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In normoxia [A], prolyl hydroxylase enzymes [PHD] utilize oxygen to hydroxylate hypoxia-inducible factors [HIF], leading to HIF-1α degradation and prevention of HIF-mediated transcriptional activation. In the setting of hypoxia, oxygen is not available as a co-factor, thereby allowing HIF-1α to stabilize and induce genes to foster cell survival and metabolism. GB004 inhibits PHD [B], preventing HIF-1α degradation and permitting for HIF-1α stabilization.
