| Size | Price | Stock | Qty |
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| 10g |
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| Other Sizes |
| Targets |
(S)-2-Allylglycine targets glutamic acid decarboxylase (GAD), the key enzyme responsible for the biosynthesis of gamma-aminobutyric acid (GABA) from glutamic acid. GAD is a rate-limiting enzyme in GABA synthesis, and its inhibition leads to depletion of GABA in the brain. By inhibiting GAD, (S)-2-Allylglycine reduces GABA levels, which can result in seizures and neuronal damage. The compound's mechanism of action involves competitive inhibition of the enzyme's active site, preventing the decarboxylation of glutamic acid. This inhibition disrupts the balance between excitatory and inhibitory neurotransmission, leading to increased neuronal excitability. The compound is used in research to study the role of GABA in epilepsy and other neurological disorders.
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| ln Vitro |
In vitro, (S)-2-Allylglycine inhibits glutamic acid decarboxylase (GAD) activity in a concentration-dependent manner. The compound's inhibitory effect on GAD has been demonstrated in various in vitro systems, including brain homogenates and purified enzyme preparations. By inhibiting GAD, (S)-2-Allylglycine reduces GABA production in vitro, providing a model for studying the effects of GABA depletion on neuronal function. The compound has been used in studies investigating the role of GABA in seizure generation and epileptogenesis. Its potency as a GAD inhibitor makes it a valuable tool for studying GABAergic neurotransmission and the pathophysiology of epilepsy. The compound is also used in research on treatment-resistant seizures.
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| ln Vivo |
In vivo, (S)-2-Allylglycine causes GABA depletion, seizures, and neuronal damage when administered to animals. The compound is used in research on treatment-resistant seizures in epilepsy. In animal models, administration of (S)-2-Allylglycine leads to a dose-dependent decrease in brain GABA levels, which is associated with the onset of seizures. The compound's effects on GABA levels and seizure activity have been studied in various animal species, including rodents. These studies have contributed to understanding the role of GABA in seizure generation and the mechanisms of action of antiepileptic drugs. The compound is also used to study the neuroprotective effects of GABA-enhancing agents in models of seizure-induced neuronal damage.
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| Enzyme Assay |
In vitro assays for (S)-2-Allylglycine typically involve measuring the inhibition of glutamic acid decarboxylase (GAD) activity. The compound is dissolved in appropriate buffer (e.g., phosphate buffer, pH 7.4) at concentrations ranging from 0.1-10 mM. GAD activity is measured by quantifying the production of GABA from glutamic acid using radiometric, fluorometric, or HPLC-based methods. The reaction mixture contains GAD enzyme, substrate (glutamic acid), pyridoxal phosphate (cofactor), and varying concentrations of (S)-2-Allylglycine. The reaction is incubated at 37°C for 30-60 minutes, and the amount of GABA produced is measured. IC50 values are calculated by plotting the percentage of inhibition against the compound concentration. The compound's solubility in water is limited (<1 mg/ml), so DMSO may be used for stock solutions.
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| Cell Assay |
In vitro cell-based assays using (S)-2-Allylglycine are conducted in neuronal cell cultures to study GABA depletion and its effects on neuronal function. Primary neuronal cultures or cell lines expressing GAD are treated with various concentrations of (S)-2-Allylglycine (typically 0.1-5 mM) for 24-72 hours. GABA levels in cell lysates or culture media are measured using ELISA, HPLC, or mass spectrometry. Cell viability is assessed using MTT or LDH assays to determine the cytotoxic effects of GABA depletion. Neuronal activity can be monitored using calcium imaging or electrophysiological recordings to assess the functional consequences of reduced GABA levels. The compound is typically dissolved in DMSO and diluted in cell culture medium, with final DMSO concentrations kept below 0.1%.
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| Animal Protocol |
In vivo animal experiments with (S)-2-Allylglycine are conducted in rodent models to study GABA depletion-induced seizures and neuronal damage. The compound is typically administered intraperitoneally or intracerebroventricularly at doses ranging from 50-200 mg/kg. After administration, animals are monitored for seizure activity using behavioral observation or EEG recording. Brain GABA levels are measured at various time points after administration using HPLC or mass spectrometry. Neuronal damage is assessed by histopathological examination of brain sections using stains such as Nissl or Fluoro-Jade B. The compound is used to model epilepsy and evaluate the efficacy of potential antiepileptic drugs that enhance GABAergic neurotransmission. Dosing formulations typically involve dissolving the compound in saline or PBS.
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| ADME/Pharmacokinetics |
(S)-2-Allylglycine is administered intraperitoneally or intracerebroventricularly in animal studies at doses typically ranging from 50-200 mg/kg. The compound has limited aqueous solubility (<1 mg/ml), so it is often dissolved in DMSO or saline with sonication. Pharmacokinetic studies in rodents show that the compound is rapidly absorbed after intraperitoneal administration and reaches the brain where it inhibits GAD. The compound's effects on GABA levels are dose-dependent and correlate with seizure severity. The half-life of (S)-2-Allylglycine in the brain is approximately 1-2 hours, and GABA levels begin to recover within 4-6 hours after administration. The compound is metabolized and excreted primarily through renal pathways. For long-term storage, the powder is kept at -20°C for up to 3 years.
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| Toxicity/Toxicokinetics |
The toxicity of (S)-2-Allylglycine is primarily related to its mechanism of action as a GAD inhibitor, which causes GABA depletion and seizures. In animal studies, administration of the compound leads to dose-dependent seizure activity and neuronal damage. The compound is used as a research tool to model epilepsy and study the pathophysiology of seizure-induced neuronal injury. At high doses, (S)-2-Allylglycine can cause status epilepticus and neuronal death, particularly in vulnerable brain regions such as the hippocampus. The compound's toxicity is mediated by the reduction of GABA levels, which leads to excessive excitatory neurotransmission and excitotoxicity. The compound is intended for research use only and is not for human use. Standard laboratory safety precautions should be followed when handling the compound.
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| Additional Infomation |
L-Allylglycine is an organic molecular entity.
(S)-2-Allylglycine (CAS 16338-48-0) is also known as L-Allylglycine and (S)-(-)-2-Amino-4-pentenoic acid. It has the molecular formula C5H9NO2 and a molecular weight of 115.13 g/mol. The compound is a potent inhibitor of glutamic acid decarboxylase (GAD), the key enzyme in GABA biosynthesis. It causes GABA depletion, seizures, and neuronal damage, and is used in research on treatment-resistant seizures in epilepsy. The compound is a peptide derivative and a bioactive peptide analogue. Its SMILES code is C=CC[C@H](N)C(O)=O. The compound is stored as a powder at -20°C for up to 3 years or in solvent at -80°C for up to 6 months. It is intended for research use only. |
| Molecular Formula |
C5H9NO2
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|---|---|
| Molecular Weight |
115.1305
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| Exact Mass |
115.063
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| CAS # |
16338-48-0
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| PubChem CID |
167529
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| Appearance |
White to off-white solid powder
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| Density |
1.0±0.1 g/cm3
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| Boiling Point |
222.7±23.0 °C at 760 mmHg
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| Melting Point |
283 °C (dec.)(lit.)
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| Flash Point |
88.5±22.6 °C
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| Vapour Pressure |
0.0±0.9 mmHg at 25°C
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| Index of Refraction |
1.461
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| LogP |
-0.06
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
8
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| Complexity |
101
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C=CC[C@@H](C(=O)O)N
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| InChi Key |
WNNNWFKQCKFSDK-BYPYZUCNSA-N
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| InChi Code |
InChI=1S/C5H9NO2/c1-2-3-4(6)5(7)8/h2,4H,1,3,6H2,(H,7,8)/t4-/m0/s1
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| Chemical Name |
(2S)-2-aminopent-4-enoic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~50 mg/mL (~434.29 mM)
DMSO :< 1 mg/mL |
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| Solubility (In Vivo) |
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.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 8.6858 mL | 43.4292 mL | 86.8583 mL | |
| 5 mM | 1.7372 mL | 8.6858 mL | 17.3717 mL | |
| 10 mM | 0.8686 mL | 4.3429 mL | 8.6858 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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