D-Lysine-d8 dihydrochloride
D-Lysine-d8 dihydrochloride is the d8-labeled D-Lysine (HY-Y1091). D-Lysine is the D-enantiomer of L-Lysine (HY-N0469). D-Lysine is metabolically inert and not utilized for protein synthesis by mammalian ribosomes. D-Lysine blocks renal uptake of 111In/90Y-Octreotide (HY-P0036)-based probes without inhibiting uptake by tumor/receptor tissues, and thus acts as a renoprotective agent in diagnostic imaging and peptide receptor radionuclide therapy (PRRT). D-Lysine specifically inhibits the early steps of non-enzymatic glycation by competing with glucose via its free amino group, theoretically, it can serve as a glycation competitor that "does not interfere with protein synthesis" under chronic hyperglycemia in diabetes. D-Lysine can be used in research related to cancer and diabetes.
For research use only. We do not sell to patients.
- Formula: C6H8D8Cl2N2O2
- Molecular Weight:227.16
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Storage:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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Unlabeled CAS 10303-72-7
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Appearance Solid
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Molecular Weight 227.16
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Formula C6H8D8Cl2N2O2
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Color White to off-white
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SMILES
N[C@H](C([2H])([2H])C([2H])([2H])C([2H])([2H])C([2H])([2H])N)C(O)=O.Cl.Cl
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Protocols
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
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Data Sheet (270 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
D-Lysine-d8 dihydrochloride Related Classifications
HY-W035399S Related Classifications
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