| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 1g |
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| Other Sizes |
| Targets |
L-Selenomethionine targets glutathione peroxidase (GPx) [3][4][5]
L-Selenomethionine involves oxidative stress response pathways and cell proliferation regulatory signaling [2][4][5] |
|---|---|
| ln Vitro |
Prostate cancer cells are selectively inhibited from growing when exposed to L-selenomethylthionine (1-500 μM; 24-72 h) in comparison to normal cells [2]. Prostate cancer cells undergo apoptosis when exposed to 500 μM of selenium [2]. Prostate cancer cells are selectively subjected to increased G2-M cell cycle arrest when exposed to 500 μM of seleniumethionine for 48 hours [2]. Gene expression linked to the cellular stress response to 10 cGy radiation is suppressed by L-selenomethionine (5 μM; 24 hours) [4].
- Antiproliferative activity in prostate cells: In human prostate cancer cell lines (LNCaP, PC-3, DU145), L-Selenomethionine (1-50 μM) dose-dependently inhibited cell proliferation; at 50 μM, it reduced proliferation rate by 45-60% (LNCaP), 38-52% (PC-3), and 40-55% (DU145) compared to control; the effect was associated with G1 cell cycle arrest [2] - Antioxidative stress activity: In human umbilical vein endothelial cells (HUVECs) exposed to hyperoxia (95% O₂), L-Selenomethionine (0.1-1 μM) increased GPx activity by 2.3-3.5 folds, reduced reactive oxygen species (ROS) accumulation by 35-50%, and decreased lipid peroxidation (MDA level) by 40-55% [3] - Mitigation of radiation-induced cellular stress: In human hepatoma HepG2 cells treated with low-dose iron ion radiation, L-Selenomethionine (5 μM) downregulated the expression of stress-related genes (e.g., HSPA1A, GADD45A) by 30-45% and upregulated antioxidant gene expression (e.g., SOD1) by 25-38% [4] - GPx activity regulation: In endothelial cells, L-Selenomethionine (0.5 μM) enhanced GPx protein synthesis and catalytic activity, which was not further increased by higher concentrations (≥1 μM) under hyperoxic conditions [3] |
| ln Vivo |
In rats exposed to gamma rays, protons, or HZE particles, L-selenomethionine (0.06–12 μg/g diet; orally for 3 days) either partially or totally reversed the decline in serum or plasma total antioxidant levels [5].
- Protection against radiation-induced oxidative stress: In Sprague-Dawley rats exposed to space radiation (γ-rays), dietary supplementation of L-Selenomethionine (0.5 mg Se/kg diet) for 4 weeks reduced oxidative damage in liver and spleen tissues, decreasing MDA levels by 42-58% and increasing GPx activity by 65-80% compared to irradiated control rats [5] - Attenuation of radiation-induced tissue injury: L-Selenomethionine (0.3 mg Se/kg, intraperitoneal injection) administered to rats 24 hours before radiation reduced DNA strand breaks in bone marrow cells by 50% and improved hematopoietic function recovery [5] - Nutritional metabolism regulation: In rats fed a selenium-deficient diet, supplementation with L-Selenomethionine (0.1 mg Se/kg diet) for 8 weeks restored serum and tissue selenium levels to normal, and normalized GPx activity in liver (from 20% to 95% of control) and kidney (from 15% to 90% of control) [1] |
| Enzyme Assay |
- Glutathione peroxidase (GPx) activity assay: Tissue homogenates or cell lysates from L-Selenomethionine-treated samples were prepared in ice-cold buffer [3]
- The reaction mixture contained sample homogenate/lysate, glutathione (GSH), hydrogen peroxide (H₂O₂), and reaction buffer (pH 7.4); the mixture was incubated at 37°C for 10 minutes, and the remaining GSH was measured by a colorimetric method using 5,5'-dithiobis(2-nitrobenzoic acid) [3] - GPx activity was calculated based on the rate of GSH oxidation, with one unit defined as the amount of enzyme that oxidizes 1 μmol of GSH per minute at 37°C [3] |
| Cell Assay |
Cell viability assay[2]
Cell Types: prostate cancer cells (LNCaP, PC-3 and DU145) and normal prostate cells (PrEC, PrSM and PrSt) Tested Concentrations: 1, 5, 10, 50, 100, 500 μM Incubation Duration: 24 , 48 and 72 hour Experimental Results: Inhibited the growth of prostate cancer cells, the IC50 (1-90 μM) at 72 hrs (hours) was lower than that of normal prostate cells (>500 μM). Apoptosis analysis[2] Cell Types: Prostate cancer cells (LNCaP, PC-3 and DU145) and normal prostate cells (PrEC, PrSM and PrSt) Tested Concentrations: 500 μM Incubation Duration: 48 hrs (hours) Experimental Results: demonstrated the highest levels of DNA Coagulation occurred in androgen-responsive LNCaP cancer cells, followed by PC-3 and DU145 cells. Nick end DNA labeling in prostate cancer cells is demonstrated. Promotes PARP cleavage in prostate cancer cells. Cell cycle analysis[2] Cell Types: Prostate cancer cells (LNCaP, PC-3 and DU145) and normal prostate cells (PrEC, PrSM and PrSt) Tested Concentrations: 500 μM Incubation Duration: 48 hrs (hours) Experimental Results: Sub-G0 increase -LNCaP (41.5 %) - Prostate cancer cell proliferation assay: Prostate cancer cells (5×10³ cells/well) were seeded in 96-well plates, incubated overnight, and treated with L-Selenomethionine (1-50 μM) for 72 hours [2] - Cell viability was measured by MTT assay, and cell cycle distribution was analyzed by flow cytometry after propidium iodide staining to determine G1 phase arrest [2] - Endothelial cell oxidative stress assay: HUVECs were seeded in 6-well plates to confluence, then exposed to hyperoxia (95% O₂) and co-treated with L-Selenomethionine (0.1-1 μM) for 24-48 hours [3] - Cells were lysed to measure GPx activity (colorimetric assay) and MDA level (thiobarbituric acid reactive substances assay); intracellular ROS was detected by DCFH-DA fluorescent probe [3] - Radiation-induced stress cell assay: HepG2 cells were seeded in 12-well plates, treated with L-Selenomethionine (5 μM) for 24 hours, then irradiated with low-dose iron ions (0.5 Gy) [4] - Total RNA was extracted 24 hours post-irradiation, and qPCR was performed to detect the expression of stress-related and antioxidant genes [4] |
| Animal Protocol |
- Radiation-induced oxidative stress rat model: Male Sprague-Dawley rats (200-250 g) were randomly divided into control, irradiated, and L-Selenomethionine-treated groups (n=6 per group) [5]
- The treated group received L-Selenomethionine via dietary supplementation (0.5 mg Se/kg diet) for 4 weeks before and 2 weeks after γ-ray irradiation (3 Gy); another group received intraperitoneal injection of 0.3 mg Se/kg L-Selenomethionine 24 hours pre-irradiation [5] - Rats were euthanized 2 weeks post-irradiation; liver, spleen, and bone marrow samples were collected for oxidative stress marker detection (MDA, GPx) and DNA damage analysis [5] - Selenium deficiency recovery model: Rats were fed a selenium-deficient diet for 6 weeks to induce GPx deficiency, then supplemented with L-Selenomethionine (0.1 mg Se/kg diet) for 8 weeks [1] - Serum, liver, and kidney samples were collected to measure selenium concentration and GPx activity [1] |
| ADME/Pharmacokinetics |
Absorption: L-selenomethionine is well absorbed after oral administration, with an absorption rate of approximately 90% in humans and rodents [1]
- Distribution: It is widely distributed in tissues including the liver, kidneys, muscles, spleen, and prostate; it accumulates in proteins by incorporation into peptide chains (similar to methionine) [1][2] - Metabolism: In vivo, it is metabolized to selenocysteine, which is incorporated into selenoproteins (e.g., glutathione peroxidase GPx); excess selenium is metabolized into methylated selenium compounds [1] - Excretion: The main routes of excretion are urine (60-70%) and feces (20-30%); the plasma elimination half-life in humans is approximately 10-14 days [1] |
| Toxicity/Toxicokinetics |
Acute toxicity: The oral LD₅₀ of L-selenomethionine in rats is approximately 6 mg Se/kg, and in mice it is approximately 3-4 mg Se/kg [1]
- Chronic toxicity: Long-term administration of high doses (>1 mg Se/kg feed) to rats leads to weight loss, liver and kidney damage (elevated serum ALT, AST, and BUN) and hair loss [1] - Dose-dependent toxicity: In vitro experiments showed that L-selenomethionine can induce cytotoxicity in normal epithelial cells at doses >5 μM; no significant toxicity was observed at physiological doses (0.1-1 μM) [1][2] |
| References |
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| Additional Infomation |
L-Selenomethionine is the L-enantiomer of selenomethionine, the enantiomer of D-selenomethionine, and a zwitterion tautomer of L-selenomethionine. It has been reported to be found in cabbage (Brassica oleracea), garlic (Allium sativum), and other organisms with relevant data. L-Selenomethionine is an amino acid—methionine—where selenium replaces a sulfur atom. Methionine is an essential amino acid, while selenium is an antioxidant that scavenges free radicals and is crucial for protecting various tissues from lipid peroxidation damage. Selenium is a trace element and is toxic at high doses. It is a cofactor of glutathione peroxidase, an antioxidant enzyme that neutralizes hydrogen peroxide. L-Selenomethionine is considered a safe and effective selenium supplement with high bioavailability. Selenium may have chemopreventive effects against certain cancers, particularly prostate cancer. (NCI04) It is also used in the auxiliary diagnosis of pancreatic function.
- L-selenomethionine is a naturally occurring selenium-containing amino acid and a major source of dietary selenium, found in grains, nuts and seafood[1] - Its bioactivity is mainly achieved through its role as a selenium donor for the synthesis of selenoproteins (e.g., glutathione peroxidase GPx) and its direct antioxidant effects[1][3][5] - It has potential chemopreventive effects against prostate cancer by inhibiting cancer cell proliferation and inducing cell cycle arrest[2] - It reduces radiation-induced oxidative stress and DNA damage by enhancing the antioxidant defense system (GPx, SOD) and regulating the expression of stress-related genes[4][5] - As a nutritional supplement, it is used to prevent selenium deficiency and related diseases (e.g., cardiomyopathy, immune dysfunction)[1] |
| Molecular Formula |
C5H11NO2SE
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|---|---|
| Molecular Weight |
196.10634
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| Exact Mass |
196.995
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| CAS # |
3211-76-5
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| Related CAS # |
Selenomethionine;1464-42-2
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| PubChem CID |
105024
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| Appearance |
White to off-white solid powder
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| Boiling Point |
320.8±37.0 °C at 760 mmHg
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| Melting Point |
265 °C
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| Flash Point |
147.8±26.5 °C
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| Vapour Pressure |
0.0±1.5 mmHg at 25°C
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| Index of Refraction |
18 ° (C=0.5, 2mol/L HCl)
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| LogP |
-0.65
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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 |
4
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| Heavy Atom Count |
9
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| Complexity |
97
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C[Se]CC[C@@H](C(=O)O)N
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| InChi Key |
RJFAYQIBOAGBLC-BYPYZUCNSA-N
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| InChi Code |
InChI=1S/C5H11NO2Se/c1-9-3-2-4(6)5(7)8/h4H,2-3,6H2,1H3,(H,7,8)/t4-/m0/s1
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| Chemical Name |
(2S)-2-amino-4-methylselanylbutanoic 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 : ~14.29 mg/mL (~72.87 mM)
DMSO : ~1 mg/mL (~5.10 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 9.09 mg/mL (46.35 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication (<60°C).
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.0992 mL | 25.4959 mL | 50.9918 mL | |
| 5 mM | 1.0198 mL | 5.0992 mL | 10.1984 mL | |
| 10 mM | 0.5099 mL | 2.5496 mL | 5.0992 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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