D-Lysine

D-Lysine is the D-enantiomer of L-Lysine (HY-N0469). It 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). In vitro, 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^[2]. In Vitro:D-Lysine (0.25-4.0 mM; 10-20 days) significantly inhibits the non-enzymatic binding of glucose to human albumin, IgG, collagen, and isolated human glomerular basement membrane in vitro. Its inhibitory effect is directly correlated with the concentration of D-Lysine and is enhanced with increasing glucose concentrations (statistically significant under 10 and 20 mM glucose conditions)^[2].
D-Lysine (0.25-2.0 mM; 10 days) reduces the formation of ketamines in human albumin (50 g/L) co-incubated with 10 mM glucose in a dose-dependent manner in vitro, and a linear correlation exists between the concentration of D-Lysine and the reduction in fructosamine levels^[2].
D-Lysine (0.25-2.0 mM; 10 days) inhibits non-enzymatic binding of glucose to human albumin at physiological concentration (50 g/L) in vitro. In undiluted samples, inhibitory effects are detectable at 0.25 mM, while in diluted samples, detection requires a concentration of 0.5 mM^[2]. In Vivo:D-Lysine (400-800 mg/kg; i.v.; single co-injection) reduces renal uptake of ¹¹¹In-DTPA (HY-B1335)-octreotide by over 50% across multiple time points without altering radiopharmaceutical distribution in receptor-positive organs^[1].
D-Lysine (400 mg/kg; i.v.; single co-injection) reduces renal uptake of ⁹⁰Y-DOTATOC (HY-106033) by 65% without altering radiopharmaceutical distribution in blood or somatostatin receptor-positive organs^[1].