| Size | Price | |
|---|---|---|
| Other Sizes |
| Targets |
- Biological pathways involving amino acid metabolism, neurotransmitter synthesis, and phospholipid biosynthesis (e.g., conversion to glycine/cysteine, production of phosphatidylserine, synthesis of D-serine) (No IC50/Ki/EC50 data available; acts as an essential substrate for these physiological processes) [1]
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|---|---|
| ln Vitro |
The primary source of one-carbon groups needed for the de novo synthesis of deoxythymidine monophosphate and purine nucleotides is L-serine. Because insufficient amounts of L-serine and its metabolites cannot be produced, they are regarded conditionally essential amino acids in cell culture. L-serine and its metabolites have been shown to be important for both cell proliferation and particular activities of the central nervous system. [1].
- In primary cultures of rat hippocampal neurons, L-Serine (0.1-1 mM) promoted neuronal survival and reduced apoptosis induced by serum deprivation. At 0.5 mM, it increased neuron viability from 45% (serum-deprived group) to 82% (MTT assay) and decreased Annexin V-positive cells from 38% to 12% (flow cytometry). It also upregulated the expression of synaptic protein synaptophysin by 1.8-fold (Western blot) [1] - In rat astrocyte cultures, L-Serine (0.2-2 mM) enhanced phosphatidylserine (PS) biosynthesis. At 1 mM, it increased [³H]-serine incorporation into PS by 2.3-fold (radioisotope labeling assay) and upregulated the activity of serine palmitoyltransferase (a key enzyme in sphingolipid synthesis) by 40% (enzymatic assay) [1] - In human hepatocyte cell lines (HepG2), L-Serine (0.5-5 mM) protected against ethanol-induced oxidative stress. At 2 mM, it reduced intracellular reactive oxygen species (ROS) by 55% (DCFH-DA staining) and increased glutathione (GSH) levels by 1.6-fold (colorimetric assay), thereby inhibiting ethanol-induced hepatocyte necrosis [1] |
| ln Vivo |
- In L-serine-deficient mouse pups (induced by maternal diet lacking L-serine during gestation/lactation), oral supplementation of L-Serine (200 mg/kg/day) from postnatal day 1 to 21 reversed neurodevelopmental abnormalities. It restored brain weight (from 85% of normal to 98%), normalized hippocampal neuron density (from 70% to 96%), and improved motor coordination (rotarod test latency increased from 15 s to 48 s) [1]
- In a rat model of hepatic steatosis (induced by high-fat diet), L-Serine (500 mg/kg/day, oral gavage for 8 weeks) reduced liver triglyceride (TG) accumulation by 42% (from 180 mg/g liver to 104 mg/g liver) and decreased serum alanine transaminase (ALT) levels from 125 U/L to 68 U/L. Histological analysis showed reduced hepatic lipid droplets and inflammation [1] - In APP/PS1 transgenic mice (Alzheimer’s disease model), L-Serine (300 mg/kg/day, drinking water for 12 weeks) improved spatial memory (Morris water maze escape latency decreased from 62 s to 28 s) and reduced brain Aβ₄₂ deposition by 35% (immunohistochemistry). It also increased brain D-serine levels by 1.7-fold (HPLC) [1] |
| Enzyme Assay |
- For serine palmitoyltransferase (SPT) activity assay: Rat astrocyte lysates were incubated with L-Serine (0.1-2 mM), palmitoyl-CoA (50 μM), and pyridoxal 5'-phosphate (10 μM) in Tris-HCl buffer (pH 7.4) at 37°C for 60 minutes. The reaction was stopped by adding trichloroacetic acid (TCA), and the product 3-ketodihydrosphingosine was measured by fluorometric assay (excitation 340 nm, emission 450 nm). SPT activity was calculated as nmol product formed per mg protein per hour [1]
- For glutathione (GSH) synthesis assay: HepG2 cell lysates were treated with L-Serine (0.5-5 mM) and cysteine (0.2 mM) in phosphate-buffered saline (PBS) at 37°C for 30 minutes. GSH levels were detected by reacting with 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB), and absorbance was measured at 412 nm. GSH concentration was calculated using a standard curve [1] |
| Cell Assay |
- Primary hippocampal neuron survival assay: Hippocampi were dissected from E18 rat embryos, and neurons were isolated by trypsin digestion and plated on poly-L-lysine-coated 96-well plates. After 3 days in culture, medium was replaced with serum-free medium containing L-Serine (0.1-1 mM) for 48 hours. Neuron viability was measured by MTT assay (490 nm absorbance). For apoptosis detection, neurons were stained with Annexin V-FITC/PI and analyzed by flow cytometry [1]
- Astrocyte phosphatidylserine (PS) biosynthesis assay: Rat astrocytes were seeded in 6-well plates and labeled with [³H]-serine (1 μCi/mL) in medium containing L-Serine (0.2-2 mM) for 24 hours. Cells were lysed, and lipids were extracted with chloroform/methanol (2:1, v/v). PS was separated by thin-layer chromatography (TLC), and radioactivity was counted by liquid scintillation spectrometry to calculate [³H]-serine incorporation into PS [1] |
| Animal Protocol |
- L-serine-deficient mouse pup supplementation experiment: Female C57BL/6 mice were fed a L-serine-free diet from gestation day 0 to lactation day 21. Pups (n=10 per group) were orally gavaged with L-Serine (200 mg/kg/day, dissolved in 0.9% saline) or saline from postnatal day 1 to 21. On postnatal day 21, pups were euthanized; brain weight was measured, and hippocampal neuron density was analyzed by hematoxylin-eosin staining. Motor coordination was evaluated by rotarod test (5 rpm, 60 s cut-off) on postnatal day 18 [1]
- Rat hepatic steatosis treatment experiment: Male Sprague-Dawley rats (250-300 g, n=8 per group) were fed a high-fat diet (45% fat) for 4 weeks to induce steatosis. They were then treated with L-Serine (500 mg/kg/day, dissolved in 0.9% saline) or saline via oral gavage for 8 weeks. Blood samples were collected every 2 weeks to measure serum ALT. At the end of treatment, rats were euthanized; liver TG content was measured by enzymatic assay, and liver histology was examined by Oil Red O staining [1] |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Serine is present in acidic mucopolysaccharides in patients aged 2–9 years. Excessive accumulation and excretion of mucopolysaccharides in urine may be associated with abnormal binding between mucopolysaccharides and proteins. In children aged 2–9 years, urinary serine excretion increased from 0.059–0.162 μmol/24 h, and plasma serine levels increased from 0.102–0.158 μmol/mL. In children aged 2–9 years, serine may not be esterified with acidic mucopolysaccharides via its β-hydroxyl group, but rather linked via its carboxyl group. Measurement of serine levels in 13 regions of the rat cerebral cortex showed no significant differences in amino acid content across different functional regions. - In Sprague-Dawley rats, oral administration of L-serine (500 mg/kg) showed rapid absorption: Tmax = 1.2 h, Cmax = 125 μg/mL, AUC₀₋₈h = 480 μg·h/mL. Oral bioavailability was approximately 90% (compared to intravenous administration). It is widely distributed in various tissues, with brain tissue concentrations reaching approximately 35% of plasma concentrations 2 hours after administration [1] - L-serine is primarily metabolized in the liver and kidneys: approximately 60% is converted to glycine via serine hydroxymethyltransferase, and approximately 25% is used to synthesize cysteine. The elimination half-life (t1/2) is approximately 1.8 h, and approximately 85% of the metabolites are excreted in the urine within 24 hours (primarily in the form of urea and amino acid derivatives) [1] |
| Toxicity/Toxicokinetics |
Toxicity Summary
L-serine plays a role in cell growth and development (cell proliferation). Serine hydroxymethyltransferase converts L-serine to glycine, forming the one-carbon unit required for the synthesis of the purine bases adenine and guanine. These bases, linked to phosphate esters of pentose sugars, are essential components of DNA and RNA, and are also the final products of energy metabolism pathways, ATP and GTP. Furthermore, the conversion of L-serine to glycine via this enzyme provides the one-carbon unit required for the synthesis of the pyrimidine nucleotide deoxythymidine monophosphate, also an important component of DNA. Interactions Intraventricular injection of alanine (0.5–2.0 μg) into the brain of rabbits resulted in a decrease in body temperature at 10°C. This effect was slightly less than the additive effect of serine. Erythroblastic leukemia cells incubated in a medium containing the essential amino acid L-serine bound approximately 30% more iodine-labeled insulin (125I) than cells incubated in a medium without serine. - Acute toxicity: In ICR mice, the oral LD50 of L-serine was >5000 mg/kg; no death or toxic symptoms (sleepiness, ataxia) were observed at doses up to 5000 mg/kg [1] - Subacute toxicity: Sprague-Dawley rats were orally administered L-serine (500, 1000, 2000 mg/kg/day) for 4 weeks. No significant changes in body weight, food intake, or organ weight (liver, kidney, brain) were observed. Serum biochemical parameters (ALT, AST, BUN, creatinine) and hematological parameters (erythrocytes, leukocytes, platelets) were within the normal range. No plasma protein binding data were reported (because L-serine exists mainly in free form in plasma) [1] |
| References | |
| Additional Infomation |
Pharmacodynamics
Serine is classified as a non-essential amino acid. Serine is essential for the production of proteins, enzymes and muscle tissue in the human body. Serine is necessary for the normal metabolism of fats and fatty acids. It also helps in the production of antibodies. Serine is used as a natural moisturizer in some cosmetics and skin care products. The main source of essential amino acids is diet, while non-essential amino acids are usually synthesized by humans and other mammals using common intermediates. - L-serine is a non-essential amino acid in the human body (endogenously synthesized through the glycolytic intermediate 3-phosphoglycerate), but becomes an essential amino acid in cases of impaired synthesis (e.g., liver disease, hereditary diseases) [1]. - Its therapeutic potential includes: 1) neuroprotection (supporting neuronal survival and improving cognitive function in neurodegenerative diseases); 2) liver protection (reducing steatosis and oxidative stress); 3) supporting fetal/neonatal neurodevelopment (preventing abnormalities in L-serine deficiency) [1] - L-serine is a precursor of D-serine (a co-agonist of NMDA receptors), phosphatidylserine (a key membrane phospholipid), and glutathione (an antioxidant), which endows L-serine with a variety of biological activities [1] |
| Molecular Formula |
C3H7NO3
|
|---|---|
| Molecular Weight |
105.0926
|
| Exact Mass |
105.042
|
| CAS # |
56-45-1
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| Related CAS # |
L-Serine-13C3;201595-68-8;L-Serine-13C;89232-77-9;L-Serine-15N;59935-32-9;L-Serine-d7;935275-35-7;L-Serine-1-13C;81201-84-5;L-Serine-13C3,15N;202407-34-9;L-Serine-d3;105591-10-4;L-Serine-15N,d3;L-Serine-13C3,15N,d3;1994299-33-0;L-Serine-2-13C;89232-76-8;L-Serine1-13C,15N;2483830-04-0;L-Serine-d2;95034-57-4;L-Serine-15N,d3
|
| PubChem CID |
5951
|
| Appearance |
White to off-white solid powder
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| Density |
1.6
|
| Boiling Point |
394.8±32.0 °C at 760 mmHg
|
| Melting Point |
222ºC
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| Flash Point |
192.6±25.1 °C
|
| Vapour Pressure |
0.0±2.1 mmHg at 25°C
|
| Index of Refraction |
1.519
|
| LogP |
-1.58
|
| Hydrogen Bond Donor Count |
3
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
2
|
| Heavy Atom Count |
7
|
| Complexity |
72.6
|
| Defined Atom Stereocenter Count |
1
|
| SMILES |
C([C@@H](C(=O)O)N)O
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| InChi Key |
MTCFGRXMJLQNBG-REOHCLBHSA-N
|
| InChi Code |
InChI=1S/C3H7NO3/c4-2(1-5)3(6)7/h2,5H,1,4H2,(H,6,7)/t2-/m0/s1
|
| Chemical Name |
(2S)-2-amino-3-hydroxypropanoic acid
|
| 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)
|
| Solubility (In Vitro) |
H2O : ~50 mg/mL (~475.78 mM)
Methanol :< 1 mg/mL |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 100 mg/mL (951.57 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 9.5157 mL | 47.5783 mL | 95.1565 mL | |
| 5 mM | 1.9031 mL | 9.5157 mL | 19.0313 mL | |
| 10 mM | 0.9516 mL | 4.7578 mL | 9.5157 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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