VIT-2763 

VIT-2763, an oral ferroportin inhibitor, inhibits hepcidin binding to ferroportin and blocks iron efflux. VIT-2763 has the potential in the treatment of β-thalassemia^[1].

VIT-2763 dose dependently reduces the fluorescence polarization signal, indicating that VIT-2763 displaces TMR-hepcidin from ferroportin (IC₅₀ of 24 ± 13 nM)^[1].
VIT-2763 induces BLA reporter gene activity with an average EC₅₀ of 140 ± 50 nM, as a consequence of increasing intracellular iron concentrations caused by blocked iron export in HEK293 cells^[1].
VIT-2763 (100 nM) triggers ubiquitination and subsequent internalization and degradation of ferroportin^[1].

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

VIT-2763 (30, 100 mg/kg, orally twice daily for 36 days) decreases serum iron and prevented liver iron loading in Hbb^th3/+ mice^[1].
VIT-2763 did not change the total liver iron^[1].
VIT-2763 (30, 100 mg/kg, orally twice daily for 36 days) significantly corrects anemia and improved RBC parameters in Hbb^th3/+ mice. VIT-2763 decreases the percentage of ROS-positive RBCs in Hbb^th3/+ mice from 67% to 30%^[1].
VIT-2763 decreases apoptosis and extends the life span of RBCs in Hbb^th3/+ mice^[1].

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

408.43

C₂₁H₂₁FN₆O₂

2095668-10-1

Solid

Off-white to light yellow

O=C(C1=COC(CCNCCC2=NC3=CC=CC=C3N2)=N1)NCC4=NC=CC=C4F

Room temperature in continental US; may vary elsewhere.

• [1]. Vania Manolova, et al. Oral Ferroportin Inhibitor Ameliorates Ineffective Erythropoiesis in a Model of β-Thalassemia. J Clin Invest. 2019 Dec 9;130(1):491-506.  [Content Brief]