Mifepristone (CHEM002284)

IdentificationTaxonomyBiological PropertiesPhysical PropertiesToxicity ProfileSpectraConcentrationsLinksReferencesTargets (23)XML
Record Information
Version1.0
Creation Date2009-07-21 20:27:46 UTC
Update Date2026-04-02 23:15:43 UTC
Accession NumberCHEM002284
Identification
Common NameMifepristone
ClassSmall Molecule
DescriptionA progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary cushing syndrome [PubChem]. The two marketed forms of mifepristone are Mifeprex® (mifepristone 200mg) and Korlym™ (mifepristone 300mg). Currently under investigation for use in psychotic depression (phase 3 trials).
Contaminant Sources
  • HMDB Contaminants - Urine
  • T3DB toxins
  • ToxCast & Tox21 Chemicals
Contaminant Type
  • Abortifacient Agent, Steroidal
  • Amine
  • Contraceptive, Oral, Synthetic
  • Contraceptive, Postcoital, Synthetic
  • Drug
  • Ester
  • Hormone Antagonist
  • Luteolytic Agent
  • Menstruation-Inducing Agent
  • Metabolite
  • Organic Compound
  • Synthetic Compound
Chemical Structure
Thumb
MOLSDFPDBSMILESInChI
Synonyms
ValueSource
11-(4-DIMETHYLAMINO-phenyl)-17-hydroxy-13-methyl-17-prop-1-ynyl-1,2,6,7,8,11,12,13,14,15,16,17-dodec ahydro-cyclopenta[a]phenanthren-3-oneChEBI
CorluxChEBI
MifegyneChEBI
MifeprexChEBI
MifepristonaChEBI
MifepristonumChEBI
RU-486ChEBI
RU486ChEBI
KorlymKegg
MifepristonHMDB
Mifepristone exelgyn brandHMDB
Mifepristone contragest brandHMDB
Mifepristone danco brandHMDB
Contragest brand OF mifepristoneHMDB
Danco brand OF mifepristoneHMDB
Exelgyn brand OF mifepristoneHMDB
MifégyneHMDB
Chemical FormulaC29H35NO2
Average Molecular Mass429.594 g/mol
Monoisotopic Mass429.267 g/mol
CAS Registry Number84371-65-3
IUPAC Name(10S,11S,14S,15S,17R)-17-[4-(dimethylamino)phenyl]-14-hydroxy-15-methyl-14-(prop-1-yn-1-yl)tetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadeca-1,6-dien-5-one
Traditional Name(10S,11S,14S,15S,17R)-17-[4-(dimethylamino)phenyl]-14-hydroxy-15-methyl-14-(prop-1-yn-1-yl)tetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadeca-1,6-dien-5-one
SMILES[H][C@@]12CC[C@@](O)(C#CC)[C@@]1(C)C[C@H](C1=CC=C(C=C1)N(C)C)C1=C3CCC(=O)C=C3CC[C@@]21[H]
InChI IdentifierInChI=1S/C29H35NO2/c1-5-15-29(32)16-14-26-24-12-8-20-17-22(31)11-13-23(20)27(24)25(18-28(26,29)2)19-6-9-21(10-7-19)30(3)4/h6-7,9-10,17,24-26,32H,8,11-14,16,18H2,1-4H3/t24-,25+,26-,28-,29-/m0/s1
InChI KeyVKHAHZOOUSRJNA-GCNJZUOMSA-N
Chemical Taxonomy
Description belongs to the class of organic compounds known as oxosteroids. These are steroid derivatives carrying a C=O group attached to steroid skeleton.
KingdomOrganic compounds
Super ClassLipids and lipid-like molecules
ClassSteroids and steroid derivatives
Sub ClassOxosteroids
Direct ParentOxosteroids
Alternative Parents
Substituents
  • 3-oxosteroid
  • Hydroxysteroid
  • Oxosteroid
  • 17-hydroxysteroid
  • Tertiary aliphatic/aromatic amine
  • Dialkylarylamine
  • Aniline or substituted anilines
  • Cyclohexenone
  • Benzenoid
  • Monocyclic benzene moiety
  • Ynone
  • Cyclic alcohol
  • Tertiary alcohol
  • Cyclic ketone
  • Tertiary amine
  • Ketone
  • Alcohol
  • Organooxygen compound
  • Organonitrogen compound
  • Organopnictogen compound
  • Organic oxygen compound
  • Organic nitrogen compound
  • Carbonyl group
  • Organic oxide
  • Amine
  • Hydrocarbon derivative
  • Aromatic homopolycyclic compound
Molecular FrameworkAromatic homopolycyclic compounds
External Descriptors
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
  • Membrane
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
Applications
Biological Roles
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting Point191-196°C
Boiling PointNot Available
SolubilityPoorly soluble
Predicted Properties
PropertyValueSource
Water Solubility0.0034 g/LALOGPS
logP5.33ALOGPS
logP5.13ChemAxon
logS-5.1ALOGPS
pKa (Strongest Acidic)12.87ChemAxon
pKa (Strongest Basic)4.89ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count3ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area40.54 ŲChemAxon
Rotatable Bond Count3ChemAxon
Refractivity132.58 m³·mol⁻¹ChemAxon
Polarizability50.69 ųChemAxon
Number of Rings5ChemAxon
Bioavailability1ChemAxon
Rule of FiveNoChemAxon
Ghose FilterNoChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash KeyView
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, Positivesplash10-0w29-0356900000-2d8af6b9cc4537ce26fdSpectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (1 TMS) - 70eV, Positivesplash10-0079-2055900000-6e525ae464b1871d9ebeSpectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, PositiveNot AvailableSpectrum
LC-MS/MSLC-MS/MS Spectrum - , positivesplash10-001i-0332900000-9cbfa7fe6866f246577aSpectrum
LC-MS/MSLC-MS/MS Spectrum - , positivesplash10-008i-2952100000-aec78774f54c2156c662Spectrum
LC-MS/MSLC-MS/MS Spectrum - 45V, Positivesplash10-008i-0931000000-ee8279dfb415bc0681f0Spectrum
LC-MS/MSLC-MS/MS Spectrum - 90V, Positivesplash10-05qc-2920000000-0d03d8c581f1c4499042Spectrum
LC-MS/MSLC-MS/MS Spectrum - 60V, Positivesplash10-001i-1930000000-99d6acb871669431c089Spectrum
LC-MS/MSLC-MS/MS Spectrum - 75V, Positivesplash10-003r-1920000000-303a5d8b0036258c0881Spectrum
LC-MS/MSLC-MS/MS Spectrum - 15V, Positivesplash10-001i-0000900000-7e417e2be2da168b3821Spectrum
LC-MS/MSLC-MS/MS Spectrum - 35V, Positivesplash10-0089-0964600000-5ddcf4202f05b45619f4Spectrum
LC-MS/MSLC-MS/MS Spectrum - 30V, Positivesplash10-0089-0953300000-18649aead8226d5457ecSpectrum
LC-MS/MSLC-MS/MS Spectrum - 45V, Positivesplash10-008i-0931000000-6b177a9fd1b11cda4eeeSpectrum
LC-MS/MSLC-MS/MS Spectrum - 90V, Positivesplash10-05qc-2920000000-d4339450b67349c7406cSpectrum
LC-MS/MSLC-MS/MS Spectrum - 30V, Positivesplash10-0089-0953300000-3040f97a5bcf7379d742Spectrum
LC-MS/MSLC-MS/MS Spectrum - 60V, Positivesplash10-001i-1930000000-75e712433c777112ab39Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-001i-0003900000-482e952a320026611e1aSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-0il0-0019500000-0f2300ca0d9d68333f18Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-006y-0239000000-3062d0e76d145ad51502Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-004i-0000900000-2424eebcdaf0cba228cbSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-004i-1003900000-0d5db361e6c6078d19c6Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-0ir9-1209300000-533594d69ffd57a0e51aSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-001i-0000900000-8a86e41d44598870ec34Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-001i-0245900000-5a92d3450ccf91b2fea2Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-000t-2419000000-7daab3ac34340f53f4f6Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-004i-0000900000-a4eb2582acf4a0d738a0Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-004i-0001900000-5e48687bc755905f2a3dSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-0gbc-0179400000-0a9aad20761af0cfe7faSpectrum
1D NMR1H NMR SpectrumNot AvailableSpectrum
1D NMR13C NMR SpectrumNot AvailableSpectrum
Toxicity Profile
Route of ExposureOral. The absolute bioavailability of a 20 mg oral dose is 69%
Mechanism of ToxicityMifepristone is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.
MetabolismHepatic. Hepatic, by Cytochrome P450 3A4 isoenzyme to the N-monodemethylated metabolite (RU 42 633); RU 42 698, which results from the loss of two methyl groups from position 11 beta; and RU 42 698, which results from terminal hydroxylation of the 17–propynyl chain. Route of Elimination: Fecal: 83%; Renal: 9%. Half Life: 18 hours
Toxicity ValuesNot Available
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesFor the medical termination of intrauterine pregnancy through 49 days' pregnancy. Also indicated to control hyperglycemia secondary to hypercortisolism in adult patients with endogenous Cushing's syndrome who have type 2 diabetes mellitus or glucose intolerance and are not candidates for surgery or have had unsuccessful surgery.
Minimum Risk LevelNot Available
Health EffectsAcute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.
SymptomsNearly all of the women who receive mifepristone will report adverse reactions, and many can be expected to report more than one such reaction. About 90% of patients report adverse reactions following administration of misoprostol on day three of the treatment procedure. Side effects include more heavy bleeding than a heavy manstrual period, abdominal pain, uterine cramping, nausea, vomiting, and diarrhea.
TreatmentIf the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.
Concentrations
Not Available
DrugBank IDDB00834
HMDB IDHMDB0014972
FooDB IDNot Available
Phenol Explorer IDNot Available
KNApSAcK IDNot Available
BiGG IDNot Available
BioCyc IDNot Available
METLIN IDNot Available
PDB ID486
Wikipedia LinkMifepristone
Chemspider ID49889
ChEBI ID50692
PubChem Compound ID55245
Kegg Compound IDC07652
YMDB IDNot Available
ECMDB IDNot Available
References
Synthesis Reference

Narendra Joshi, Anil Khile, Nitin Pradhan, “Novel polymorph form M of mifepristone and process for its preparation.” U.S. Patent US20070105828, issued May 10, 2007.

MSDSLink
General References
1. Spitz IM, Bardin CW, Benton L, Robbins A: Early pregnancy termination with mifepristone and misoprostol in the United States. N Engl J Med. 1998 Apr 30;338(18):1241-7.
2. Heikinheimo O, Kekkonen R, Lahteenmaki P: The pharmacokinetics of mifepristone in humans reveal insights into differential mechanisms of antiprogestin action. Contraception. 2003 Dec;68(6):421-6.
3. Piaggio G, von Hertzen H, Heng Z, Bilian X, Cheng L: Meta-analyses of randomized trials comparing different doses of mifepristone in emergency contraception. Contraception. 2003 Dec;68(6):447-52.
4. Chabbert-Buffet N, Meduri G, Bouchard P, Spitz IM: Selective progesterone receptor modulators and progesterone antagonists: mechanisms of action and clinical applications. Hum Reprod Update. 2005 May-Jun;11(3):293-307. Epub 2005 Mar 24.
5. Fiala C, Gemzel-Danielsson K: Review of medical abortion using mifepristone in combination with a prostaglandin analogue. Contraception. 2006 Jul;74(1):66-86. Epub 2006 May 19.
6. Simons K, Toomre D: Lipid rafts and signal transduction. Nat Rev Mol Cell Biol. 2000 Oct;1(1):31-9.
7. Watson AD: Thematic review series: systems biology approaches to metabolic and cardiovascular disorders. Lipidomics: a global approach to lipid analysis in biological systems. J Lipid Res. 2006 Oct;47(10):2101-11. Epub 2006 Aug 10.
8. Sethi JK, Vidal-Puig AJ: Thematic review series: adipocyte biology. Adipose tissue function and plasticity orchestrate nutritional adaptation. J Lipid Res. 2007 Jun;48(6):1253-62. Epub 2007 Mar 20.
9. Lingwood D, Simons K: Lipid rafts as a membrane-organizing principle. Science. 2010 Jan 1;327(5961):46-50. doi: 10.1126/science.1174621.
10. The lipid handbook with CD-ROM