α7 nicotinic acetylcholine receptor (α7 nAChR). No IC50, Ki, EC50, or binding affinity values are provided. The study suggests S-ORC acts indirectly by inhibiting AChE rather than directly binding to α7 nAChR. [1]
The targets of S-Oxiracetam involve multiple neuronal pathways. It is primarily described as a positive allosteric modulator of the AMPA receptor, exerting nootropic effects by enhancing AMPA receptor-mediated excitatory synaptic transmission . Furthermore, studies indicate that (S)-oxiracetam activates the α7 nicotinic acetylcholine receptor, subsequently activating the PI3K/Akt/GSK3β signaling pathway to inhibit neuronal apoptosis . Additionally, S-oxiracetam participates in regulating cerebral energy metabolism, affecting ATP metabolism, the glutamine-glutamate cycle, and antioxidant systems .
α7 nicotinic acetylcholine receptor (α7 nAChR) – no binding affinity (IC₅₀, Ki, EC₅₀, DC₅₀) values reported.

- Cell viability (MTT assay): In primary rat cortical neurons subjected to OGD/R, cell viability was significantly decreased compared to control (p < 0.01). Treatment with S-ORC at 1 μM, 10 μM, and 100 μM for 24 hours increased neuronal survival to 58.82%, 64.82%, and 79.15%, respectively, compared to the OGD/R group (p < 0.05, p < 0.01). [1]
- LDH release assay: LDH activity in the OGD/R group (725.22 U/L) was significantly higher than in the control group (346.59 U/L) (p < 0.01). S-ORC treatment at 1 μM, 10 μM, and 100 μM decreased LDH activity to 567.59 U/L, 484.89 U/L, and 428.15 U/L, respectively (p < 0.05, p < 0.01). [1]
- Apoptosis rate (Annexin V/PI flow cytometry): The apoptotic rate in the OGD/R group (65.02%) was significantly higher than in the control group (5.86%) (p < 0.01). S-ORC treatment at 1 μM, 10 μM, and 100 μM for 24 hours significantly reduced the apoptotic rate to 34.48%, 16.15%, and 10.05%, respectively (p < 0.05, p < 0.01). [1]
- α7 nAChR protein expression (Western blot): OGD/R decreased α7 nAChR expression to 32.34% of control (83.6%). S-ORC at 1 μM, 10 μM, and 100 μM upregulated α7 nAChR expression to 46.95%, 58.67%, and 72.97%, respectively (p < 0.05, p < 0.01). [1]
- PI3K/Akt/GSK3β phosphorylation (Western blot): OGD/R significantly decreased phosphorylation of PI3K, Akt, and GSK3β compared to control (p < 0.01). S-ORC at 1, 10, and 100 μM markedly increased the phosphorylation of all three proteins (p < 0.05, p < 0.01). [1]
- α7 nAChR siRNA silencing: When α7 nAChR was silenced (transfection efficiency ~80%), S-ORC no longer improved cell viability or increased phosphorylation of PI3K, Akt, or GSK3β after OGD/R injury, confirming that the neuroprotective effect is α7 nAChR-dependent. [1]

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(S)-Oxiracetam (1, 10, 100 μM; 24 h) stimulates PI3K/Akt/GSK3β signaling that is reliant on α7 nAChR and shields the shell of fetal rat primary cortical neurons from OGD/R injury[1]. [1]

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S-Oxiracetam exhibits significant neuroprotective activity in vitro. In an oxygen-glucose deprivation/reoxygenation (OGD/R) injury model, treatment of fetal rat primary cortical neurons with (S)-oxiracetam at concentrations of 1, 10, and 100 μmol/L for 24 hours significantly protected neurons from ischemia-reperfusion injury and activated the PI3K/Akt/GSK3β signaling pathway in an α7 nAChR-dependent manner . Comparative studies of chiral oxiracetam demonstrate that both oxiracetam and (S)-oxiracetam exert good neuroprotective effects against primary neuronal damage induced by glutamate and calcium ions, with (S)-oxiracetam showing superior efficacy compared to the racemate and (R)-oxiracetam .

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(1) In primary cortical neurons subjected to OGD/R, (S)-Oxiracetam (1, 10, 100 μM) significantly increased cell viability to 58.82%, 64.82%, and 79.15% respectively (vs. OGD/R group, p<0.05, p<0.01) as measured by MTT assay. [1]
(2) (S)-Oxiracetam dose‑dependently decreased LDH release: LDH activities were 567.59, 484.89, and 428.15 U/L at 1, 10, 100 μM respectively (vs. OGD/R 725.22 U/L, p<0.05, p<0.01). [1]
(3) (S)-Oxiracetam reduced neuronal apoptosis rate: apoptotic rates were 34.48%, 16.15%, and 10.05% at 1, 10, 100 μM (vs. OGD/R 65.02%, p<0.05, p<0.01) as determined by Annexin V/PI flow cytometry. [1]
(4) Western blot analysis showed that (S)-Oxiracetam (1, 10, 100 μM) upregulated α7 nAChR protein expression (46.95%, 58.67%, 72.97% of control, vs. OGD/R 32.34%) and increased phosphorylation of PI3K, Akt, and GSK3β (Ser9) in a dose‑dependent manner. [1]
(5) In α7 nAChR siRNA‑silenced neurons, (S)-Oxiracetam failed to improve cell viability or activate PI3K/Akt/GSK3β phosphorylation, confirming the dependence on α7 nAChR. [1]

- Infarct size (TTC staining): In rats subjected to MCAO/R, the infarct size was 32.24 ± 5.00% in the MCAO/R group. S-ORC at 0.12 g/kg, 0.24 g/kg, and 0.48 g/kg (intravenous, once daily for 7 days) reduced infarct size to 26.04 ± 1.07%, 21.66 ± 2.27%, and 12.26 ± 5.59%, respectively (p < 0.05, p < 0.01). ORC at 0.24 g/kg reduced infarct size to 21.07 ± 3.02%. [1]
- Neurological deficit scores: Neurological scores in S-ORC treatment groups (0.12, 0.24, and 0.48 g/kg) were significantly improved (scores increased, indicating less deficit) compared to the MCAO/R group (p < 0.05, p < 0.01). [1]
- Neuronal apoptosis (TUNEL/NeuN staining): Most TUNEL-positive cells (72.6 ± 12.4%) in the penumbral area co-stained with NeuN, indicating apoptotic neurons. S-ORC treatment significantly reduced the number of NeuN+/TUNEL+ cells (p < 0.05, p < 0.01). [1]
- α7 nAChR expression in brain cortex (Western blot): MCAO/R significantly reduced α7 nAChR expression compared to sham (p < 0.01). S-ORC at 0.12, 0.24, and 0.48 g/kg markedly elevated α7 nAChR expression (p < 0.05, p < 0.01). [1]
- PI3K/Akt/GSK3β phosphorylation in brain cortex: MCAO/R significantly decreased phosphorylation of PI3K, Akt, and GSK3β compared to sham (p < 0.01). S-ORC at all doses markedly increased phosphorylation of these proteins (p < 0.05, p < 0.01). [1]
- GSH-PX concentration: S-ORC (0.12, 0.24, and 0.48 g/kg) and ORC (0.24 g/kg) significantly increased GSH-PX concentration in rat brain (189.54, 193.07, 203.98, and 186.65 units, respectively) (see Supplementary Figure S1). [1]
- AChE activity: S-ORC reduced AChE activity in rat brain (see Supplementary Figure S2). [1]

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(S)-Oxiracetam (IV once daily for seven days; 0.12, 0.24, and 0.48 g/kg) considerably minimizes the extent of the infarct and mildly modifies Sprague behavior-MACO/R model in solution caused by Dawson simulation Inhibitory and dysfunctional When administered intraperitoneally 60 minutes before to apomorphine, salted remoxipride (0.1-100 μM/kg) prevents vomiting in dogs and apomorphine-induced behavior in rats [1]. In striatal and extrastriatal areas, (S)-Remopride hydrochloride (0.1–10 mg/kg; intraperitoneally; 30 minutes prior to apomorphine) displaces [3H]spiperone [1].

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S-Oxiracetam demonstrates cognitive improvement and neuroprotective effects in various in vivo models. In the chronic cerebral hypoperfusion (2-VO) rat model, (S)-oxiracetam (100, 200 mg/kg) and racemic oxiracetam (400 mg/kg) significantly improved spatial learning and memory impairments, reduced astrocyte activation in the hippocampal CA1 region, increased cerebral blood flow, and regulated ATP metabolism, glutamine-glutamate cycling, and antioxidant levels in the cortex . Morris water maze tests confirmed that (S)-oxiracetam-treated groups exhibited significantly shortened escape latency and better memory retention in probe trials following platform removal . Furthermore, in a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model, (S)-oxiracetam (0.12, 0.24, 0.48 g/kg, intravenous injection once daily for 7 days) significantly reduced infarct size and ameliorated behavioral dysfunction .
(1) In rat MCAO/R model, intravenous administration of (S)-Oxiracetam (0.12, 0.24, 0.48 g/kg, once daily for 7 days, starting 2.5 h after reperfusion) significantly reduced infarct size to 26.04 ± 1.07%, 21.66 ± 2.27%, and 12.26 ± 5.59% respectively (vs. MCAO/R 32.24 ± 5.00%, p<0.05, p<0.01). [1]
(2) Neurological deficit scores were significantly improved in all (S)-Oxiracetam treatment groups compared to MCAO/R (p<0.05, p<0.01). [1]
(3) TUNEL/NeuN co‑staining showed that (S)-Oxiracetam significantly reduced the percentage of apoptotic neurons (NeuN⁺TUNEL⁺) in the penumbral area (p<0.05, p<0.01). [1]
(4) Western blot analysis of brain tissues revealed that (S)-Oxiracetam upregulated α7 nAChR expression and increased phosphorylation of PI3K, Akt, and GSK3β (Ser9) in a dose‑dependent manner (p<0.05, p<0.01). [1]
(5) (S)-Oxiracetam significantly increased GSH‑PX concentration in rat brain (189.54, 193.07, 203.98 units for 0.12, 0.24, 0.48 g/kg vs. MCAO/R) (Supplementary data). [1]

- Acetylcholinesterase (AChE) activity assay: After the MCAO/R model in rats, brain tissues were collected and homogenized. AChE activity was measured using an AChE assay kit following the manufacturer’s instructions. S-ORC treatment reduced AChE activity (Supplementary Figure S2). [1]
- Glutathione peroxidase (GSH-PX) assay: After animals were sacrificed, brain tissues were collected and prepared as homogenate. GSH-PX concentration was determined using a GSH-PX assay kit according to the manufacturer’s instruction. S-ORC treatment increased GSH-PX concentration. [1]

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As a positive allosteric modulator of the AMPA receptor, cell-free assays for S-Oxiracetam primarily focus on receptor binding studies. A typical protocol includes: 1) Prepare membrane fragments containing AMPA receptors or cell membranes expressing recombinant AMPA receptors; 2) Incubate radiolabeled AMPA receptor ligand (e.g., [³H]-AMPA) with varying concentrations of S-Oxiracetam (0.1-100 μmol/L) in binding buffer for 60 minutes at room temperature; 3) Separate bound and free ligands by rapid filtration, and measure radioactivity using a liquid scintillation counter; 4) Calculate inhibition rates to evaluate the modulatory effect of S-Oxiracetam on ligand binding. Positive allosteric modulation is typically verified through [³H]-AMPA binding enhancement assays.

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(1) Acetylcholinesterase (AChE) activity assay: Brain homogenates or cell supernatants were prepared and AChE activity was measured using a commercial colorimetric kit following the manufacturer's instructions; absorbance was read and activity calculated. (S)-Oxiracetam reduced AChE activity both in vivo and in vitro (Supplementary Figure S2). [1]
(2) Glutathione peroxidase (GSH‑PX) assay: Brain tissue homogenates were prepared and GSH‑PX concentration was determined using a commercial kit according to the manufacturer's protocol; the results showed significant increase after (S)-Oxiracetam treatment. [1]
(3) Lactate dehydrogenase (LDH) release assay: After OGD/R and drug treatment, culture supernatants were collected and LDH activity was measured using a commercial kit; absorbance at 490 nm was read and activity calculated from a standard curve. [1]

Cell Viability Assay[1]
Cell Types: fetal mouse primary cortical neurons
Tested Concentrations: 1, 10, 100 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: Compared with OGD/R, the survival rate of cortical neurons was increased (58.82%, 64.82% respectively and 79.15%) groups.

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Cytotoxicity assay [1]
Cell Types: fetal mouse primary cortical neurons
Tested Concentrations: 1, 10, 100 μM
Incubation Duration: 24 h
Experimental Results: LDH activity diminished to 567.59 U/L, 484.89 U/L and 428.15 U/ L compared with the OGD/R group (725.22 U/L), were μM, 10 μM and 100 μM respectively.

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Apoptosis analysis [1]
Cell Types: fetal mouse primary cortical neurons
Tested Concentrations: 1, 10, 100 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: The apoptosis rate of cortical neurons dependent on α7 nAChR was diminished (34.48%, 16.15% and 10.05%) ) compared with the OGD/R group.

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Western Blot Analysis [1]
Cell Types: fetal mouse primary cortical neurons
Tested Concentrations: 1, 10, 100 μM
Incubation Duration: 24 h
Experimental Results: α7 nAChR expression increased (1 μM increased by 46.95%, 58\n

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\n- Primary rat cortical neuron culture: Primary cortical neurons were cultured from E15-18 rat embryos in Neurobasal Medium supplemented with 2% B27 at 37°C in 95% air and 5% CO2. Cells were maintained for 5-7 days before experiments. [1]
\n- OGD/R model in vitro: To mimic ischemia/reperfusion injury, cortical neurons were incubated with Na2S2O4 (20 mM, pH 7.2) for 1.5 hours at 37°C (OGD), then returned to normal Neurobasal Medium for 2 hours (reoxygenation), followed by 24 hours of drug treatment. [1]
\n- MTT cell viability assay: After OGD/R treatment, 50 mL of MTT solution (5 g/L) was added to each well and incubated for 4 hours at 37°C. The formazan crystals were dissolved in DMSO for 15 minutes. Optical density was measured at 570 nm using a microplate reader. [1]
\n- LDH release assay: LDH activity in the supernatant was measured using a rat LDH assay kit following the manufacturer’s instructions after OGD/R. [1]
\n- AChE activity assay in vitro: After OGD/R, AChE activity in the supernatant of cortical neurons was measured using an AChE assay kit according to the manufacturer’s instruction. [1]
\n- Flow cytometry for apoptosis (Annexin V/PI staining): After OGD/R and drug treatment, cortical neurons were collected and stained with Annexin V/PI-FITC. Apoptotic rate was detected by flow cytometry, and data were analyzed using Cell Quest Pro software. [1]
\n- α7 nAChR siRNA transfection: After 5-6 days in culture, cortical neurons were transfected with synthesized siRNA targeting α7 nAChR using RNAimax and serum-free medium according to the manufacturer’s protocol. Negative control siRNA was used. Twenty-four hours after transfection, cells were subjected to OGD/R and S-ORC treatment. Knockdown efficiency (~80%) was confirmed by real-time PCR and Western blot. [1]
\n- Real-time PCR: Total RNA was extracted using Total RNA extraction reagent. cDNA was generated using random primers and a Prime Script RT reagent kit. Real-time PCR was performed using SYBR Premix Ex Taq II on a 7500 Real-Time PCR System. α7 nAChR mRNA expression was normalized against GAPDH. Primers used: α7 nAChR sense 5′-TCCTCCAGGCATATTCAAGAGC-3′, antisense 5′-ATTTGCAGGTCCAGTGACCACTC-3′; GAPDH sense 5′-AGGGCTCATGACCACAGTCCT-3′, antisense 5′-ATGCCAGTGAGCTTCCCGTT-3′. [1]
\n- Western blot analysis: Protein extracts from brain tissues or cultured neurons were separated by 10% SDS-PAGE and transferred to PVDF membranes. Membranes were blocked with 5% skim milk in TBST, incubated with primary antibodies overnight at 4°C, then with HRP-conjugated secondary antibodies for 2 hours. Bands were visualized by enhanced chemiluminescence. α7 nAChR expression was normalized to β-actin. Phosphorylated protein levels were expressed as a ratio of phosphorylated protein to total protein. [1]\n

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(1) Cell viability (MTT assay): Primary cortical neurons were seeded in 96‑well plates, subjected to OGD/R, treated with (S)-Oxiracetam for 24 h, then MTT solution (5 g/L) was added for 4 h; formazan crystals were dissolved in DMSO and absorbance read at 570 nm. Viability was expressed as percentage of control. [1]
(2) LDH release assay: After OGD/R and treatment, cell culture supernatants were collected and LDH activity measured using a kit; absorbance read and activity calculated. [1]
(3) Apoptosis detection by flow cytometry: Cells were harvested after OGD/R and treatment, stained with Annexin V‑FITC and PI, and analyzed on a flow cytometer; apoptotic rate (early + late) was quantified. [1]
(4) Western blotting: Protein extracts from cells or tissues were separated by SDS‑PAGE, transferred to PVDF membranes, and probed with antibodies against α7 nAChR, phospho‑PI3K, total PI3K, phospho‑Akt, total Akt, phospho‑GSK3β (Ser9), total GSK3β, and β‑actin; bands were visualized by ECL and quantified. [1]
(5) Real‑time PCR: Total RNA was extracted, reverse‑transcribed, and amplified using specific primers for α7 nAChR and GAPDH; relative expression was calculated by 2⁻ΔΔCt method. [1]
(6) siRNA transfection: Primary cortical neurons were transfected with siRNA targeting α7 nAChR using RNAimax; after 24 h, cells were subjected to OGD/R and (S)-Oxiracetam treatment; silencing efficiency was confirmed by RT‑PCR and Western blot. [1]

Animal/Disease Models: Swiss albino mouse scopolamine-induced amnesia model [1].
Doses: 0.12, 0.24, 0.48 g/kg, one time/day for 7 days
Route of Administration: intravenous (iv) (iv)injection
Experimental Results: Compared with the sham operation group, the infarct area of rats was diminished to 26.04 ± 1.07%, 21.66 ± 2.27% , 12.26 ± 5.59% group were 0.12 g/kg, 0.24 g/kg, and 0.48 g/kg respectively. Neurologic scores improved compared with the MCAO/R group. Neurons were protected from apoptosis compared with the sham group. Compared with the MCAO/R group, the phosphorylated expression of α7 nAChR, as well as PI3K, Akt and GSK3β was increased. GSH-PX concentrations increased (189.54 units, 193.07 units, and 203.98 units, respectively).

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- MCAO/R model in rats: Male Sprague-Dawley rats (250-280 g) were anesthetized with chloral hydrate (300 mg/kg, i.p.). Middle cerebral artery occlusion (MCAO) was performed for 1.5 hours using the intraluminal filament method, followed by reperfusion by withdrawing the filament. Sham group underwent the same surgical procedure without filament insertion. [1]
- Drug administration: At 2.5 hours after MCAO, S-ORC (0.12, 0.24, or 0.48 g/kg) or ORC (0.24 g/kg) was administered intravenously once daily for seven days. The injection volume was 0.5 mL/100 g body weight/day. The control and MCAO/R groups received saline. [1]
- Neurological deficit assessment: Seven days after MCAO, neurological deficit scores were assessed on a 5-point scale (0: no deficits; 1: contralateral forelimb flexion; 2: decreased resistance to lateral push; 3: spontaneous circling; 4: no spontaneous movement). [1]
- Infarct size measurement: Seven days after MCAO, rats were sacrificed. Brains were sectioned into 2-mm thick coronal slices and stained with 2% TTC at 37°C for 15 minutes in the dark. Infarct area was calculated as (total infarct area / whole brain section area) × 100% using Image-Pro Plus software. [1]
- Tissue collection for biochemical assays: After animals were sacrificed, brain tissues were collected, homogenized, and used for GSH-PX and AChE activity assays according to kit instructions. [1]
- Immunofluorescence and TUNEL staining: Three days after MCAO, rats were perfused with normal saline followed by 4% paraformaldehyde. Brains were post-fixed and cryosectioned at 30 μm. Sections were stained with anti-NeuN antibody (1:200) overnight at 4°C, followed by Cy3-conjugated secondary antibody. TUNEL staining was performed using a TUNEL kit. Nuclei were counterstained with DAPI. Images were captured using a fluorescence microscope. [1]

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The typical in vivo animal assay protocol for S-Oxiracetam is as follows : 1) Establish disease animal models, such as the chronic cerebral hypoperfusion (2-VO) rat model or middle cerebral artery occlusion/reperfusion (MCAO/R) rat model. 2) Randomize animals into sham, model, positive control, and S-Oxiracetam treatment groups (multiple doses: 30, 100, 200 mg/kg or 0.12-0.48 g/kg), with 8-10 animals per group. 3) Administration routes: oral gavage or intravenous injection, with treatment duration ranging from 5 days to 7 weeks. 4) Assess learning and memory abilities using Morris water maze and step-down tests. 5) After euthanasia, collect brain tissue for histopathological analysis (Nissl staining, GFAP immunohistochemistry) or detect spatial distribution changes of small molecule metabolites in the brain using MALDI-MSI and LC-MS/MS.

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(1) Animal model: Male Sprague‑Dawley rats (250‑280 g) were subjected to middle cerebral artery occlusion (MCAO) for 1.5 h using the intraluminal filament method, followed by reperfusion. Sham rats underwent same surgery without filament insertion. [1]
(2) Drug administration: (S)-Oxiracetam was dissolved in saline and administered intravenously (0.5 mL/100 g/day) at doses of 0.12, 0.24, or 0.48 g/kg, starting 2.5 h after MCAO, once daily for 7 consecutive days. The reference compound oxiracetam (ORC) was given at 0.24 g/kg. [1]
(3) Neurological deficit scoring: At 7 days post‑MCAO, motor functions were scored on a 0‑4 scale (0=no deficit, 4=no spontaneous movement) according to Longa's method. [1]
(4) Infarct size measurement: Brains were removed, sectioned into 2‑mm coronal slices, stained with 2% TTC at 37 °C for 15 min, and photographed; infarct area was measured using Image‑Pro Plus and expressed as percentage of whole brain section. [1]
(5) Immunofluorescence and TUNEL staining: At 3 days post‑MCAO, rats were perfused with paraformaldehyde; brain sections (30 μm) were stained with anti‑NeuN antibody (neuronal marker), followed by Cy3‑conjugated secondary antibody, then TUNEL staining was performed using a kit; images were captured and apoptotic neurons (NeuN⁺TUNEL⁺) were counted. [1]
(6) Tissue collection for biochemistry: Brain tissues were homogenized for determination of GSH‑PX and AChE activities using commercial kits. [1]

The manuscript does not provide original ADME or pharmacokinetic data for S-ORC. It cites previous work (Zhang et al., 2015a, 2015b) stating that S-ORC has higher absorption and slower elimination compared to the racemate oxiracetam, making it a better therapeutic agent, but no specific values (half-life, bioavailability, etc.) are given in this study. [1]

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[1]. S-oxiracetam ameliorates ischemic stroke induced neuronal apoptosis through up-regulating α7 nAChR and PI3K / Akt / GSK3β signal pathway in rats. Neurochem Int. 2018 May;115:50-60.

- S-ORC is the S-enantiomer of oxiracetam (ORC), a nootropic drug. Previous studies indicate that the desired pharmacological activities of oxiracetam reside almost exclusively in the S-enantiomer. [1]
- The study proposes that S-ORC exerts its neuroprotective effect by decreasing acetylcholinesterase (AChE) activity, thereby increasing acetylcholine (ACh) levels, which then activates α7 nAChR and the downstream PI3K/Akt/GSK3β signaling pathway, ultimately inhibiting neuronal apoptosis. This mechanism is supported by the fact that α7 nAChR siRNA silencing abolished the protective effects of S-ORC. [1]
- S-ORC also increased GSH-PX levels, suggesting an anti-oxidative stress effect. [1]
- The study concludes that S-ORC could be developed as an effective agent for preventing neuronal death after ischemic stroke. [1]

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(S)-Oxiracetam is the S‑enantiomer of the nootropic agent oxiracetam. This study reveals that its neuroprotective mechanism against ischemic stroke involves up‑regulation of α7 nAChR, which leads to activation of the PI3K/Akt/GSK3β signaling pathway, resulting in inhibition of neuronal apoptosis. S‑ORC also reduces AChE activity (thereby increasing acetylcholine levels) and enhances antioxidant capacity (increased GSH‑PX). The protective effect is dependent on α7 nAChR, as siRNA silencing abolished its efficacy. S‑ORC demonstrates both in vitro and in vivo efficacy in reducing infarct size, neurological deficits, and neuronal apoptosis. No FDA warnings or clinical indications are mentioned. [1]

C6H10N2O3

158.15

158.069

C, 62.75; H, 6.58; Br, 26.09; N, 4.57

88929-35-5

(R)-Oxiracetam;68252-28-8;Oxiracetam;62613-82-5

6603951

Typically exists as solid at room temperature

1.4±0.1 g/cm3

494.6±40.0 °C at 760 mmHg

252.9±27.3 °C

0.0±2.9 mmHg at 25°C

1.570

-2.48

2

3

2

11

192

1

C(N1C(=O)C[C@H](O)C1)C(=O)N

IHLAQQPQKRMGSS-BYPYZUCNSA-N

InChI=1S/C6H10N2O3/c7-5(10)3-8-2-4(9)1-6(8)11/h4,9H,1-3H2,(H2,7,10)/t4-/m0/s1

2-[(4S)-4-hydroxy-2-oxopyrrolidin-1-yl]acetamide

S-Oxiracetam (S)-ISF-2522 (S)-Oxiracetam

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~250 mg/mL (~1580.68 mM)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)