejniece et al., 2011). Model: mice.

The dopamine transporter

Merz Pharmaceuticals coded the R-form MRZ-9547 (Dekundy et al., 2015). In vitro and in rat microdialysis, it selectively inhibited the dopamine transporter (DAT). It also moderately raised striatal dopamine release. Its mirror image, MRZ-9546, was much weaker. MRZ-9547 also raised rats' lever pressing for food on progressive ratio schedules. It did so more than methylphenidate did (Sommer et al., 2014). DAT was the only significant target for the R-form in a radioligand binding panel (Zvejniece et al., 2020).

The S-form is also called a selective DAT inhibitor. It was given daily by mouth to Western diet-fed mice for 8 weeks. Obese Zucker rats were given it the same way for 12 weeks. It lowered body weight gain and fat mass gain. It also lowered plasma glucose and leptin. It did not change locomotor activity (Zvejniece et al., 2017). Models: rats, mice and in vitro assays.

Neuroprotection and inflammation models

One study used Wistar rats with cerebral ischemia. The ischemia came from bilateral carotid occlusion or gravitational overload. Phenylpiracetam reduced neurological deficit. It preserved locomotor, exploratory and memory measures. It also raised survival and helped restore local cerebral blood flow. Piracetam had the same effects, but weaker (Tiurenkov et al., 2007).

Male mice were given bacterial lipopolysaccharide. One intraperitoneal exposure to the R-form lessened their fall in body temperature. It also lessened the rise in brain TNF-α, IL-1β and inducible nitric oxide synthase gene expression. A week of oral pretreatment reduced carrageenan-induced paw edema (Zvejniece et al., 2020). Models: rats and mice.

Clinical studies in Russia

A double-blind, randomized, placebo-controlled trial studied 90 adults with symptomatic focal epilepsy. They received phenylpiracetam at one of two daily amounts, or placebo. This was on top of standard antiepileptic drugs. The authors reported fewer seizures and better cognitive scores in those without epileptiform EEG abnormalities (Grebeniuk et al., 2014).

A 2025 meta-analysis pooled 11 studies in 549 people with asthenia, a fatigue syndrome. It reported MFI-20 fatigue scores 16.3 points lower on average after a one-month course. This was change over time rather than against placebo. Side effects were seen in 5.5 percent (Devlikamova and Safina, 2025). Model: human clinical studies.