2. Stem Cell/Wnt TGF-beta/Smad
  3. TGF-beta/Smad
  4. Luspatercept (mIgG2a)

Luspatercept (mIgG2a)  (Synonyms: RAP-536)

Cat. No.: HY-P99720A
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Luspatercept (mIgG2a) (RAP-536) is a fusion protein, consisting of a modified extracellular domain of human ActRIIB linked to the murine IgG2a Fc domain. Luspatercept (mIgG2a) inhibits Smad2/3 signaling, promotes differentiation of late-stage erythroid precursors and mitigates ineffective erythropoiesis (IE) in murine β-thalassemia. Luspatercept (mIgG2a) reduces anemia, α-globin aggregates, hemolysis, and disease complications of IE such as iron overload, splenomegaly, and bone defects.

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Luspatercept (mIgG2a) Chemical Structure

Luspatercept (mIgG2a) Chemical Structure

CAS No. : 1373715-00-4

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Description

Luspatercept (mIgG2a) (RAP-536) is a fusion protein, consisting of a modified extracellular domain of human ActRIIB linked to the murine IgG2a Fc domain. Luspatercept (mIgG2a) inhibits Smad2/3 signaling, promotes differentiation of late-stage erythroid precursors and mitigates ineffective erythropoiesis (IE) in murine β-thalassemia. Luspatercept (mIgG2a) reduces anemia, α-globin aggregates, hemolysis, and disease complications of IE such as iron overload, splenomegaly, and bone defects[1].

In Vivo

Luspatercept (mIgG2a) (RAP-536) (1 mg/kg, s.c., twice weekly for 2 months) alleviates anemia by promoting late-stage erythroid differentiation, reduces α-globin aggregates and hemolysis, and mitigates IE and related disease complications in murine β-thalassemia mice model[1].
Luspatercept (mIgG2a) (30 mg/kg, i.p., once for 12 h) inhibits overactivation of Smad2/3 in splenic erythroid precursors in murine β-thalassemia mice model[1].
Luspatercept (mIgG2a) (1-10 mg/kg, s.c., twice weekly for 2 months or once for 72 h) promotes terminal erythroid differentiation in the bone marrow and spleen and increases peripheral red cells in EPO-pretreated wild-type mice [1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Hbbth1/th1 mice of the B6.D2-Hbbd3th/BrkJ strain (3-4 months old) with hydrogen peroxidenot (50 μM) or not[1].
Dosage: 1 mg/kg
Administration: s.c., twice weekly for 2 months and then collected bone marrow, spleen and liver tissues.
Result: Significantly increased 29% RBC number, 16% hemoglobin concentration, and 19% hematocrit.
Decreased 8% mean cell volume, 10% mean cell hemoglobin, and 2% mean cell hemoglobin concentration.
Reduced 33% reticulocytes and a 19% red cell distribution width area.
Induced an overall increase in the proportion of late-stage erythroid precursors, significantly decreased the cell population of R1 while an increase of R3 in bone marrow, and reduced R1 and R2 with a significant increase in R3 in the spleen.
Reduced ∼60% serum EPO level, 36% splenomegaly, serum concentrations of ferritin (15%) and iron (28%), 29% transferrin saturation.
Reduced iron levels in liver (1464 μg/mg dry weight) and kidney (648 μg/mg dry weight) and altered the iron distribution with restoration of architecture in spleen.
Increased Hamp mRNA levels approximately 2 times without the expression changes of Bmp6 in liver and Gdf15 or Twsg1 in spleen.
Reduced 40% mean concentrations of total bilirubin and occurrence of abnormal erythrocyte morphology and hemolytic debris, but increased mean erythrocyte life span (28 vs 20 days).
Markedly reduced heinz bodies and 38% mean membrane-associated α-globin aggregates in peripheral erythrocytes.
Reduced ROS levels significantly in immature (CD71+Ter119+) and mature (CD71−Ter119+) erythroblasts as well as in peripheral red cells.
Reduced peroxide-stimulated ROS levels and significantly increased 17% bone mineral density, 100% trabecular bone volume (100%), number (14%), and thickness (14%).
Increased cortical thickness with a decrease in marrow space.
Animal Model: Hbbth1/th1 mice of the B6.D2-Hbbd3th/BrkJ strain (3-4 months old)[1].
Dosage: 30 mg/kg
Administration: i.p., once for 12 h, and then collected bone marrow, spleen and liver tissues.
Result: Reduced phosphorylated Smad2/3 level in erythroid precursors of spleens within 12 h.
Inhibited phospho-Smad2 protein expression in erythroid precursors of spleens within 12 h.
Animal Model: C57BL/6 wild-type mice were injected intraperitoneally with EPO (1500 units/kg) or not[1].
Dosage: 1, 10 mg/kg
Administration: s.c., (1 mg/kg) twice weekly for 2 months, (10 mg/kg) once for 72 h, and then collected bone marrow, spleen and liver tissues.
Result: Promoted terminal erythroid differentiation in the bone marrow and spleen and increased peripheral red cells in EPO-pretreated wild-type mice at 10 mg/kg with EPO stimulation in C57BL/6 wild-type mice.
Did not affect iron parameters and Hamp expression in C57BL/6 wild-type mice.
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[Luspatercept (mIgG2a)]
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Luspatercept (mIgG2a) Related Classifications

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Keywords:

Luspatercept (mIgG2a)1373715-00-4RAP-536RAP536RAP 536TGF-beta/SmadTransforming growth factor betaFusion proteinInhibitorIneffective erythropoiesisIEβ-thalassemiaAnemiaα-globin aggregatesHemolysisinhibitorinhibit

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