Anticoagulant that retains platelets functionality. Buffers Ca2+ activity in physiological range (~1mM). Bypasses the metabolic blockade, may permit heme biosynthesis but does not suffice to reverse the iron-restriction response. Stabilizes the iron-sulfur cluster and is predicted to restore aconitase to its ‘high iron’ conformation and thereby dissociates the PKC-associated signaling complexes whose hyperactivation impairs Epo responsiveness. Binds IDH (isocitrate dehydrogenase), an excellent candidate for participating, along with aconitase and PKC, in an iron restriction signalosome. Contributes to heme biosynthesis which may account for its greater potency in restoring erythroid differentiation.