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Identification
NameEdetic Acid
Accession NumberDB00974  (APRD01327)
TypeSmall Molecule
GroupsApproved
Description

A chelating agent (chelating agents) that sequesters a variety of polyvalent cations. It is used in pharmaceutical manufacturing and as a food additive. [PubChem]

Structure
Thumb
Synonyms
SynonymLanguageCode
(Ethylenedinitrilo)tetraacetic acid, ion(4-)Not AvailableNot Available
{[-(bis-carboxymethyl-amino)-ethyl]-carboxymethyl-amino}-acetic acidNot AvailableNot Available
2,2',2'',2'''-(ethane-1,2-diyldinitrilo)tetraacetateNot AvailableNot Available
Acide edetiqueNot AvailableNot Available
Acide ethylenediaminetetracetiqueNot AvailableNot Available
Acido edeticoNot AvailableNot Available
Acidum edeticumNot AvailableNot Available
Edetic acidNot AvailableNot Available
EDTANot AvailableNot Available
EDTA, ion(4-)Not AvailableNot Available
EthylenediaminetetraacetateNot AvailableNot Available
Ethylenediaminetetraacetic acidNot AvailableNot Available
H4EdtaNot AvailableNot Available
N,N'-1,2-Ethane diylbis-(N-(carboxymethyl)glycine)Not AvailableNot Available
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Calcium Disodium Versenateinjection200 mg/mLintramuscular3 M Pharmaceuticals2009-07-092015-12-31Us 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Generic Prescription ProductsNot Available
Over the Counter ProductsNot Available
International Brands
NameCompany
CheladratePharmex
Diso-TateO'Neal, Jones
EndrateBersworth
Uni WashUnited
Brand mixturesNot Available
Salts
Name/CASStructureProperties
Edetate calcium disodium
Thumb
  • InChI Key: SHWNNYZBHZIQQV-UHFFFAOYSA-J
  • Monoisotopic Mass: 374.001495875
  • Average Mass: 374.268
DBSALT000837
Edetate disodium
Thumb
  • InChI Key: ZGTMUACCHSMWAC-UHFFFAOYSA-L
  • Monoisotopic Mass: 336.054554784
  • Average Mass: 336.2063
DBSALT000838
Categories
CAS number62-33-9
WeightAverage: 292.2426
Monoisotopic: 292.090665498
Chemical FormulaC10H16N2O8
InChI KeyKCXVZYZYPLLWCC-UHFFFAOYSA-N
InChI
InChI=1S/C10H16N2O8/c13-7(14)3-11(4-8(15)16)1-2-12(5-9(17)18)6-10(19)20/h1-6H2,(H,13,14)(H,15,16)(H,17,18)(H,19,20)
IUPAC Name
2-({2-[bis(carboxymethyl)amino]ethyl}(carboxymethyl)amino)acetic acid
SMILES
OC(=O)CN(CCN(CC(O)=O)CC(O)=O)CC(O)=O
Taxonomy
DescriptionThis compound belongs to the class of organic compounds known as tetracarboxylic acids and derivatives. These are carboxylic acids containing exactly four carboxyl groups.
KingdomOrganic compounds
Super ClassOrganic acids and derivatives
ClassCarboxylic acids and derivatives
Sub ClassTetracarboxylic acids and derivatives
Direct ParentTetracarboxylic acids and derivatives
Alternative Parents
Substituents
  • Tetracarboxylic acid or derivatives
  • Alpha-amino acid or derivatives
  • Alpha-amino acid
  • Tertiary aliphatic amine
  • Tertiary amine
  • Carboxylic acid
  • Hydrocarbon derivative
  • Organooxygen compound
  • Organonitrogen compound
  • Carbonyl group
  • Amine
  • Aliphatic acyclic compound
Molecular FrameworkAliphatic acyclic compounds
External Descriptors
Pharmacology
IndicationFor the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults.
PharmacodynamicsEdetate calcium is a heavy metal chelating agent. The calcium in edetate calcium can be displaced by divalent or trivalent metals to form a stable water soluble complex that can be excreted in the urine. In theory, 1 g of edetate calcium can theoretically bind 620 mg of lead, but in reality only about 5 mg per gram is actually excreted into the urine in lead poisoned patients. In addition to chelating lead, edetate calcium also chelates and eliminates zinc from the body. Edetate calcium also binds cadmium, copper, iron and manganese, but to a much lesser extent than either lead or zinc. Edetate calcium is relatively ineffective for use in treating mercury, gold or arsenic poisoning.
Mechanism of actionThe pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate will form with any metal that has the ability to displace calcium from the molecule, a feature shared by lead, zinc, cadmium, manganese, iron and mercury. The amounts of manganese and iron metabolized are not significant. Copper is not mobilized and mercury is unavailable for chelation because it is too tightly bound to body ligands or it is stored in inaccessible body compartments. The excretion of calcium by the body is not increased following intravenous administration of edetate calcium disodium, but the excretion of zinc is considerably increased.
AbsorptionPoorly absorbed from the gastrointestinal tract. Well absorbed following intramuscular injection.
Volume of distributionNot Available
Protein bindingNot Available
Metabolism

Almost none of the compound is metabolized.

Route of eliminationIt is excreted primarily by the kidney, with about 50% excreted in one hour and over 95% within 24 hours.2 Almost none of the compound is metabolized.
Half lifeThe half life of edetate calcium disodium is 20 to 60 minutes.
ClearanceNot Available
ToxicityInadvertent administration of 5 times the recommended dose, infused intravenously over a 24 hour period, to an asymptomatic 16 month old patient with a blood lead content of 56 mcg/dl did not cause any ill effects. Edetate calcium disodium can aggravate the symptoms of severe lead poisoning, therefore, most toxic effects (cerebral edema, renal tubular necrosis) appear to be associated with lead poisoning. Because of cerebral edema, a therapeutic dose may be lethal to an adult or a pediatric patient with lead encephalopathy. Higher dosage of edetate calcium disodium may produce a more severe zinc deficiency.
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 Absorption-0.8668
Blood Brain Barrier-0.7126
Caco-2 permeable-0.5739
P-glycoprotein substrateSubstrate0.6377
P-glycoprotein inhibitor INon-inhibitor0.9296
P-glycoprotein inhibitor IINon-inhibitor0.972
Renal organic cation transporterNon-inhibitor0.8473
CYP450 2C9 substrateNon-substrate0.8457
CYP450 2D6 substrateNon-substrate0.8271
CYP450 3A4 substrateNon-substrate0.7616
CYP450 1A2 substrateNon-inhibitor0.8959
CYP450 2C9 substrateNon-inhibitor0.9225
CYP450 2D6 substrateNon-inhibitor0.9306
CYP450 2C19 substrateNon-inhibitor0.9174
CYP450 3A4 substrateNon-inhibitor0.9288
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.9891
Ames testNon AMES toxic0.9132
CarcinogenicityNon-carcinogens0.7715
BiodegradationNot ready biodegradable0.8307
Rat acute toxicity1.8974 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.8158
hERG inhibition (predictor II)Non-inhibitor0.9341
Pharmacoeconomics
Manufacturers
  • Graceway pharmaceuticals llc
  • Watson laboratories inc
  • 3m pharmaceuticals inc
Packagers
Dosage forms
FormRouteStrength
Injectionintramuscular200 mg/mL
Prices
Unit descriptionCostUnit
Endrate 150 mg/ml ampul1.44USD ml
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
PatentsNot Available
Properties
StateSolid
Experimental Properties
PropertyValueSource
melting point237 °CNot Available
water solubility1000000 mg/L at 25 °CMEYLAN,WM et al. (1996)
logP-2.6Not Available
Predicted Properties
PropertyValueSource
Water Solubility9.26 mg/mLALOGPS
logP-1.2ALOGPS
logP-5.2ChemAxon
logS-1.5ALOGPS
pKa (Strongest Acidic)1.49ChemAxon
pKa (Strongest Basic)8.13ChemAxon
Physiological Charge-3ChemAxon
Hydrogen Acceptor Count10ChemAxon
Hydrogen Donor Count4ChemAxon
Polar Surface Area155.68 Å2ChemAxon
Rotatable Bond Count11ChemAxon
Refractivity62.35 m3·mol-1ChemAxon
Polarizability25.64 Å3ChemAxon
Number of Rings0ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Download (10.2 KB)
SpectraGC-MS
References
Synthesis Reference

Bersworth, F.C.; U.S. Patent 2,407,645; September 17,1946; assigned to The Martin Dennis Co.

General ReferenceNot Available
External Links
ATC CodesNot Available
AHFS CodesNot Available
PDB Entries
FDA labelNot Available
MSDSNot Available
Interactions
Drug Interactions
Drug
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AcenocoumarolMay enhance the anticoagulant effect of other Anticoagulants.
Acetylsalicylic acidAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
AlteplaseThrombolytic Agents may enhance the anticoagulant effect of Anticoagulants.
Aminosalicylic AcidSalicylates may enhance the anticoagulant effect of Anticoagulants.
AnagrelideAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
ApixabanApixaban may enhance the anticoagulant effect of Anticoagulants.
ArgatrobanMay enhance the anticoagulant effect of other Anticoagulants.
Bismuth SubsalicylateSalicylates may enhance the anticoagulant effect of Anticoagulants.
BivalirudinMay enhance the anticoagulant effect of other Anticoagulants.
CelecoxibNonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Anticoagulants.
CilostazolAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
CitalopramAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
ClopidogrelAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
Cyproterone acetateProgestins may diminish the therapeutic effect of Anticoagulants. More specifically, the potential prothrombotic effects of some progestins and progestin-estrogen combinations may counteract anticoagulant effects.
Dabigatran etexilateDabigatran Etexilate may enhance the anticoagulant effect of Anticoagulants.
DalteparinMay enhance the anticoagulant effect of other Anticoagulants.
DanaparoidMay enhance the anticoagulant effect of other Anticoagulants.
DasatinibDasatinib may enhance the anticoagulant effect of Anticoagulants.
DeferasiroxMay enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased.
DesogestrelEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
DesvenlafaxineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
DiflunisalAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
DipyridamoleAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
DrospirenoneEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
DuloxetineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
EnoxaparinMay enhance the anticoagulant effect of other Anticoagulants.
EpoprostenolProstacyclin Analogues may enhance the adverse/toxic effect of Anticoagulants. Specifically, the antiplatelet effects of these agents may lead to an increased risk of bleeding with the combination.
EptifibatideAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
EscitalopramAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
EstropipateEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
Ethinyl EstradiolEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
EthynodiolEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
EtodolacAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
EtonogestrelProgestins may diminish the therapeutic effect of Anticoagulants. More specifically, the potential prothrombotic effects of some progestins and progestin-estrogen combinations may counteract anticoagulant effects.
FenoprofenAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
FloctafenineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
FluoxetineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
FluvoxamineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
Fondaparinux sodiumMay enhance the anticoagulant effect of other Anticoagulants.
HeparinMay enhance the anticoagulant effect of other Anticoagulants.
HomoharringtonineMay enhance the adverse/toxic effect of Omacetaxine. Specifically, the risk for bleeding-related events may be increased.
IbritumomabMay enhance the adverse/toxic effect of Ibritumomab. Both agents may contribute to an increased risk of bleeding.
IbuprofenAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
IcosapentOmega-3 Fatty Acids may enhance the anticoagulant effect of Anticoagulants.
Icosapent ethylOmega-3 Fatty Acids may enhance the anticoagulant effect of Anticoagulants.
IloprostProstacyclin Analogues may enhance the adverse/toxic effect of Anticoagulants. Specifically, the antiplatelet effects of these agents may lead to an increased risk of bleeding with the combination.
IndomethacinAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
KetoprofenAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
KetorolacAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
LevomilnacipranAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
LevonorgestrelProgestins may diminish the therapeutic effect of Anticoagulants. More specifically, the potential prothrombotic effects of some progestins and progestin-estrogen combinations may counteract anticoagulant effects.
Magnesium salicylateSalicylates may enhance the anticoagulant effect of Anticoagulants.
Medroxyprogesterone AcetateProgestins may diminish the therapeutic effect of Anticoagulants. More specifically, the potential prothrombotic effects of some progestins and progestin-estrogen combinations may counteract anticoagulant effects.
Mefenamic acidAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
Megestrol acetateProgestins may diminish the therapeutic effect of Anticoagulants. More specifically, the potential prothrombotic effects of some progestins and progestin-estrogen combinations may counteract anticoagulant effects.
MeloxicamAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
MestranolEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
MilnacipranAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
NabumetoneAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
NadroparinMay enhance the anticoagulant effect of other Anticoagulants.
NaproxenAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
NorelgestrominEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
NorethindroneProgestins may diminish the therapeutic effect of Anticoagulants. More specifically, the potential prothrombotic effects of some progestins and progestin-estrogen combinations may counteract anticoagulant effects.
NorgestimateEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
ObinutuzumabMay enhance the adverse/toxic effect of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased.
OxaprozinAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
ParoxetineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
Pentosan PolysulfatePentosan Polysulfate Sodium may enhance the anticoagulant effect of Anticoagulants.
PiperazineEstrogen Derivatives may diminish the anticoagulant effect of Anticoagulants. More specifically, the potential prothrombotic effects of some estrogens and progestin-estrogen combinations may counteract anticoagulant effects.
PiroxicamAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
PrasugrelAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
ProgesteroneProgestins may diminish the therapeutic effect of Anticoagulants. More specifically, the potential prothrombotic effects of some progestins and progestin-estrogen combinations may counteract anticoagulant effects.
ReteplaseThrombolytic Agents may enhance the anticoagulant effect of Anticoagulants.
RivaroxabanMay enhance the anticoagulant effect of Rivaroxaban.
SalsalateSalicylates may enhance the anticoagulant effect of Anticoagulants.
SertralineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
SulindacAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
TenecteplaseThrombolytic Agents may enhance the anticoagulant effect of Anticoagulants.
Tiaprofenic acidAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
TicagrelorAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
TiclopidineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
TinzaparinMay enhance the anticoagulant effect of other Anticoagulants.
TipranavirTipranavir may enhance the anticoagulant effect of Anticoagulants.
TirofibanAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
TolmetinAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
TositumomabMay enhance the adverse/toxic effect of Tositumomab and Iodine I 131 Tositumomab. Specifically, the risk of bleeding-related adverse effects may be increased.
TreprostinilProstacyclin Analogues may enhance the adverse/toxic effect of Anticoagulants. Specifically, the antiplatelet effects of these agents may lead to an increased risk of bleeding with the combination.
VenlafaxineAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
VilazodoneAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
Vitamin EVitamin E may enhance the anticoagulant effect of Anticoagulants. Vitamin E may also increase the overall risk for bleeding.
VorapaxarVorapaxar may enhance the adverse/toxic effect of Anticoagulants. More specifically, this combination is expected to increase the risk of bleeding.
Food InteractionsNot Available

Targets

1. Lead

Kind: small molecule

Organism: Human

Pharmacological action: yes

Actions: chelator

Components

Name UniProt ID Details

References:

  1. Onnby L, Giorgi C, Plieva FM, Mattiasson B: Removal of heavy metals from water effluents using supermacroporous metal chelating cryogels. Biotechnol Prog. 2010 Sep;26(5):1295-302. Pubmed
  2. Chakraborty N, Banerjee A, Pal R: Accumulation of lead by free and immobilized cyanobacteria with special reference to accumulation factor and recovery. Bioresour Technol. 2010 Dec 13. Pubmed
  3. Tian SK, Lu LL, Yang XE, Huang HG, Brown P, Labavitch J, Liao HB, He ZL: The impact of EDTA on lead distribution and speciation in the accumulator Sedum alfredii by synchrotron X-ray investigation. Environ Pollut. 2010 Dec 17. Pubmed

2. Iron

Kind: small molecule

Organism: Human

Pharmacological action: unknown

Actions: chelator

Components

Name UniProt ID Details

References:

  1. Hasegawa H, Rahman IM, Kinoshita S, Maki T, Furusho Y: Separation of dissolved iron from the aqueous system with excess ligand. Chemosphere. 2011 Jan 3. Pubmed

3. Manganese cation

Kind: small molecule

Organism: Human

Pharmacological action: unknown

Actions: chelator

Components

Name UniProt ID Details

References:

  1. Broncel M, Wagner SC, Paul K, Hackenberger CP, Koksch B: Towards understanding secondary structure transitions: phosphorylation and metal coordination in model peptides. Org Biomol Chem. 2010 Jun 7;8(11):2575-9. Epub 2010 Mar 29. Pubmed

Enzymes

1. Adenosine deaminase

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

Name UniProt ID Details
Adenosine deaminase P00813 Details

References:

  1. Abu-Shady MR, Elshafei AM, el-Beih FM, Mohamed LA: Properties of adenosine deaminase in extracts of Asperigillus terricola. Acta Microbiol Pol. 1994;43(3-4):305-11. Pubmed

2. Cytochrome P450 1A2

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

Name UniProt ID Details
Cytochrome P450 1A2 P05177 Details

References:

  1. Bournique B, Petry M, Gousset G: Usefulness of statistic experimental designs in enzymology: example with recombinant hCYP3A4 and 1A2. Anal Biochem. 1999 Dec 1;276(1):18-26. Pubmed

3. Serum paraoxonase/lactonase 3

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

Name UniProt ID Details
Serum paraoxonase/lactonase 3 Q15166 Details

References:

  1. Pla A, Rodrigo L, Hernandez AF, Gil F, Lopez O: Effect of metal ions and calcium on purified PON1 and PON3 from rat liver. Chem Biol Interact. 2007 Apr 5;167(1):63-70. Epub 2007 Jan 16. Pubmed

4. Cytochrome P450 19A1

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 19A1 P11511 Details

References:

  1. Moslemi S, Vibet A, Papadopoulos V, Camoin L, Silberzahn P, Gaillard JL: Purification and characterization of equine testicular cytochrome P-450 aromatase: comparison with the human enzyme. Comp Biochem Physiol B Biochem Mol Biol. 1997 Sep;118(1):217-27. Pubmed
  2. Bellino FL, Holben L: Placental estrogen synthetase (aromatase): evidence for phosphatase-dependent inactivation. Biochem Biophys Res Commun. 1989 Jul 14;162(1):498-504. Pubmed
  3. Zhang F, Zhou D, Kao YC, Ye J, Chen S: Expression and purification of a recombinant form of human aromatase from Escherichia coli. Biochem Pharmacol. 2002 Nov 1;64(9):1317-24. Pubmed
  4. Milczarek R, Sokolowska E, Hallmann A, Kaletha K, Klimek J: NADPH- and iron-dependent lipid peroxidation inhibit aromatase activity in human placental microsomes. J Steroid Biochem Mol Biol. 2008 Jun;110(3-5):230-5. Epub 2008 Apr 20. Pubmed

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Drug created on June 13, 2005 07:24 / Updated on April 16, 2014 14:02