Glycine transporter type 1 (GlyT1) inhibitor; Positive allosteric modulator of NMDA receptors [1][2]

Sarcosine enhanced NMDA receptor-mediated excitatory postsynaptic field potentials (fEPSPs) in rat hippocampal slices. This potentiation was blocked by the NMDA antagonist AP5, confirming NMDA receptor dependence [2]

Sarcosine (100–300 μM) increased the amplitude and slope of fEPSPs in a concentration-dependent manner without affecting non-NMDA receptor-mediated responses [2]

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Commercial ergot supplements have been made from amino acids and their derivatives. They affect the release of anabolic hormones, the availability of fuel for activity, the ability to think clearly under pressure, and the prevention of muscular damage brought on by exertion. They are regarded as advantageous synergistic food ingredients [1].

In the pentylenetetrazol (PTZ)-induced seizure model, intraperitoneal Sarcosine (600 mg/kg) significantly delayed seizure onset latency (by 48%) and reduced mortality rate (from 100% to 30%) compared to controls [1]

In maximal electroshock (MES) tests, Sarcosine (600 mg/kg i.p.) decreased seizure duration by 35% and protected 40% of mice from tonic hindlimb extension [1]
The electroconvulsive threshold is markedly elevated by Sarcosine (400–800 mg/kg; ip) [2].

Animal/Disease Models: Albino Swiss mouse body weight (25-30 g)[2]
Doses: 100 mg/kg, 200 mg/kg, 400 mg/kg, 800 mg/kg
Route of Administration: intraperitoneal (ip) injection
Experimental Results: in mice MEST In trials, epilepsy thresholds were elevated at doses of 400 mg/kg and 800 mg/kg.

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For PTZ seizures: Mice received PTZ (85 mg/kg, s.c.) 30 min after Sarcosine (300 or 600 mg/kg, i.p.) dissolved in saline. Seizure latency and mortality were monitored for 30 min [1]

For MES seizures: Mice were pretreated with Sarcosine (600 mg/kg i.p.) 30 min before electrical stimulation (50 mA, 0.2 sec). Tonic extension duration and protection rates were recorded [1]

For hippocampal slice studies: Rats were sacrificed, and brain slices (400 μm) were perfused with artificial CSF. fEPSPs were evoked by Schaffer collateral stimulation [2]

Metabolism / Metabolites
Sarcosine is metabolized to glycine by sarcosine dehydrogenase, while glycine-N-methyltransferase converts glycine into sarcosine.

Toxicity Summary
Creatine is an oncogenic metabolite. Exogenous creatine appears to upregulate the expression of human epidermal growth factor receptor 2 (HER2/neu), a potent oncoprotein, in androgen-dependent prostate cancer cells. Therefore, creatine may induce prostate cancer progression by increasing HER2/neu expression. Toxicity Data
Not Applicable In mice, no death or behavioral toxicity (e.g., ataxia, sedation) was observed at anticonvulsant doses (≤600 mg/kg) [1]

[1]. Effects of sarcosine, a glycine transporter type 1 inhibitor, in two mouse seizure models. Pharmacol Rep. Mar-Apr 2010;62(2):392-7.

[2]. Effects of sarcosine and N, N-dimethylglycine on NMDA receptor-mediated excitatory field potentials. J Biomed Sci. 2017; 24: 18.

Hygroscopic crystals or powder. Slightly sweet taste. (NTP, 1992)
sarcosine is an N-methyl derivative of glycine, belonging to the N-alkylglycine family. It is an intermediate in the glycine metabolic pathway. It can act as an inhibitor of glycine transporter 1, a glycine receptor agonist, a human metabolite, an E. coli metabolite, and a mouse metabolite. It is an N-alkylglycine, N-methyl amino acid, belonging to the N-methylglycine family. It is the conjugate base of sarcosine salts and the conjugate acid of sarcosine acids. It is a zwitterion of sarcosine.
sarcosine has been studied for the treatment of schizophrenia.
sarcosine is present in or produced by E. coli (K12 strain, MG1655 strain).
sarcosine has been reported to exist in lancelet worms, fruit flies, and other organisms with relevant data.
sarcosine is an amino acid, an intermediate and byproduct of glycine synthesis and degradation, with potential antidepressant and antischizophrenic activity. Sarcosine is a product of dietary choline and creatine and is rapidly converted into glycine. Oral administration of sarcosine in combination with certain antipsychotic drugs can increase glycine concentration in the brain, thereby enhancing NMDA receptor activation and alleviating symptoms. Sarcosine is an N-methyl derivative of glycine. Sarcosine is metabolized to glycine by sarcosine dehydrogenase, while glycine-N-methyltransferase converts glycine back to sarcosine. Sarcosine is a natural amino acid found in muscles and other body tissues. In the laboratory, it can be synthesized from chloroacetic acid and methylamine. Sarcosine is naturally present in the process of choline metabolism to glycine. Sarcosine has a sweet taste and is readily soluble in water. It is used in the manufacture of biodegradable surfactants and toothpaste, among other applications. Sarcosine is widely found in organisms, including egg yolks, turkey, ham, vegetables, and legumes. Sarcosine is produced from dietary choline and methionine and is rapidly degraded into glycine. Creatine itself is non-toxic, as evidenced by the deficiency phenotype of sarcinemia (a congenital abnormality in sarcin metabolism). Sarcinemia can be caused by severe folate deficiency, as folate is required for the conversion of sarcin to glycine (Wikipedia). Sarcin has recently been identified as a biomarker for invasive prostate cancer. Studies have found that sarcin levels are significantly elevated during the progression of prostate cancer to metastasis and can be detected in urine. Sarcin levels are also elevated in invasive prostate cancer cell lines compared to benign prostatic epithelial cells (A3519). Sarcin is an amino acid intermediate in choline metabolism.

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sarcosine (N-methylglycine) is an endogenous glycine derivative that inhibits GlyT1, thereby increasing glycine levels in the synaptic cleft and enhancing NMDA receptor function [1][2]
It has shown anticonvulsant effects in pentylenetetrazol (PTZ) and maximal electroshock (MES) models, supporting its potential application in the treatment of epilepsy [1]
NMDA receptor enhancement suggests its potential application in neurological disorders involving NMDA dysfunction (e.g., schizophrenia) [2]
An amino acid intermediate in choline metabolism.

C3H8CLNO2

125.55

125.024

637-96-7

107-97-1; 2-(Methylamino)acetic acid-d3 hydrochloride;347840-04-4;2-(Methylamino)acetic acid-d5 hydrochloride;1219794-62-3

69483

White to off-white solid powder

1.48 g/cm3

195.1ºC at 760 mmHg

173-175 °C(lit.)

71.8ºC

0.483

3

3

2

7

52.8

0

Cl[H].O([H])C(C([H])([H])N([H])C([H])([H])[H])=O

WVKIFIROCHIWAY-UHFFFAOYSA-N

InChI=1S/C3H7NO2.ClH/c1-4-2-3(5)6;/h4H,2H2,1H3,(H,5,6);1H

2-(methylamino)acetic acid;hydrochloride

Sarcosine hydrochloride; Glycine, N-methyl-, hydrochloride; n-methylglycine hydrochloride; CCRIS 3353; Sarcosine, hydrochloride; EINECS 211-310-2; UNII-W50V8R1ZE9; ...; 637-96-7;

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

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.)