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Identification
NameEstropipate
Accession NumberDB04574
TypeSmall Molecule
GroupsApproved
Description

Estropipate is a form of estrogen. It has several uses such as: Alleviate symptoms of menopause as hormone replacement therapy, treatment some types of infertility, treatment of some conditions leading to underdevelopment of female sexual characteristics,treatment of vaginal atrophy,treatment of some types of breast cancer (particularly in men and postmenopausal women), treatment of prostate cancer and prevention of osteoporosis.

Structure
Thumb
Synonyms
SynonymLanguageCode
3-Hydroxyestra-1,3,5(10)-trien-17-one hydrogen sulphateNot AvailableNot Available
Estrone 3-sulfateNot AvailableNot Available
Estrone hydrogen sulfateNot AvailableNot Available
Estrone sulfateNot AvailableNot Available
Estrone sulphateNot AvailableNot Available
EstropipateNot AvailableUSP
OGENNot AvailableNot Available
Ogen (TN)Not AvailableNot Available
Ogen 2.5Not AvailableNot Available
Prescription ProductsNot Available
Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Estropipatetablet.75 mgoralWatson Laboratories, Inc.1993-09-23Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Estropipatetablet1.5 mgoralWatson Laboratories, Inc.1993-09-23Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Estropipatetablet3 mgoralWatson Laboratories, Inc.1993-09-23Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Estropipatetablet.75 mgoralPhysicians Total Care, Inc.2003-03-21Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Estropipatetablet1.5 mgoralPhysicians Total Care, Inc.2003-03-21Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Estropipatetablet3 mgoralPhysicians Total Care, Inc.2003-03-26Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Over the Counter ProductsNot Available
International Brands
NameCompany
OgenNot Available
ORTHO-ESTNot Available
Brand mixturesNot Available
SaltsNot Available
Categories
CAS number7280-37-7
WeightAverage: 350.429
Monoisotopic: 350.118794504
Chemical FormulaC18H22O5S
InChI KeyJKKFKPJIXZFSSB-CBZIJGRNSA-N
InChI
InChI=1S/C18H22O5S/c1-18-9-8-14-13-5-3-12(23-24(20,21)22)10-11(13)2-4-15(14)16(18)6-7-17(18)19/h3,5,10,14-16H,2,4,6-9H2,1H3,(H,20,21,22)/t14-,15-,16+,18+/m1/s1
IUPAC Name
[(1S,10R,11S,15S)-15-methyl-14-oxotetracyclo[8.7.0.0²,⁷.0¹¹,¹⁵]heptadeca-2(7),3,5-trien-5-yl]oxidanesulfonic acid
SMILES
C[C@]12CC[C@H]3[C@@H](CCC4=C3C=CC(OS(O)(=O)=O)=C4)[C@@H]1CCC2=O
Taxonomy
DescriptionThis compound belongs to the class of organic compounds known as sulfated steroids. These are sterol lipids containing a sulfate group attached to the steroid skeleton.
KingdomOrganic compounds
Super ClassLipids and lipid-like molecules
ClassSteroids and steroid derivatives
Sub ClassSulfated steroids
Direct ParentSulfated steroids
Alternative Parents
Substituents
  • Sulfated steroid
  • 3-sulfated steroid
  • Sulfated steroid skeleton
  • Oxosteroid
  • 17-oxosteroid
  • Estrane-skeleton
  • Phenanthrene
  • Tetralin
  • Sulfuric acid monoester
  • Benzenoid
  • Sulfuric acid ester
  • Sulfate-ester
  • Organic sulfuric acid or derivatives
  • Ketone
  • Hydrocarbon derivative
  • Organooxygen compound
  • Carbonyl group
  • Aromatic homopolycyclic compound
Molecular FrameworkAromatic homopolycyclic compounds
External Descriptors
Pharmacology
IndicationEstropipate is used for the treatment of moderate to severe vasomotor symptoms associated with the monopause, and moderate to severe symptoms of vulval and vaginal atrophy associated with the menopause. It is also used to treat hypoestrogenism due to hypogonadism, castration or primary ovarian failure, and prevent postmenopausal osteoporosis.
PharmacodynamicsEstropipate is an estrogenic substance. It acts as naturally produced estrogen does. Estrogens act through binding to nuclear receptors in estrogen-responsive tissues. Circulating estrogens modulate the pituitary secretion of the gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH), through a negative feedback mechanism. Estrogens act to reduce the elevated levels of these hormones seen in postmenopausal women.
Mechanism of actionEstradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.
AbsorptionEstropipate is well absorbed through the skin and gastrointestinal tract. When applied for a local action, absorption is usually sufficient to cause systemic effects.
Volume of distributionNot Available
Protein bindingNot Available
Metabolism

Exogenous estrogens are metabolized in the same manner as endogenous estrogens. Circulating estrogens exist in a dynamic equilibrium of metabolic interconversions. These transformations take place mainly in the liver. Estradiol is converted reversibly to estrone, and both can be converted to estriol, which is the major urinary metabolite. Estrogens also undergo enterohepatic recirculation via sulfate and glucuronide conjugation in the liver, biliary secretion of conjugates into the intestine, and hydrolysis in the gut followed by reabsorption. In postmenopausal women, a significant proportion of the circulating estrogens exist as sulfate conjugates, especially estrone sulfate, which serves as a circulating reservoir for the formation of more active estrogens.

SubstrateEnzymesProduct
Estropipate
Not Available
EstroneDetails
Estropipate
Not Available
EstriolDetails
Route of eliminationEstradiol, estrone and estriol are excreted in the urine along with glucuronide and sulfate conjugates
Half lifeNot Available
ClearanceNot Available
ToxicityNot Available
Affected organisms
  • Humans and other mammals
Pathways
PathwayCategorySMPDB ID
Sulfite oxidase deficiencyDiseaseSMP00532
Sulfate/Sulfite MetabolismMetabolicSMP00041
17-Beta Hydroxysteroid Dehydrogenase III DeficiencyDiseaseSMP00356
Aromatase deficiencyDiseaseSMP00565
Androgen and Estrogen MetabolismMetabolicSMP00068
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+0.9974
Blood Brain Barrier+0.935
Caco-2 permeable-0.8343
P-glycoprotein substrateNon-substrate0.5376
P-glycoprotein inhibitor INon-inhibitor0.5591
P-glycoprotein inhibitor IINon-inhibitor0.9751
Renal organic cation transporterNon-inhibitor0.8407
CYP450 2C9 substrateNon-substrate0.7526
CYP450 2D6 substrateNon-substrate0.8214
CYP450 3A4 substrateSubstrate0.6275
CYP450 1A2 substrateNon-inhibitor0.9046
CYP450 2C9 substrateNon-inhibitor0.9071
CYP450 2D6 substrateNon-inhibitor0.923
CYP450 2C19 substrateNon-inhibitor0.9026
CYP450 3A4 substrateNon-inhibitor0.9421
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.8808
Ames testNon AMES toxic0.5621
CarcinogenicityCarcinogens 0.5507
BiodegradationNot ready biodegradable0.9558
Rat acute toxicity2.2402 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Strong inhibitor0.5746
hERG inhibition (predictor II)Inhibitor0.8077
Pharmacoeconomics
ManufacturersNot Available
PackagersNot Available
Dosage forms
FormRouteStrength
Tabletoral.75 mg
Tabletoral1.5 mg
Tabletoral3 mg
PricesNot Available
PatentsNot Available
Properties
StateSolid
Experimental PropertiesNot Available
Predicted Properties
PropertyValueSource
Water Solubility0.0059 mg/mLALOGPS
logP0.29ALOGPS
logP3.83ChemAxon
logS-4.8ALOGPS
pKa (Strongest Acidic)-1.7ChemAxon
pKa (Strongest Basic)-7.5ChemAxon
Physiological Charge-1ChemAxon
Hydrogen Acceptor Count4ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area80.67 Å2ChemAxon
Rotatable Bond Count2ChemAxon
Refractivity89.07 m3·mol-1ChemAxon
Polarizability36.64 Å3ChemAxon
Number of Rings4ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Not Available
SpectraNot Available
References
Synthesis ReferenceNot Available
General ReferenceNot Available
External Links
ATC CodesNot Available
AHFS Codes
  • 68:16.04
PDB EntriesNot Available
FDA labelNot Available
MSDSNot Available
Interactions
Drug Interactions
Drug
AbciximabEstrogen 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.
AcenocoumarolEstrogen 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.
AcetohexamideHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
AlogliptinHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
AnastrozoleEstrogen Derivatives may diminish the therapeutic effect of Anastrozole.
BosentanMay decrease the serum concentration of CYP3A4 Substrates.
CanagliflozinHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
ChlorpropamideHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Citric AcidEstrogen 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.
DabrafenibMay decrease the serum concentration of CYP3A4 Substrates.
DalteparinEstrogen 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.
DeferasiroxMay decrease the serum concentration of CYP3A4 Substrates.
DehydroepiandrosteroneMay enhance the adverse/toxic effect of Estrogen Derivatives.
DicoumarolEstrogen 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.
Edetic AcidEstrogen 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.
EnoxaparinEstrogen 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.
Ethyl biscoumacetateEstrogen 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.
ExemestaneEstrogen Derivatives may diminish the therapeutic effect of Exemestane.
Fondaparinux sodiumEstrogen 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.
GliclazideHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
GlimepirideHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
GliquidoneHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
GlyburideHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
HeparinEstrogen 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.
HyaluronidaseEstrogen Derivatives may diminish the therapeutic effect of Hyaluronidase.
Insulin AspartHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Insulin DetemirHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Insulin GlargineHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Insulin GlulisineHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Insulin LisproHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Insulin RegularHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Insulin, isophaneHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
LenalidomideEstrogen Derivatives may enhance the thrombogenic effect of Lenalidomide.
LinagliptinHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
MetforminHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
MitotaneMay decrease the serum concentration of CYP3A4 Substrates.
OspemifeneEstrogen Derivatives may enhance the adverse/toxic effect of Ospemifene. Estrogen Derivatives may diminish the therapeutic effect of Ospemifene.
PhenindioneEstrogen 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.
PhenprocoumonEstrogen 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.
RepaglinideHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
RopiniroleEstrogen Derivatives may increase the serum concentration of ROPINIRole.
SaxagliptinHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
SiltuximabMay decrease the serum concentration of CYP3A4 Substrates.
SulodexideEstrogen 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.
TeriflunomideMay decrease the serum concentration of CYP1A2 Substrates.
ThalidomideEstrogen Derivatives may enhance the thrombogenic effect of Thalidomide.
TipranavirEstrogen Derivatives may enhance the dermatologic adverse effect of Tipranavir. The combination of tipranavir/ritonavir and ethinyl estradiol/norethindrone was associated with a high incidence of skin rash. Tipranavir may decrease the serum concentration of Estrogen Derivatives.
TocilizumabMay decrease the serum concentration of CYP3A4 Substrates.
TolbutamideHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
TreprostinilEstrogen 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.
VildagliptinHyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents.
Vitamin CMay increase the serum concentration of Estrogen Derivatives.
WarfarinEstrogen 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.
Food Interactions
  • Take with food to decrease nausea

Targets

1. Estrogen receptor

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: agonist

Components

Name UniProt ID Details
Estrogen receptor P03372 Details

References:

  1. Brama M, Gnessi L, Basciani S, Cerulli N, Politi L, Spera G, Mariani S, Cherubini S, d’Abusco AS, Scandurra R, Migliaccio S: Cadmium induces mitogenic signaling in breast cancer cell by an ERalpha-dependent mechanism. Mol Cell Endocrinol. 2007 Jan 29;264(1-2):102-8. Epub 2006 Nov 27. Pubmed
  2. Lehnes K, Winder AD, Alfonso C, Kasid N, Simoneaux M, Summe H, Morgan E, Iann MC, Duncan J, Eagan M, Tavaluc R, Evans CH Jr, Russell R, Wang A, Hu F, Stoica A: The effect of estradiol on in vivo tumorigenesis is modulated by the human epidermal growth factor receptor 2/phosphatidylinositol 3-kinase/Akt1 pathway. Endocrinology. 2007 Mar;148(3):1171-80. Epub 2006 Nov 30. Pubmed
  3. Sasson S: Equilibrium binding analysis of estrogen agonists and antagonists: relation to the activation of the estrogen receptor. Pathol Biol (Paris). 1991 Jan;39(1):59-69. Pubmed
  4. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

2. Estrogen receptor beta

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: agonist

Components

Name UniProt ID Details
Estrogen receptor beta Q92731 Details

References:

  1. Vijayanathan V, Greenfield NJ, Thomas TJ, Ivanova MM, Tyulmenkov VV, Klinge CM, Gallo MA, Thomas T: Effects of estradiol and 4-hydroxytamoxifen on the conformation, thermal stability, and DNA recognition of estrogen receptor beta. Biochem Cell Biol. 2007 Feb;85(1):1-10. Pubmed
  2. Sasson S: Equilibrium binding analysis of estrogen agonists and antagonists: relation to the activation of the estrogen receptor. Pathol Biol (Paris). 1991 Jan;39(1):59-69. Pubmed

Enzymes

1. Cytochrome P450 1A2

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 1A2 P05177 Details

References:

  1. Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). Accessed May 28, 2010.
  2. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed
  3. Lee AJ, Cai MX, Thomas PE, Conney AH, Zhu BT: Characterization of the oxidative metabolites of 17beta-estradiol and estrone formed by 15 selectively expressed human cytochrome p450 isoforms. Endocrinology. 2003 Aug;144(8):3382-98. Pubmed

2. Cytochrome P450 3A4

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 3A4 P08684 Details

References:

  1. Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). Accessed May 28, 2010.
  2. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed
  3. Lee AJ, Cai MX, Thomas PE, Conney AH, Zhu BT: Characterization of the oxidative metabolites of 17beta-estradiol and estrone formed by 15 selectively expressed human cytochrome p450 isoforms. Endocrinology. 2003 Aug;144(8):3382-98. Pubmed
  4. Williams ET, Leyk M, Wrighton SA, Davies PJ, Loose DS, Shipley GL, Strobel HW: Estrogen regulation of the cytochrome P450 3A subfamily in humans. J Pharmacol Exp Ther. 2004 Nov;311(2):728-35. Epub 2004 Jul 28. Pubmed

3. Cytochrome P450 2C9

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inducer

Components

Name UniProt ID Details
Cytochrome P450 2C9 P11712 Details

References:

  1. Egnell AC, Eriksson C, Albertson N, Houston B, Boyer S: Generation and evaluation of a CYP2C9 heteroactivation pharmacophore. J Pharmacol Exp Ther. 2003 Dec;307(3):878-87. Epub 2003 Oct 13. Pubmed

Carriers

1. Sex hormone-binding globulin

Kind: protein

Organism: Human

Pharmacological action: unknown

Components

Name UniProt ID Details
Sex hormone-binding globulin P04278 Details

References:

  1. Campusano M C, Brusco G F, Campino J C, Rodriguez P L, Arteaga U E: [Assessment of androgenic decline in the elderly] Rev Med Chil. 2006 Sep;134(9):1123-8. Epub 2006 Dec 12. Pubmed
  2. Kuba R, Pohanka M, Zakopcan J, Novotna I, Rektor I: Sexual dysfunctions and blood hormonal profile in men with focal epilepsy. Epilepsia. 2006 Dec;47(12):2135-40. Pubmed
  3. Bendlova B, Zavadilova J, Vankova M, Vejrazkova D, Lukasova P, Vcelak J, Hill M, Cibula D, Vondra K, Starka L, Vrbikova J: Role of D327N sex hormone-binding globulin gene polymorphism in the pathogenesis of polycystic ovary syndrome. J Steroid Biochem Mol Biol. 2007 Apr;104(1-2):68-74. Epub 2007 Jan 26. Pubmed
  4. Sablik Z, Samborska-Sablik A, Bolinska-Soltysiak H, Goch JH, Kula K: [Hyperandrogenism as a risk factor of coronary artery disease in young women] Pol Arch Med Wewn. 2006 Feb;115(2):118-24. Pubmed
  5. Mohamad MJ, Mohammad MA, Karayyem M, Hairi A, Hader AA: Serum levels of sex hormones in men with acute myocardial infarction. Neuro Endocrinol Lett. 2007 Apr;28(2):182-6. Pubmed
  6. O’Connell MB: Pharmacokinetic and pharmacologic variation between different estrogen products. J Clin Pharmacol. 1995 Sep;35(9 Suppl):18S-24S. Pubmed
  7. Pardridge WM: Serum bioavailability of sex steroid hormones. Clin Endocrinol Metab. 1986 May;15(2):259-78. Pubmed

2. Serum albumin

Kind: protein

Organism: Human

Pharmacological action: unknown

Components

Name UniProt ID Details
Serum albumin P02768 Details

References:

  1. O’Connell MB: Pharmacokinetic and pharmacologic variation between different estrogen products. J Clin Pharmacol. 1995 Sep;35(9 Suppl):18S-24S. Pubmed

Transporters

1. Solute carrier family 22 member 1

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

Name UniProt ID Details
Solute carrier family 22 member 1 O15245 Details

References:

  1. Hayer-Zillgen M, Bruss M, Bonisch H: Expression and pharmacological profile of the human organic cation transporters hOCT1, hOCT2 and hOCT3. Br J Pharmacol. 2002 Jul;136(6):829-36. Pubmed
  2. Wu X, Kekuda R, Huang W, Fei YJ, Leibach FH, Chen J, Conway SJ, Ganapathy V: Identity of the organic cation transporter OCT3 as the extraneuronal monoamine transporter (uptake2) and evidence for the expression of the transporter in the brain. J Biol Chem. 1998 Dec 4;273(49):32776-86. Pubmed

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Drug created on September 07, 2007 15:12 / Updated on September 16, 2013 17:25