(5Z)-7-[(1R,2R,3R)-3-hydroxy-2-[(1E,3S)-3-hydroxyoct-1-en-1-yl]-5-oxocyclopentyl]hept-5-enoic acid

• ChemBase ID: 793
• Molecular Formular: C20H32O5
• Molecular Mass: 352.46508
• Monoisotopic Mass: 352.22497412
• SMILES: O[C@H]1[C@@H]([C@H](C(=O)C1)C/C=C\CCCC(=O)O)/C=C/[C@@H](O)CCCCC
• Canonical SMILES: CCCCC[C@@H](/C=C/[C@H]1[C@H](O)CC(=O)[C@@H]1C/C=C\CCCC(=O)O)O
• InChI: InChI=1S/C20H32O5/c1-2-3-6-9-15(21)12-13-17-16(18(22)14-19(17)23)10-7-4-5-8-11-20(24)25/h4,7,12-13,15-17,19,21,23H,2-3,5-6,8-11,14H2,1H3,(H,24,25)/b7-4-,13-12+/t15-,16+,17+,19+/m0/s1
• InChIKey: XEYBRNLFEZDVAW-ARSRFYASSA-N

NAMES AND DATABASE IDS

Names

• IUPAC name: (5Z)-7-[(1R,2R,3R)-3-hydroxy-2-[(1E,3S)-3-hydroxyoct-1-en-1-yl]-5-oxocyclopentyl]hept-5-enoic acid
• IUPAC Traditional name: dinoprostone
• Brand Name: Cervidil; Prepidil; Prostarmon E; Prostin E; Prostin E2; Propess
• Synonyms: (5Z,11α,13E,15S)-11,15-Dihydroxy-9-oxoprosta-5,13-dienoic acid; Dinoprostone; Prostaglandin E2; Dinoprostone Prostaglandin E2; PGE2; Prostaglandin E2; Dinoprostone; (5Z,11α,13E,15S)-11,15-Dihydroxy-9-oxoprosta-5,13-dien-1-oic Acid; 7-[3-Hydroxy-2-(3-hydroxy-1-octenyl)-5-oxocyclopentyl]-5-heptenoic Acid; (-)-Prostaglandin E2; (15S)-Prostaglandin E2; Cervidil; Cerviprime; Cerviprost; Minprostin E2; Prepidil; Primiprost; Prostin E2; l-PGE2; Prostaglandin E2

Database IDs

• CAS Number: 363-24-6
• EC Number: 206-656-6
• MDL Number: MFCD00077861
• Beilstein Number: 4709356
• PubChem SID: 24898683; 24898775; 160964256; 46505549; 24898100
• PubChem CID: 5280360

CALCULATED PROPERTIES

JChem

• Acid pKa: 4.3033595
• H Acceptors: 5
• H Donor: 3
• LogD (pH = 5.5): 2.0038702
• LogD (pH = 7.4): 0.2647247
• Log P: 3.22527
• Molar Refractivity: 99.4351 cm^3
• Polarizability: 38.188305 Å^3
• Polar Surface Area: 94.83 Å^2
• Rotatable Bonds: 12
• Lipinski's Rule of Five: true

ALOGPS 2.1

• Log P: 3.31
• LOG S: -3.9
• Solubility (Water): 4.40e-02 g/l

PROPERTIES

Physical Property

• Solubility: 58.1 mg/L; Chloroform; Ethanol; ethanol: soluble1 mg/mL; Methanol
• Apperance: powder; White Solid
• Melting Point: 65-66°C
• Hydrophobicity(logP): 2.8

Safety Information

• Storage Condition: Amber Vial, -20°C Freezer, Under Inert Atmosphere
• RTECS: UK8000000
• European Hazard Symbols: Toxic (T)
• German water hazard class: 3
• Risk Statements: 60-61-22
• Safety Statements: 53-22-26-36/37/39-45
• GHS Pictograms: GHS07; GHS08
• GHS Signal Word: Danger
• GHS Hazard statements: H302-H360
• GHS Precautionary statements: P201-P308 + P313
• Personal Protective Equipment: Eyeshields, Faceshields, full-face particle respirator type N100 (US), Gloves, respirator cartridge type N100 (US), type P1 (EN143) respirator filter, type P3 (EN 143) respirator cartridges
• Storage Temperature: -20°C

Pharmacology Properties

• Gene Information: human ... PTGER1(5731), PTGER2(5732), PTGER3(5733), PTGER4(5734), PTGIR(5739)mouse ... Ptger1(19216), Ptger2(19217), Ptger3(19218), Ptger4(19219)

Product Information

• Purity: ≥93% (HPLC); ≥98% (TLC)
• Potency: 0.25-100 ng/mL
• Suitability: suitable for cell culture
• Biological Source: synthetic
• Sterility: γ-irradiated

DETAILS

DrugBank - DB00917

• Drug Groups: approved
• Description: Dinoprostone is a naturally occurring prostaglandin E2 (PGE2). It has important effects in labour. It also stimulates osteoblasts to release factors which stimualtes bone resorption by osteoclasts. As a prescription drug it is used as a vaginal suppository, to prepare the cervix for labour and to induce labour.
• Indication: For the termination of pregnancy during the second trimester (from the 12th through the 20th gestational week as calculated from the first day of the last normal menstrual period), as well as for evacuation of the uterine contents in the management of missed abortion or intrauterine fetal death up to 28 weeks of gestational age as calculated from the first day of the last normal menstrual period. Also used in the management of nonmetastatic gestational trophoblastic disease (benign hydatidiform mole). Other indications include improving the cervical inducibility (cervical "ripening") in pregnant women at or near term with a medical or obstetrical need for labor induction, and the management of postpartum hemorrhage.
• Pharmacology: Dinoprostone is equivalent to prostaglandin E2 (PGE2). It stimulates labor and delivery by stimulating the uterine, and thus terminates pregnancy. Dinoprostone is also capable of stimulating the smooth muscle of the gastrointestinal tract of man. This activity may be responsible for the vomiting and/or diarrhea that is not uncommon when dinoprostone is used to terminate pregnancy.
• Toxicity: Oral, mouse: LD₅₀ = 750 mg/kg; Oral, rat: LD₅₀ = 500 mg/kg.
• Affected Organisms: Humans and other mammals
• Biotransformation: Rapid metabolism of dinoprostone occurs primarily in the local tissues; any systemic absorption of the medication is cleared mainly in the maternal lungs and, secondarily, at sites such as the liver and kidneys.
• Absorption: Absorbed at a rate of 0.3 mg per hour over 12 hours while the vaginal system is in place.
• Half Life: Less than 5 minutes.
• Protein Binding: 73%, to albumin
• Elimination: The major route of elimination of the products of PGE2 metabolism is the kidneys.
• External Links: Wikipedia; RxList; Drugs.com

Sigma Aldrich - P0409

Physical form
powder -20 °C; stock-frozen in working aliquots, avoid repeated freeze/thaw
Biochem/physiol Actions
Most biologically active prostaglandin. PGE2 induces cervical ripening and parturition; mediates bradykinin-induced vasodilation; regulates adenylyl cyclase. Tumor cells that over-express cyclooxygenase 2 display increased invasiveness, angiogenesis, and resistance to apoptosis that may be due to the PGE2-induced expression of angiogenic factors and stabilization of the anti-apoptotic protein, survivin.The effect of PGE2 on the immune system is mixed. It inhibits T cell activation in vitro, suggesting it is an immunosuppressant. However, in vivo, it appears to effect expansion of the Th17 subset and differentiation of the Th1 subset of T helper cells, marking it as an immunoactivator.1
Prostaglandin E2 is a signaling molecule produced by activated platelets. The release of PGE2 by activated platelets is part of a mechanism by which activated platelets utilize adjacent erythrocytes to help in clot formation. This product was shown to lower the filterability of human erythrocytes by approximately 30% at a concentration of 10-10sup M and also caused a reduction in mean cell volume by about 10%. The cause of cell shrinkage was the induction of a PGE2- stimulated K+ efflux pathway leading to rapid loss of cellular K+ ions. This loss was shown to be Ca2+dependent. PGE2 has been shown to stimulate the production of interleukin-6 (IL-6) by neonatal mouse parietal bones. After 6 hours in culture, cells stimulated with 10-8sup M PGE2 produced significantly more IL-6 than controls. The pyrogenic activity of PGE2 was not inhibited by dexamethasone, unlike prostaglandin F2α.Most biologically active prostaglandin. PGE2 induces cervical ripening and parturition; mediates bradykinin-induced vasodilation; regulates adenylyl cyclase. Tumor cells that over-express cyclooxygenase 2 display increased invasiveness, angiogenesis, and resistance to apoptosis that may be due to the PGE2-induced expression of angiogenic factors and stabilization of the anti-apoptotic protein, survivin.

Sigma Aldrich - P4172

Biochem/physiol Actions
Most biologically active prostaglandin. PGE2 induces cervical ripening and parturition; mediates bradykinin-induced vasodilation; regulates adenylyl cyclase. Tumor cells that over-express cyclooxygenase 2 display increased invasiveness, angiogenesis, and resistance to apoptosis that may be due to the PGE2-induced expression of angiogenic factors and stabilization of the anti-apoptotic protein, survivin.The effect of PGE2 on the immune system is mixed. It inhibits T cell activation in vitro, suggesting it is an immunosuppressant. However, in vivo, it appears to effect expansion of the Th17 subset and differentiation of the Th1 subset of T helper cells, marking it as an immunoactivator.1

Sigma Aldrich - P5640

Biochem/physiol Actions
Most biologically active prostaglandin. PGE2 induces cervical ripening and parturition; mediates bradykinin-induced vasodilation; regulates adenylyl cyclase. Tumor cells that over-express cyclooxygenase 2 display increased invasiveness, angiogenesis, and resistance to apoptosis that may be due to the PGE2-induced expression of angiogenic factors and stabilization of the anti-apoptotic protein, survivin.The effect of PGE2 on the immune system is mixed. It inhibits T cell activation in vitro, suggesting it is an immunosuppressant. However, in vivo, it appears to effect expansion of the Th17 subset and differentiation of the Th1 subset of T helper cells, marking it as an immunoactivator.1

Sigma Aldrich - P6532

Application
For use in cell culture applications for the study of prostaglandin regulated cell signaling and gene regulation.
Physical form
powder -20 °C; stock-frozen in working aliquots, avoid repeated freeze/thaw
Biochem/physiol Actions
Most biologically active prostaglandin. PGE2 induces cervical ripening and parturition; mediates bradykinin-induced vasodilation; regulates adenylyl cyclase. Tumor cells that over-express cyclooxygenase 2 display increased invasiveness, angiogenesis, and resistance to apoptosis that may be due to the PGE2-induced expression of angiogenic factors and stabilization of the anti-apoptotic protein, survivin.The effect of PGE2 on the immune system is mixed. It inhibits T cell activation in vitro, suggesting it is an immunosuppressant. However, in vivo, it appears to effect expansion of the Th17 subset and differentiation of the Th1 subset of T helper cells, marking it as an immunoactivator.1

Toronto Research Chemicals - P838610

The most common and most biologically potent of mammalian prostaglandins. Isolated from sheep prostate. Oxytocic; abortifacient.

REFERENCES

• Van Dorp, D.A., et al.: Biochem. Biopphys. Acta, 90, 204 (1964)
• Hamberg, M., et al.: J. Biol. Chem., 246, 6713 (1964)