Ferroheme is formed when iron is inserted into protoporphyrin IX. The active center of hemoglobin and myoglobin consists of iron Ferroheme complex bound through a single, “proximal”, axial histidine (His) to the protein It is an iron containing cofactor that is involved with a wide range of cellular functions including oxygen transport. The antimalarial activity of a number of artemisinin derivatives, both newly synthesized and currently used as drugs, against Plasmodium falciparum in culture shows a correlation with their affinity of binding with Ferroheme.

Gliotoxin is a potent crystalline antibiotic substance produced during the growth of the imperfect fungus Gliocladium jimbriatum. It is a natural mycotoxin with immunosuppressive and antimicrobial activity. Gliotoxin acts as NOTCH2 transactivation inhibitor in human neoplasias. It induced growth inhibition and apoptosis in multiple colorectal cancer cell lines with mutations of the Wnt signaling pathway. Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats. Gliotoxin is a dual inhibitor of farnesyltransferase and geranylgeranyltransferase I with pronounced antitumor activity and favorable toxicity profile against breast cancer in vitro and in vivo.

Bilirubin is an orange-yellow pigment made during the normal breakdown of red blood cells. Bilirubin passes through the liver and is excreted out of the body. Occasionally, higher bilirubin levels may indicate an increased rate of destruction of red blood cells (hemolysis). A high level of bilirubin in the blood is called hyperbilirubinemia. High bilirubin levels can cause jaundice. Jaundice makes the skin and the whites of the eyes appear yellow, due to the brown and yellow bilirubin in the blood. Phototherapy for neonatal is one of the treatment methods against hyperbilirubinemia. Light absorption by bilirubin in the skin transforms the native Z,Z-bilirubin to conformational photoisomers Z,E-bilirubin and E,Z-bilirubin and structural photoisomers E,Z-lumirubin and E,E-lumirubin. Formation and excretion of Z,E-bilirubin and E,Z-lumirubin are both important routes of elimination of bilirubin through bile and urine, although the precise contributions of the various photoisomers to the overall elimination of bilirubin are still unknown.

Verteporfin (trade name Visudyne), a benzoporphyrin derivative, is a medication used for the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis syndrome. Verteporfin can also be used to destroy tumors. Verteporfin is a 1:1 mixture of two regioisomers (I and II), VISUDYNE therapy is a two-stage process requiring administration of both verteporfin for injection and nonthermal red light. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 689 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to the endothelium and blockage of the vessels. Verteporfin is also used off-label for the treatment of central serous retinopathy. Verteporfin is given intravenously, 15 minutes before laser treatment. Light activation of verteporfin results in local damage to neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neovasculature. However, animal models indicate that the drug is also present in the retina. Therefore, there may be collateral damage to retinal structures following photoactivation including the retinal pigmented epithelium and outer nuclear layer of the retina. The temporary occlusion of choroidal neovascularization (CNV) following VISUDYNE therapy has been confirmed in humans by fluorescein angiography.

Hemin (trade name Panhematin) is a protoporphyrin IX containing a ferric iron ion (heme B) with a chloride ligand, which is is indicated for the amelioration of recurrent attacks of acute intermittent porphyria temporally related to the menstrual cycle in susceptible women. Manifestations such as pain, hypertension, tachycardia, abnormal mental status and mild to progressive neurologic signs may be controlled in selected patients with this disorder. the therapy for the acute porphyrias is not curative. Heme acts to limit the hepatic and/or marrow synthesis of porphyrin. This action is likely due to the inhibition of δ-aminolevulinic acid synthetase, the enzyme which limits the rate of the porphyrin/heme biosynthetic pathway. The exact mechanism by which hematin produces symptomatic improvement in patients with acute episodes of the hepatic porphyrias has not been elucidated.