Abstract
The hemoglobin (Hb) sickle cell mutation, Glu6Val, promotes Hb polymerization under cellular concentrations/conditions. Deoxy Hb is most susceptible to form polymers in the mutant. However, we know that normal Hb, even without the mutation, will polymerize under very high concentrations. Therefore, our goal was to assess if other types of Hb could polymerize, in this case, if methemoglobin (ferric iron, +3) could polymerize. If it did, we asked if the recently developed anti-sickling drug, GBT440 (Voxelotor), would decrease the polymerization.
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