Structure

L-(+)-Ergothioneine (>98%)

CAS
497-30-3
Catalog Number
ALC-FP-497303
Category
Featured Products
Molecular Weight
229.30 g/mol
Molecular Formula
C9H15N3O2S

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Specification

Melting Point
270 - 271 °C
Appearance
White crystals
Assay
≥ 99.9% (HPLC)
Bulk Density
0.55 - 0.75 g/mL
D50
50 mesh pass rate 100%
Drying Loss
< 0.5% (105 °C, 2h)
Odor
Characteristic
Optical Rotation
[ɑ]D≥(+)122° (c=1, H2O)
pH
6.0-7.5 (50 mg/mL, 20 °C)
Sample Lot No.
A24Q0821
Total Solvent Residue
≤ 200 ppm

L-Ergothioneine Protects Retinal Pigment Epithelial Cells through NRF2-Mediated Antioxidant Mechanisms

Screening and evaluation of antioxidants for retinal pigment epithelial cell protection: L-ergothioneine as a novel therapeutic candidate through NRF2 activation Gu S, et al. Experimental Eye Research, 2024, 242, 109862.

L-Ergothioneine (EGT) was evaluated for its protective role against oxidative stress-induced injury in retinal pigment epithelial (RPE) cells. In vitro, RPE cells exposed to sodium iodate were treated with EGT, which significantly reduced oxidative damage and preserved redox homeostasis. Transcriptomic analysis revealed that EGT counteracted stress-induced gene dysregulation and upregulated antioxidant-related genes. In vivo, mice subjected to oxidative stress exhibited preserved retinal structure following EGT administration. Mechanistic studies confirmed that inhibition of NRF2 signaling abolished EGT's cytoprotective effect, demonstrating that EGT mitigates oxidative stress via NRF2 activation, highlighting its potential as a novel therapeutic antioxidant for age-related macular degeneration.

Ergothioneine Enhances Mitochondrial Function via Activation of MPST

Ergothioneine controls mitochondrial function and exercise performance via direct activation of MPST Sprenger H-G, et al. Cell Metabolism, 2025, 37(4), 857-869.e9

Ergothioneine (EGT) was investigated for its role in regulating mitochondrial metabolism during exercise. Using metabolomic and proteomic analyses of exercised mouse muscle, researchers observed that EGT selectively accumulated in mitochondria following training. Proteome-wide thermal stability assays identified 3-mercaptopyruvate sulfurtransferase (MPST) as a direct molecular target of EGT. Biochemical assays confirmed that EGT binding enhanced MPST catalytic activity, leading to elevated mitochondrial respiration and improved exercise endurance in vivo. These findings demonstrate that EGT directly modulates mitochondrial bioenergetics through MPST activation, defining the EGT-MPST axis as a key mechanism underlying enhanced muscular performance.

Ergothioneine Attenuates Cisplatin-Induced AKI-CKD Transition via Complement and Antioxidant Regulation

Proteomic analysis reveals the potential mechanism of ergothioneine in preventing acute kidney injury to chronic kidney disease transition Peng J, et al. Archives of Biochemistry and Biophysics, 2025, 772, 110534.

In a cisplatin-induced acute kidney injury to chronic kidney disease (AKI-CKD) mouse model, ergothioneine (EGT) demonstrated potent renal protection. Mice received multiple low doses of cisplatin, followed by EGT administration. Biochemical assays and histopathological analysis revealed significant recovery of renal structure and function. Proteomic profiling identified 35 differentially expressed proteins, while GO and KEGG enrichment analyses highlighted complement activation as a major regulatory pathway. Network pharmacology, molecular docking, and Western blot confirmed C4B and PON1 as core EGT targets. These results suggest EGT mitigates AKI-CKD progression by enhancing antioxidant defenses and modulating complement-mediated injury.

Ergothioneine as a Therapeutic Antioxidant in Metabolic Disease Research

The roles and functions of ergothioneine in metabolic diseases Wen T, et al. The Journal of Nutritional Biochemistry, 2025, 141, 109895.

Ergothioneine (EGT) has been experimentally investigated for its therapeutic potential in metabolic disorders. In vitro and in vivo assays employed high-performance liquid chromatography (HPLC) to quantify EGT uptake via the OCTN1 transporter in intestinal epithelial cells, followed by distribution analysis in hepatic and renal tissues. Cellular assays assessed its antioxidant and anti-inflammatory effects through ROS quantification and cytokine profiling. Animal models of obesity and diabetes further demonstrated EGT's modulation of oxidative stress and apoptosis. These experiments collectively confirmed EGT's biochemical role in mitigating metabolic dysfunction and its promise as a metabolic disease modulator.

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