Fetal hemoglobin is a critical player in management of sickle cell disease and an important target. Last year at ASH, Peter Bruun-Rasmussen demonstrated, looking at data back from the multi-center study of hydroxyurea, as well as a cooperative study of sickle cell disease, demonstrating that even small increments in fetal hemoglobin, for example, 1% to 3% led to a reduction in vaso-occlusive crises by 5% to 8%...
Fetal hemoglobin is a critical player in management of sickle cell disease and an important target. Last year at ASH, Peter Bruun-Rasmussen demonstrated, looking at data back from the multi-center study of hydroxyurea, as well as a cooperative study of sickle cell disease, demonstrating that even small increments in fetal hemoglobin, for example, 1% to 3% led to a reduction in vaso-occlusive crises by 5% to 8%. But that was going back to data that we already had on patients. And more recently, as you noticed, I presented that data at ASCAT using Picnic Health data set, which is a real-world data set of patients, predominantly in the United States, older than two years of age across all genotypes, where there was a correlation between increasing levels of fetal hemoglobin and improved rates of crises. And it was actually really interesting because it seemed even going from 0% to 5% fetal hemoglobin led to an incremental improvement in the rate of VOCs that were observed. So certainly looking at well-established trials and analyzing that data again, and as well as the real-world data that’s not always the cleanest because it’s more of EMR data that has been abstracted. There seems to be a correlation between increasing levels of fetal hemoglobin and improved rates of vaso-occlusive crises.
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