| Identification | Back Directory | [Name]
L-Lysinamide, N-(3-methyl-1-oxobutyl)-L-α-aspartyl-L-threonyl-L-histidyl-L-phenylalanyl-L-prolyl-L-cysteinyl-L-isoleucyl-N6-[N-(1-oxohexadecyl)-L-γ-glutamyl]-L-lysyl-L-phenylalanyl-L-α-glutamyl-L-prolyl-L-arginyl-L-seryl-L-lysylglycyl-L-cysteinyl-, cyclic (6→16)-disulfide | [CAS]
1628323-80-7 | [Synonyms]
Rusfertide
L-Lysinamide, N-(3-methyl-1-oxobutyl)-L-α-aspartyl-L-threonyl-L-histidyl-L-phenylalanyl-L-prolyl-L-cysteinyl-L-isoleucyl-N6-[N-(1-oxohexadecyl)-L-γ-glutamyl]-L-lysyl-L-phenylalanyl-L-α-glutamyl-L-prolyl-L-arginyl-L-seryl-L-lysylglycyl-L-cysteinyl-, cyclic (6→16)-disulfide | [Molecular Formula]
C114H181N27O28S2 | [MOL File]
1628323-80-7.mol | [Molecular Weight]
2441.98 |
| Chemical Properties | Back Directory | [density ]
1.41±0.1 g/cm3(Predicted) | [form ]
Solid | [color ]
White to off-white | [Sequence]
{Asp(N-(3-methyl-1-oxobutyl))}-Thr-His-Phe-Pro-Cys-Ile-{Lys(γGlu-C16 acid)}-Phe-Glu-Pro-Arg-Ser-Lys-Gly-Cys-Lys-NH2 (disulfide bridge: Cys6-Cys16) |
| Hazard Information | Back Directory | [Uses]
Rusfertide is a peptide mimetic of natural hepcidin, which targets and degrades ferroportin, reduces serum iron and transferrin-saturation, and thus regulates the production of red blood cells. Rusfertide ameliorates the polycythemia vera, β-thalassemia and hereditary hemochromatosis[1][2]. | [in vivo]
Rusfertide limits the iron toxicity in red blood cells (RBCs) (1 mg/kg, s.c., once every two days, for 49 days) and transferrin-saturation (2.5 mg/kg, s.c., once every two days, for 2 weeks), improves oxygen carrying capacity of RBCs, attenuates the anemia and iron deposition in mice models for β-thalassemia and hereditary hemochromatosis[1]. | Animal Model: | Hbbth3/+ mice model for β-thalassemia and hereditary hemochromatosis[1] | | Dosage: | 1 and 2.5 mg/kg | | Administration: | s.c., once every two days, for 49 days (1 mg/kg); or for 2 weeks (2.5 mg/kg) | | Result: | Improved the survival rate of RBCs in β-thalassemia model.
Reduced transferrin-saturation and iron deposition. |
| [References]
[1] Taranath R, et al., Regulation of iron homeostasis by PTG-300 improves disease parameters in mouse models for beta-thalassemia and hereditary hemochromatosis[J]. Blood, 2019, 134: 3540.
[2] Kremyanskaya M, et al., PTG-300 eliminates the need for therapeutic phlebotomy in both low and high-risk polycythemia vera patients[J]. Blood, 2020, 136: 33-35. |
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YantaiBio
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