Neonatal jaundice is the most common cause of hospital readmission for term- and near term infants and its management poses a significant burden on the healthcare system.

Infants with isoimmune hemolytic disease, such as ABO or Rhesus (Rh) incompatibility, or glucose-6-phosphate dehydrogenase (G6PD deficiency), have an increased rate of red cell destruction and, thus, an increase in bilirubin production. Newborn infants have immature liver function and do not conjugate bilirubin well, which results in accumulation of unconjugated bilirubin. Thus, bilirubin levels may rise rapidly and intervention may be required. At present, phototherapy (PT) is the most frequently used treatment for hyperbilirubinemia; it converts unconjugated bilirubin to less toxic water soluble photoisomers that are then excreted in the urine without need for conjugation. Infants who do not respond to PT are treated by exchange transfusion (ET), considered a therapy of last resort because of associated morbidity and mortality. Both PT and ET enhance the elimination of, but have no impact on the production of bilirubin.

Stannsoporfin is a heme oxygenase inhibitor that acts to reduce bilirubin production. It is being developed for the management of neonatal jaundice.