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Identification
NameStannsoporfin
Accession NumberDB04912
TypeSmall Molecule
GroupsInvestigational
DescriptionStannsoporfin is a competitive heme oxygenase (HO) inhibitor being developed by InfaCare, a subsidiary of WellSpring Pharmaceuticals, for the prevention of hyperbilirubinemia in infants at risk of developing jaundice.
Structure
Thumb
Synonyms
SnMP
Tin (IV) mesoporphyrin IX dichloride
tin-mesoporphyrin
External Identifiers Not Available
Approved Prescription ProductsNot Available
Approved Generic Prescription ProductsNot Available
Approved Over the Counter ProductsNot Available
Unapproved/Other Products Not Available
International Brands
NameCompany
StanateNot Available
Brand mixturesNot Available
SaltsNot Available
Categories
UNII0KAE1U0G7Q
CAS number106344-20-1
WeightNot Available
Chemical FormulaNot Available
InChI KeyNot Available
InChINot Available
IUPAC NameNot Available
SMILESNot Available
Taxonomy
ClassificationNot classified
Pharmacology
IndicationInvestigated for use/treatment in liver disease, metabolic disease, and pediatric indications.
PharmacodynamicsStannsoporfin is a chemical compound being investigated for use as a medicament in the treatment of infant jaundice. Stannsoporfin is also known to inhibit heme metabolism in mammals, to control the rate of tryptophan metabolism in mammals, and to increase the rate at which heme is excreted by mammals.
Mechanism of actionKernicterus is attributed to high levels of bilirubin, a by-product of heme metabolism. Bilirubin is a bile pigment, which is normally eliminated from the body after conversion into a water-soluble form by the liver. Stannsoporfin's mechanism of action specifically inhibits the enzyme that blocks the conversion of heme into bilirubin.
Related Articles
AbsorptionNot absorbed orally
Volume of distributionNot Available
Protein bindingNot Available
MetabolismNot Available
Route of eliminationNot Available
Half life3.8 hours following i.v. administration of 1 mumole per kg body weight
ClearanceNot Available
ToxicityNot Available
Affected organisms
  • Humans and other mammals
PathwaysNot Available
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal AbsorptionNot AvailableNot Available
Blood Brain BarrierNot AvailableNot Available
Caco-2 permeableNot AvailableNot Available
P-glycoprotein substrateNot AvailableNot Available
P-glycoprotein inhibitor INot AvailableNot Available
P-glycoprotein inhibitor IINot AvailableNot Available
Renal organic cation transporterNot AvailableNot Available
CYP450 2C9 substrateNot AvailableNot Available
CYP450 2D6 substrateNot AvailableNot Available
CYP450 3A4 substrateNot AvailableNot Available
CYP450 1A2 substrateNot AvailableNot Available
CYP450 2C9 inhibitorNot AvailableNot Available
CYP450 2D6 inhibitorNot AvailableNot Available
CYP450 2C19 inhibitorNot AvailableNot Available
CYP450 3A4 inhibitorNot AvailableNot Available
CYP450 inhibitory promiscuityNot AvailableNot Available
Ames testNot AvailableNot Available
CarcinogenicityNot AvailableNot Available
BiodegradationNot AvailableNot Available
Rat acute toxicityNot AvailableNot applicable
hERG inhibition (predictor I)Not AvailableNot Available
hERG inhibition (predictor II)Not AvailableNot Available
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397 )
Pharmacoeconomics
ManufacturersNot Available
PackagersNot Available
Dosage formsNot Available
PricesNot Available
PatentsNot Available
Properties
StateSolid
Experimental PropertiesNot Available
Predicted PropertiesNot Available
Spectra
Mass Spec (NIST)Not Available
Spectra
Spectrum TypeDescriptionSplash Key
References
Synthesis ReferenceNot Available
General References
  1. Galbraith RA, Kappas A: Pharmacokinetics of tin-mesoporphyrin in man and the effects of tin-chelated porphyrins on hyperexcretion of heme pathway precursors in patients with acute inducible porphyria. Hepatology. 1989 Jun;9(6):882-8. [PubMed:2714739 ]
External Links
ATC CodesNot Available
AHFS CodesNot Available
PDB EntriesNot Available
FDA labelNot Available
MSDSNot Available
Interactions
Drug InteractionsNot Available
Food InteractionsNot Available

Targets

Kind
Protein
Organism
Human
Pharmacological action
unknown
General Function:
Signal transducer activity
Specific Function:
Heme oxygenase cleaves the heme ring at the alpha methene bridge to form biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. Under physiological conditions, the activity of heme oxygenase is highest in the spleen, where senescent erythrocytes are sequestrated and destroyed. Exhibits cytoprotective effects since excess of free heme sensitizes cells to undergo a...
Gene Name:
HMOX1
Uniprot ID:
P09601
Molecular Weight:
32818.345 Da
References
  1. Drummond GS, Kappas A: Chemoprevention of severe neonatal hyperbilirubinemia. Semin Perinatol. 2004 Oct;28(5):365-8. [PubMed:15686268 ]
  2. Cannon JB, Martin C, Drummond GS, Kappas A: Targeted delivery of a heme oxygenase inhibitor with a lyophilized liposomal tin mesoporphyrin formulation. Pharm Res. 1993 May;10(5):715-21. [PubMed:8321837 ]
  3. Boni RE, Huch Boni RA, Galbraith RA, Drummond GS, Kappas A: Tin-mesoporphyrin inhibits heme oxygenase activity and heme-iron absorption in the intestine. Pharmacology. 1993 Nov;47(5):318-29. [PubMed:8265722 ]
  4. Wagner KR, Hua Y, de Courten-Myers GM, Broderick JP, Nishimura RN, Lu SY, Dwyer BE: Tin-mesoporphyrin, a potent heme oxygenase inhibitor, for treatment of intracerebral hemorrhage: in vivo and in vitro studies. Cell Mol Biol (Noisy-le-grand). 2000 May;46(3):597-608. [PubMed:10872746 ]
  5. Nalos M, Vassilev D, Pittner A, Asfar P, Bruckner UB, Schneider EM, Georgieff M, Radermacher P, Froeba G: Tin-mesoporphyrin for inhibition of heme oxygenase during long-term hyperdynamic porcine endotoxemia. Shock. 2003 Jun;19(6):526-32. [PubMed:12785007 ]
Kind
Protein
Organism
Human
Pharmacological action
unknown
General Function:
Metal ion binding
Specific Function:
Heme oxygenase cleaves the heme ring at the alpha methene bridge to form biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. Under physiological conditions, the activity of heme oxygenase is highest in the spleen, where senescent erythrocytes are sequestrated and destroyed. Heme oxygenase 2 could be implicated in the production of carbon monoxide in brain wher...
Gene Name:
HMOX2
Uniprot ID:
P30519
Molecular Weight:
36032.615 Da
References
  1. Drummond GS, Kappas A: Chemoprevention of severe neonatal hyperbilirubinemia. Semin Perinatol. 2004 Oct;28(5):365-8. [PubMed:15686268 ]
  2. Cannon JB, Martin C, Drummond GS, Kappas A: Targeted delivery of a heme oxygenase inhibitor with a lyophilized liposomal tin mesoporphyrin formulation. Pharm Res. 1993 May;10(5):715-21. [PubMed:8321837 ]
  3. Boni RE, Huch Boni RA, Galbraith RA, Drummond GS, Kappas A: Tin-mesoporphyrin inhibits heme oxygenase activity and heme-iron absorption in the intestine. Pharmacology. 1993 Nov;47(5):318-29. [PubMed:8265722 ]
  4. Wagner KR, Hua Y, de Courten-Myers GM, Broderick JP, Nishimura RN, Lu SY, Dwyer BE: Tin-mesoporphyrin, a potent heme oxygenase inhibitor, for treatment of intracerebral hemorrhage: in vivo and in vitro studies. Cell Mol Biol (Noisy-le-grand). 2000 May;46(3):597-608. [PubMed:10872746 ]
  5. Nalos M, Vassilev D, Pittner A, Asfar P, Bruckner UB, Schneider EM, Georgieff M, Radermacher P, Froeba G: Tin-mesoporphyrin for inhibition of heme oxygenase during long-term hyperdynamic porcine endotoxemia. Shock. 2003 Jun;19(6):526-32. [PubMed:12785007 ]
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Drug created on October 21, 2007 16:23 / Updated on August 17, 2016 12:24