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Record Information
Creation Date2014-09-11 05:17:08 UTC
Update Date2014-12-24 20:26:57 UTC
Accession NumberT3D4799
Common NameAzelaic Acid
ClassSmall Molecule
DescriptionAzelaic acid is a saturated dicarboxylic acid found naturally in wheat, rye, and barley. It is a natural substance that is produced by Malassezia furfur (also known as Pityrosporum ovale), a yeast that lives on normal skin. It is effective against a number of skin conditions, such as mild to moderate acne, when applied topically in a cream formulation of 20%. It works in part by stopping the growth of skin bacteria that cause acne, and by keeping skin pores clear. Azelaic acid's antimicrobial action may be attributable to inhibition of microbial cellular protein synthesis.
Compound Type
  • Antineoplastic Agent
  • Dermatologic Agent
  • Drug
  • Food Toxin
  • Metabolite
  • Natural Compound
  • Organic Compound
  • Plant Toxin
Chemical Structure
1,7-Heptanedicarboxylic acid
1,9-Nonanedioic acid
Acide azélaïque
Ácido azelaico
Acidum acelaicum
Acidum azelaicum
Anchoic acid
Azalaic acid
Azelaic acid
Azelainic acid
Emerox 1110
Emerox 1144
Emery'S L-110
Heptanedicarboxylic acid
Lepargylic acid
N-Nonanedioic acid
Nonanedioic acid
Nonanedioic acid azelaic acid
Nonanedioic acid homopolymer
Poly(azelaic anhydride)
Polyazelaic anhydride
Chemical FormulaC9H16O4
Average Molecular Mass188.221 g/mol
Monoisotopic Mass188.105 g/mol
CAS Registry Number123-99-9
IUPAC Namenonanedioic acid
Traditional Nameazelaic acid
InChI IdentifierInChI=1S/C9H16O4/c10-8(11)6-4-2-1-3-5-7-9(12)13/h1-7H2,(H,10,11)(H,12,13)
Chemical Taxonomy
Description belongs to the class of organic compounds known as medium-chain fatty acids. These are fatty acids with an aliphatic tail that contains between 4 and 12 carbon atoms.
KingdomOrganic compounds
Super ClassLipids and lipid-like molecules
ClassFatty Acyls
Sub ClassFatty acids and conjugates
Direct ParentMedium-chain fatty acids
Alternative Parents
  • Medium-chain fatty acid
  • Dicarboxylic acid or derivatives
  • Carboxylic acid
  • Carboxylic acid derivative
  • Organic oxygen compound
  • Organic oxide
  • Hydrocarbon derivative
  • Organooxygen compound
  • Carbonyl group
  • Aliphatic acyclic compound
Molecular FrameworkAliphatic acyclic compounds
External Descriptors
Biological Properties
StatusDetected and Not Quantified
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue Locations
  • Prostate
  • Skin
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
AppearanceWhite powder.
Experimental Properties
Melting Point106.5°C
Boiling Point286.5°C at 1.00E+02 mm Hg
Solubility2400 mg/L (at 20°C)
Predicted Properties
Water Solubility2.28 g/LALOGPS
pKa (Strongest Acidic)4.15ChemAxon
Physiological Charge-2ChemAxon
Hydrogen Acceptor Count4ChemAxon
Hydrogen Donor Count2ChemAxon
Polar Surface Area74.6 ŲChemAxon
Rotatable Bond Count8ChemAxon
Refractivity46.54 m³·mol⁻¹ChemAxon
Polarizability20.5 ųChemAxon
Number of Rings0ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectrum TypeDescriptionSplash KeyView
GC-MSGC-MS Spectrum - GC-MS (2 TMS)splash10-0v0r-4920000000-5a3ed693b1c4083f1f15JSpectraViewer | MoNA
GC-MSGC-MS Spectrum - GC-MS (Non-derivatized)splash10-0v0r-4920000000-5a3ed693b1c4083f1f15JSpectraViewer | MoNA
GC-MSGC-MS Spectrum - GC-EI-TOF (Non-derivatized)splash10-00mk-1910000000-83ba58dac4b0698643d0JSpectraViewer | MoNA
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, Positivesplash10-000f-9600000000-24638c458fa83f47c259JSpectraViewer
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (2 TMS) - 70eV, Positivesplash10-00y0-9740000000-d157d08c3a7c87244190JSpectraViewer
LC-MS/MSLC-MS/MS Spectrum - Quattro_QQQ 10V, Negative (Annotated)splash10-000i-0900000000-a118e433f0bd27a95b89JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - Quattro_QQQ 25V, Negative (Annotated)splash10-006t-9600000000-93b3a375b722791cb5c9JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - Quattro_QQQ 40V, Negative (Annotated)splash10-052k-9500000000-6b069f2fed947651b284JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ (API3000, Applied Biosystems) 10V, Negativesplash10-000i-0900000000-7980b5eadcca6ee1eaddJSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ (API3000, Applied Biosystems) 20V, Negativesplash10-004i-0900000000-462585874f7661d40d5bJSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ (API3000, Applied Biosystems) 30V, Negativesplash10-004j-4900000000-0f65eeeed8c8a6ff3cc9JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ (API3000, Applied Biosystems) 40V, Negativesplash10-0002-9300000000-d654ca3c764066f98358JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ (API3000, Applied Biosystems) 50V, Negativesplash10-0002-9000000000-60a08bb384f2b4cbfca8JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ , negativesplash10-000i-0900000000-7980b5eadcca6ee1eaddJSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ , negativesplash10-004i-0900000000-462585874f7661d40d5bJSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ , negativesplash10-004j-4900000000-0f65eeeed8c8a6ff3cc9JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ , negativesplash10-0002-9300000000-fcefbd80852c2625bc0eJSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-QQ , negativesplash10-0002-9000000000-60a08bb384f2b4cbfca8JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - Linear Ion Trap , negativesplash10-004i-0900000000-26216115e75cad833509JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - Linear Ion Trap , negativesplash10-004i-0900000000-7bef8272c481ea57a60bJSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - Linear Ion Trap , negativesplash10-004i-0900000000-751bf479539d4bd2b5e1JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - Linear Ion Trap , negativesplash10-00di-0900000000-9a056a45b27896966bf9JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - Linear Ion Trap , negativesplash10-00di-0900000000-3155fd845eec8f32ce93JSpectraViewer | MoNA
LC-MS/MSLC-MS/MS Spectrum - , negativesplash10-004r-0900000000-544110f97ebc0f97e15bJSpectraViewer | MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-00dr-0900000000-b1b7c1ab57d58a2405a8JSpectraViewer
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-00g3-2900000000-d0ba7fbbe987efa4c818JSpectraViewer
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-05qd-9100000000-8d65a19b998d18ad08acJSpectraViewer
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-000i-0900000000-a7edc3ac66d27685b9d1JSpectraViewer
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-00kr-1900000000-c56b9d972f88c58dc65bJSpectraViewer
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-0a4l-9300000000-47cbefe19a788d7f36b9JSpectraViewer
MSMass Spectrum (Electron Ionization)splash10-06rx-9100000000-6db2acb47ad4c6163063JSpectraViewer | MoNA
1D NMR1H NMR SpectrumNot AvailableJSpectraViewer
1D NMR1H NMR SpectrumNot AvailableJSpectraViewer
1D NMR13C NMR SpectrumNot AvailableJSpectraViewer
2D NMR[1H,13C] 2D NMR SpectrumNot AvailableJSpectraViewer
Toxicity Profile
Route of ExposureApproximately 4% of the topically applied azelaic acid is systemically absorbed.
Mechanism of ToxicityThe exact mechanism of action of azelaic acid is not known. It is thought that azelaic acid manifests its antibacterial effects by inhibiting the synthesis of cellular protein in anaerobic and aerobic bacteria, especially Staphylococcus epidermidis and Propionibacterium acnes. In aerobic bacteria, azelaic acid reversibly inhibits several oxidoreductive enzymes including tyrosinase, mitochondrial enzymes of the respiratory chain, thioredoxin reductase, 5-alpha-reductase, and DNA polymerases. In anaerobic bacteria, azelaic acid impedes glycolysis. Along with these actions, azelaic acid also improves acne vulgaris by normalizing the keratin process and decreasing microcomedo formation. Azelaic acid may be effective against both inflamed and noninflamed lesions. Specifically, azelaic acid reduces the thickness of the stratum corneum, shrinks keratohyalin granules by reducing the amount and distribution of filaggrin (a component of keratohyalin) in epidermal layers, and lowers the number of keratohyalin granules.
MetabolismMainly excreted unchanged in the urine but undergoes some b-oxidation to shorter chain dicarboxylic acids. Route of Elimination: Azelaic acid is mainly excreted unchanged in the urine, but undergoes some нф-oxidation to shorter chain dicarboxylic acids. Half Life: The observed half-lives in healthy subjects are approximately 45 minutes after oral dosing and 12 hours after topical dosing, indicating percutaneous absorption rate-limited kinetics.
Toxicity ValuesOral LD50 in rat: >5 g/kg
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesFor the topical treatment of mild-to-moderate inflammatory acne vulgaris.
Minimum Risk LevelNot Available
Health EffectsNot Available
SymptomsNot Available
TreatmentNot Available
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDDB00548
PubChem Compound ID2266
ChemSpider ID2179
UniProt IDNot Available
ChEBI ID48131
BioCyc IDNot Available
CTD IDNot Available
Stitch IDNot Available
ACToR IDNot Available
Wikipedia LinkNonanedioic acid
Synthesis Reference

Abdul Malek, Clevys J. Monasterios, G. Ronald Brown, Ved P. Gupta, “Two step oxidation process for the production of carboxylic acids such as azelaic acid from unsaturated substrates.” U.S. Patent US5380928, issued October, 1981.

General References
  1. Mayer-da-Silva A, Gollnick H, Detmar M, Gassmuller J, Parry A, Muller R, Orfanos CE: Effects of azelaic acid on sebaceous gland, sebum excretion rate and keratinization pattern in human skin. An in vivo and in vitro study. Acta Derm Venereol Suppl (Stockh). 1989;143:20-30. [2475995 ]
  2. Hermanns JF, Petit L, Martalo O, Pierard-Franchimont C, Cauwenbergh G, Pierard GE: Unraveling the patterns of subclinical pheomelanin-enriched facial hyperpigmentation: effect of depigmenting agents. Dermatology. 2000;201(2):118-22. [11053913 ]
  3. Hoffmann GF, Meier-Augenstein W, Stockler S, Surtees R, Rating D, Nyhan WL: Physiology and pathophysiology of organic acids in cerebrospinal fluid. J Inherit Metab Dis. 1993;16(4):648-69. [8412012 ]
  4. Korman SH, Mandel H, Gutman A: Characteristic urine organic acid profile in peroxisomal biogenesis disorders. J Inherit Metab Dis. 2000 Jun;23(4):425-8. [10896310 ]
  5. Rocamora V, Puig L, Romani J, de Moragas JM: Amelanotic lentigo maligna melanoma: report of a case and review of the literature. Cutis. 1999 Jul;64(1):53-6. [10431675 ]
  6. Russell JJ: Topical therapy for acne. Am Fam Physician. 2000 Jan 15;61(2):357-66. [10670502 ]
  7. Webster G: Combination azelaic acid therapy for acne vulgaris. J Am Acad Dermatol. 2000 Aug;43(2 Pt 3):S47-50. [10898830 ]
  8. Del Rosso JQ: A status report on the medical management of rosacea: focus on topical therapies. Cutis. 2002 Nov;70(5):271-5. [12469780 ]
  9. Liao DC: Management of acne. J Fam Pract. 2003 Jan;52(1):43-51. [12540312 ]
  10. Del Rosso JQ: Medical treatment of rosacea with emphasis on topical therapies. Expert Opin Pharmacother. 2004 Jan;5(1):5-13. [14680431 ]
  11. Wolf JE Jr: The role of topical metronidazole in the treatment of rosacea. Cutis. 2004 Jan;73(1 Suppl):19-28. [14959942 ]
  12. Frampton JE, Wagstaff AJ: Azelaic acid 15% gel: in the treatment of papulopustular rosacea. Am J Clin Dermatol. 2004;5(1):57-64. [14979745 ]
  13. Halder RM, Richards GM: Management of dyschromias in ethnic skin. Dermatol Ther. 2004;17(2):151-7. [15113282 ]
  14. Halder RM, Richards GM: Topical agents used in the management of hyperpigmentation. Skin Therapy Lett. 2004 Jun-Jul;9(6):1-3. [15334278 ]
  15. Lindow KB: Rosacea. An overview of diagnosis and management. Adv Nurse Pract. 2004 Dec;12(12):27-32. [15615217 ]
  16. Cayce KA, McMichael AJ, Feldman SR: Hyperpigmentation: an overview of the common afflictions. Dermatol Nurs. 2004 Oct;16(5):401-6, 413-6; quiz 417. [15624705 ]
  17. Wolf JE Jr: Present and future rosacea therapy. Cutis. 2005 Mar;75(3 Suppl):4-7; discussion 33-6. [15810803 ]
  18. van Zuuren EJ, Graber MA: The rigor of trials evaluating Rosacea treatments. Cutis. 2005 Mar;75(3 Suppl):13-6; discussion 33-6. [15810805 ]
  19. Purdy S: Acne vulgaris. Clin Evid. 2005 Jun;(13):2038-59. [16135322 ]
  20. Roebuck HL: Face up to rosacea. Nurse Pract. 2005 Sep;30(9):24-30, 35; quiz 36-7. [16151303 ]
  21. Callender VD: Considerations for treating acne in ethnic skin. Cutis. 2005 Aug;76(2 Suppl):19-23. [16164153 ]
  22. Nally JB, Berson DS: Topical therapies for rosacea. J Drugs Dermatol. 2006 Jan;5(1):23-6. [16468288 ]
  23. Fleischer AB Jr: The evolution of azelaic acid. Cutis. 2006 Feb;77(2 Suppl):4-6. [16566281 ]
  24. Draelos ZD: The rationale for advancing the formulation of azelaic acid vehicles. Cutis. 2006 Feb;77(2 Suppl):7-11. [16566282 ]
  25. Elewski B, Thiboutot D: A clinical overview of azelaic acid. Cutis. 2006 Feb;77(2 Suppl):12-6. [16566283 ]
  26. Del Rosso JQ: The use of topical azelaic acid for common skin disorders other than inflammatory rosacea. Cutis. 2006 Feb;77(2 Suppl):22-4. [16566285 ]
  27. Worret WI, Fluhr JW: [Acne therapy with topical benzoyl peroxide, antibiotics and azelaic acid]. J Dtsch Dermatol Ges. 2006 Apr;4(4):293-300. [16638058 ]
  28. Liu RH, Smith MK, Basta SA, Farmer ER: Azelaic acid in the treatment of papulopustular rosacea: a systematic review of randomized controlled trials. Arch Dermatol. 2006 Aug;142(8):1047-52. [16924055 ]
  29. Goodman G: Managing acne vulgaris effectively. Aust Fam Physician. 2006 Sep;35(9):705-9. [16969442 ]
  30. Purdy S: Acne vulgaris. Clin Evid. 2006 Jun;(15):2183-201. [16973084 ]
  31. Gupta AK, Gover MD, Nouri K, Taylor S: The treatment of melasma: a review of clinical trials. J Am Acad Dermatol. 2006 Dec;55(6):1048-65. Epub 2006 Sep 28. [17097400 ]
  32. Fitton A, Goa KL: Azelaic acid. A review of its pharmacological properties and therapeutic efficacy in acne and hyperpigmentary skin disorders. Drugs. 1991 May;41(5):780-98. [1712709 ]
  33. van Zuuren EJ, Gupta AK, Gover MD, Graber M, Hollis S: Systematic review of rosacea treatments. J Am Acad Dermatol. 2007 Jan;56(1):107-15. Epub 2006 Nov 7. [17190628 ]
  34. Gupta AK, Gover MD: Azelaic acid (15% gel) in the treatment of acne rosacea. Int J Dermatol. 2007 May;46(5):533-8. [17472690 ]
  35. Sreekumar A, Poisson LM, Rajendiran TM, Khan AP, Cao Q, Yu J, Laxman B, Mehra R, Lonigro RJ, Li Y, Nyati MK, Ahsan A, Kalyana-Sundaram S, Han B, Cao X, Byun J, Omenn GS, Ghosh D, Pennathur S, Alexander DC, Berger A, Shuster JR, Wei JT, Varambally S, Beecher C, Chinnaiyan AM: Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression. Nature. 2009 Feb 12;457(7231):910-4. doi: 10.1038/nature07762. [19212411 ]
  36. Nguyen QH, Bui TP: Azelaic acid: pharmacokinetic and pharmacodynamic properties and its therapeutic role in hyperpigmentary disorders and acne. Int J Dermatol. 1995 Feb;34(2):75-84. [7737781 ]
  37. Mackrides PS, Shaughnessy AF: Azelaic acid therapy for acne. Am Fam Physician. 1996 Dec;54(8):2457-9. [8961845 ]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available


General Function:
Protein homodimerization activity
Specific Function:
This is a copper-containing oxidase that functions in the formation of pigments such as melanins and other polyphenolic compounds. Catalyzes the rate-limiting conversions of tyrosine to DOPA, DOPA to DOPA-quinone and possibly 5,6-dihydroxyindole to indole-5,6 quinone.
Gene Name:
Uniprot ID:
Molecular Weight:
60392.69 Da
  1. Schallreuter KU, Wood JW: A possible mechanism of action for azelaic acid in the human epidermis. Arch Dermatol Res. 1990;282(3):168-71. [2114832 ]
  2. Nazzaro-Porro M: Azelaic acid. J Am Acad Dermatol. 1987 Dec;17(6):1033-41. [2963038 ]
  3. Picardo M, Passi S, Sirianni MC, Fiorilli M, Russo GD, Cortesi E, Barile G, Breathnach AS, Nazzaro-Porro M: Activity of azelaic acid on cultures of lymphoma- and leukemia-derived cell lines, normal resting and stimulated lymphocytes and 3T3 fibroblasts. Biochem Pharmacol. 1985 May 15;34(10):1653-8. [4004885 ]
  4. Nazzaro-Porro M, Passi S, Balus L, Breathnach A, Martin B, Morpurgo G: Effect of dicarboxylic acids on lentigo maligna. J Invest Dermatol. 1979 Jun;72(6):296-305. [448162 ]
General Function:
Sterol 5-alpha reductase activity
Specific Function:
Converts testosterone (T) into 5-alpha-dihydrotestosterone (DHT) and progesterone or corticosterone into their corresponding 5-alpha-3-oxosteroids. It plays a central role in sexual differentiation and androgen physiology.
Gene Name:
Uniprot ID:
Molecular Weight:
28393.015 Da
  1. Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. [17139284 ]
  2. Imming P, Sinning C, Meyer A: Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct;5(10):821-34. [17016423 ]
  3. Stamatiadis D, Bulteau-Portois MC, Mowszowicz I: Inhibition of 5 alpha-reductase activity in human skin by zinc and azelaic acid. Br J Dermatol. 1988 Nov;119(5):627-32. [3207614 ]
General Function:
Steroid binding
Specific Function:
Efficiently catalyzes the reduction of progesterone, androstenedione, 17-alpha-hydroxyprogesterone and testosterone to 5-beta-reduced metabolites. The bile acid intermediates 7-alpha,12-alpha-dihydroxy-4-cholesten-3-one and 7-alpha-hydroxy-4-cholesten-3-one can also act as substrates.
Gene Name:
Uniprot ID:
Molecular Weight:
37376.615 Da
  1. Stamatiadis D, Bulteau-Portois MC, Mowszowicz I: Inhibition of 5 alpha-reductase activity in human skin by zinc and azelaic acid. Br J Dermatol. 1988 Nov;119(5):627-32. [3207614 ]
General Function:
Zinc ion binding
Specific Function:
Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Isoform 3 is involved in activation of NOS3 and endothelial nitric oxide production. Isoforms lacking one or several functional domains are thought to modulate transcriptional activity by competitive ligand or DNA binding and/or heterodimerization with the full length receptor. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3. Isoform 3 can bind to ERE and inhibit isoform 1.
Gene Name:
Uniprot ID:
Molecular Weight:
66215.45 Da
Binding/Activity Constants
TypeValueAssay TypeAssay Source
AC508.63 uMTox21_ERa_LUC_BG1_AgonistTox21/NCGC
  1. Sipes NS, Martin MT, Kothiya P, Reif DM, Judson RS, Richard AM, Houck KA, Dix DJ, Kavlock RJ, Knudsen TB: Profiling 976 ToxCast chemicals across 331 enzymatic and receptor signaling assays. Chem Res Toxicol. 2013 Jun 17;26(6):878-95. doi: 10.1021/tx400021f. Epub 2013 May 16. [23611293 ]