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1. Acocantherin
2. Acolongifloroside K
3. G Strophanthin
4. G-strophanthin
1. G-strophanthin
2. Ouabaine
3. Acocantherin
4. Ouabagenin L-rhamnoside
5. Oubain
6. Purostrophan
7. Ouabain Anhydrous
8. Gratus Strophanthin
9. Strodival
10. Astrobain
11. Gratibain
12. Ouabain Octahydrate
13. 630-60-4
14. Strophoperm
15. Acocantherine
16. Ouabagenin-l-rhamnosid
17. Strophalen
18. Kombetin
19. Uabaina
20. Rectobaina
21. Solufantina
22. Strophosan
23. G-strophicor
24. Chebi:472805
25. G-strophanthin (jan)
26. Uabanin
27. Mls000069786
28. Chembl222863
29. Nsc-25485
30. 5acl011p69
31. Strophantin-g
32. Quabain
33. Smr000058492
34. Strophanthin-g
35. Dsstox_cid_23765
36. Dsstox_rid_80072
37. Dsstox_gsid_43765
38. G-strophanthin [jan]
39. 3-(alpha-l-rhamnopyranosyloxy)-1beta,5beta,11alpha,14,19-pentahydroxy-5beta-card-20(22)-enolide
40. Card-20(22)-enolide, 3-[(6-deoxy-.alpha.-l-mannopyranosyl)oxy]-1,5,11,14,19-pentahydroxy-, (1.beta.,3.beta.,5.beta.,11.alpha.)-
41. Obn
42. Ouabain, Octahydrate
43. Cardiac Glycoside
44. 4-[(1s,2r,3r,5s,7s,10r,11s,14r,15r,17r)-3,7,11,17-tetrahydroxy-2-(hydroxymethyl)-15-methyl-5-{[(2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxy}tetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadecan-14-yl]-2,5-dihydrofuran-2-one
45. Cas-630-60-4
46. Ouabagenin-l-rhamnosid [german]
47. Sr-01000076047
48. Ccris 965
49. Unii-5acl011p69
50. Hsdb 3519
51. 1ibg
52. Ncgc00163473-01
53. 3-[(1r,3s,5s,8r,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-[(2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydropyran-2-yl]oxy-2,3,4,6,7,8,9,11,12,15,16,17-dodecahydro-1h-cyclopenta[a]phenanthren-17-yl]-2h-furan-5-one
54. Card-20(22)-enolide, 3-((6-deoxy-.alpha.-l-mannopyranosyl)oxy)-1,5,11,14,19-pentahydroxy-, (1.beta.,3.beta.,5.beta.,11.alpha.)-
55. Einecs 211-139-3
56. Nsc 25485
57. Brn 0101712
58. 3a3y
59. Opera_id_395
60. Ouabain [mi]
61. Ouabain [mart.]
62. Prestwick0_000471
63. Prestwick1_000471
64. Prestwick2_000471
65. Prestwick3_000471
66. Ouabain [who-dd]
67. Epitope Id:161502
68. O 3125
69. G-strophanthin [mi]
70. Lopac0_000943
71. Schembl15433
72. Bspbio_000602
73. 5-18-05-00625 (beilstein Handbook Reference)
74. Card-20(22)-enolide, 3-((6-deoxy-alpha-l-mannopyranosyl)oxy)-1,5,11,14,19-pentahydroxy-, (1beta,3beta,5beta,11alpha)-
75. Spbio_002541
76. Ouabain [ep Monograph]
77. Bpbio1_000664
78. Cid_439501
79. Gtpl4826
80. Dtxsid0043765
81. Ouabain Anhydrous [hsdb]
82. Regid_for_cid_439501
83. 3n23
84. Hms2089j19
85. Hms2235a07
86. Hms3262n08
87. Zinc8143614
88. Tox21_110024
89. Tox21_112057
90. Tox21_301547
91. Tox21_500943
92. Bdbm50286739
93. Akos024285581
94. Tox21_112057_1
95. Ccg-205024
96. Ccg-208243
97. Db01092
98. Lp00943
99. Sdccgsbi-0050917.p002
100. 3-((6-deoxy-alpha-l-mannopyranosyl)oxy)-1,5,11alpha,14,19-pentahydroxycard-20(22)-enolide
101. 3-(6-deoxy-alpha-l-mannopyranosyloxy)-1,5,11a,14,19-pentahydroxycard-20(22)-enolide
102. Smp1_000142
103. Ncgc00013319-01
104. Ncgc00015769-17
105. Ncgc00015769-32
106. Ncgc00017394-02
107. Ncgc00017394-07
108. Ncgc00017394-11
109. Ncgc00255970-01
110. Ncgc00261628-01
111. Ncgc00263656-01
112. Eu-0100943
113. C01443
114. D00112
115. Q285911
116. Sr-01000721848
117. Sr-01000076047-1
118. Sr-01000076047-5
119. Sr-01000721848-2
120. Sr-01000721848-4
121. Brd-k35708212-331-03-1
122. (1.beta.,3.beta.,5.beta.,11.alpha.)-3-((6-deoxy-.alpha.-l-mannopyranosyl)oxy)-1,5,11,14,19-pentahydroxycard-20(22)-enolide
123. (1alpha,3beta,5beta,11alpha,17alpha)-3-[(6-deoxy-alpha-l-mannopyranosyl)oxy]-1,5,11,14,19-pentahydroxycard-20(22)-enolide
124. 3-[(6-deoxy-.alpha.-l-mannopyranosyl)oxy]-1,5,11.alpha.,14,19-pentahydroxycard-20(22)-enolide
125. 4-((1r,3s,5s,8r,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydro-2h-pyran-2-yloxy)-hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one
126. 4-((1r,3s,5s,8r,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-(((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyltetrahydro-2h-pyran-2-yl)oxy)hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one
127. 4-((1r,3s,5s,8r,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydro-2h-pyran-2-yloxy)-hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one
128. 4-((1r,3s,5s,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyltetrahydro-2h-pyran-2-yloxy)hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one
129. 4-[(1r,3s,5s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one
130. 4-[(r)-1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one
131. 4-[1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one
132. 4-[1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one(ouabain)
133. Ouabain4-[1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one
| Molecular Weight | 584.7 g/mol |
|---|---|
| Molecular Formula | C29H44O12 |
| XLogP3 | -1.7 |
| Hydrogen Bond Donor Count | 8 |
| Hydrogen Bond Acceptor Count | 12 |
| Rotatable Bond Count | 4 |
| Exact Mass | 584.28327683 g/mol |
| Monoisotopic Mass | 584.28327683 g/mol |
| Topological Polar Surface Area | 207 Ų |
| Heavy Atom Count | 41 |
| Formal Charge | 0 |
| Complexity | 1080 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 15 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Ouabain is included in the database.
NIH/NLM; ClinicalTrials.Gov. Available from, as of February 1, 2017: https://clinicaltrials.gov/ct2/results?term=Ouabain&Search=Search
/EXPL THER/ Up-regulation of placental soluble fms-like tyrosine kinase 1 (sFlt1) contributes to the pathogenesis of preeclampsia. To evaluate novel upstream pathways that regulate placental sFlt1 production, we screened a library of natural compounds (n=502) in human placental cell lines. Here, we report 3 compounds in the cardiac glycoside family, ouabain, gitoxigenin, and digitoxin, that inhibit placental sFlt1 production at nanomolar concentrations in vitro. We further characterized ouabain and demonstrated that it inhibits sFlt1 mRNA and protein expression in human placental cytotrophoblasts and explant cultures in a dose- and time-dependent manner. Ouabain down-regulated sFlt1 production by inhibiting hypoxia-inducible factor 1 (HIF-1alpha) protein expression in the placenta. Furthermore, we found that phosphorylation of heat-shock protein 27 (HSP27) was necessary for ouabain to inhibit HIF-1alpha translation. In a rat model of pregnancy-induced hypertension, ouabain reduced mean arterial pressure and enhanced placental HSP27 phosphorylation without any adverse effects on pups ...
PMID:24970393 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202104 Rana S et al; FASEB J 28 (10): 4324-34 (2014)
/EXPL THER/ Cytotoxicity and proliferative effects of ouabain on H460 lung cancer cells were evaluated by the MTT assay. The levels of integrin proteins in response to ouabain were determined by western blotting. Anchorage-independent growth and migration behaviors were performed by the wound healing assay and colony formation assay, respectively. Herein, the results suggested that exposure of the lung cancer cells to physiological concentrations of ouabain significantly altered the level of integrins. Ouabain suppressed integrin alpha-4, alpha-5, alpha-v, beta-3 and beta-4, whereas it had no significant effect on integrin beta-1 and beta-4. According to the switch patterns of integrins, ouabain treatment resulted in a dramatic reduction of cell colony size and inhibition of cancer cell migration. However, ouabain-induced integrin switch had only a slight effect on chemotherapeutic drug susceptibility. Ouabain may have a role in suppressing cancer metastasis via integrin regulation.
PMID:25275046 Ninsontia C, Chanvorachote P; Anticancer Res 34 (10): 5495-502 (2014)
A recent study confirmed the long-known clinical experience that ouabain has an inhibitory effect on cardiotoxicity induced by digitalis glycosides. Ouabain at a low dosage delayed the start of arrythmia induced by digoxin on guinea pig papillary muscle. In addition, ouabain at a low dosage but not at a high dosage delayed the development of digoxin-induced arrhythmia in anesthetized guinea pigs. Thus, the long-known characteristic dose dependency of ouabain effects has been confirmed.
Furstenwerth H; lnt J Clin Pract 64 (12) 1591-4 (2010)
For more Therapeutic Uses (Complete) data for Ouabain (11 total), please visit the HSDB record page.
For the treatment of atrial fibrillation and flutter and heart failure
Ouabain, a cardiac glycoside similar to digitoxin, is used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation.
Enzyme Inhibitors
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)
Cardiotonic Agents
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE). (See all compounds classified as Cardiotonic Agents.)
C - Cardiovascular system
C01 - Cardiac therapy
C01A - Cardiac glycosides
C01AC - Strophanthus glycosides
C01AC01 - G-strophanthin
The effect of i.v.-administered ouabain starts immediately after injection, reaches a maximum after 5 min, last 5-7 hr and then rapidly declines.
Furstenwerth H; lnt J Clin Pract 64 (12) 1591-4 (2010)
It is poorly absorbed from alimentary tract, where much of oral dose appears to be destroyed.
Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-842
Four, 7 and 10% of (3)H-ouabain had been absorbed 1, 5 and 15 hr respectively after oral administration to guinea pigs. Percentage absorbed was constant at each of 3 dose levels. ... Similar results obtained in man. ... /It/ was absorbed from GI tract of rats by passive diffusion. Absorption of im dose probably depended more on tissue-blood flow than on rates of diffusion ... 67% of iv dose was excreted in 30-min bile of rats. ... /It/ was actively transported from liver to bile, and carbon tetrachloride pretreatment of rats reduced biliary excretion by depressing this transport.
The Chemical Society. Foreign Compound Metabolism in Mammals. Volume 2: A Review of the Literature Published Between 1970 and 1971. London: The Chemical Society, 1972., p. 67
Plasma clearance of ouabain following iv admin was much faster in rat than in rabbit or dog. Levels of radioactivity in plasma, bile, and liver ... determined 20 min after iv administration ... showed that rat exhibited overall bile to plasma concentration ratio of 1500, whereas same ratio was much less for rabbit (2.9) and dog (9.3). Liver/plasma and bile/liver concentration ratios ... were ... much greater in rat (20 and 71) than in rabbit (2.5 and 1.3) or dog (3.3 and 2.7). This species variation is thought to be important factor in resistance of rat to toxic effects of ouabain relative to rabbit and dog.
The Chemical Society. Foreign Compound Metabolism in Mammals Volume 3. London: The Chemical Society, 1975., p. 575
For more Absorption, Distribution and Excretion (Complete) data for Ouabain (7 total), please visit the HSDB record page.
Ouabain ... is not bound extensively to plasma albumin and ... /is/ excreted largely unchanged.
Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 673
... Almost entirely eliminated by renal excretion, with a biological-half-life ... about 21 hr in normal adults but longer in elderly persons & much longer in renal failure.
Osol, A. (ed.). Remington's Pharmaceutical Sciences. 16th ed. Easton, Pennsylvania: Mack Publishing Co., 1980., p. 798
Ouabain inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Ouabain also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
Ouabain, an endogenous digitalis compound, has been detected in nanomolar concentrations in the plasma of several mammals and is associated with the development of hypertension. In addition, plasma ouabain is increased in several hypertension models, and the acute or chronic administration of ouabain increases blood pressure in rodents. These results suggest a possible association between ouabain and the genesis or development and maintenance of arterial hypertension. One explanation for this association is that ouabain binds to the alpha-subunit of the Na(+) pump, inhibiting its activity. Inhibition of this pump increases intracellular Na(+), which reduces the activity of the sarcolemmal Na(+)/Ca(2+) exchanger and thereby reduces Ca(2+) extrusion. Consequently, intracellular Ca(2+) increases and is taken up by the sarcoplasmic reticulum, which, upon activation, releases more calcium and increases the vascular smooth muscle tone. In fact, acute treatment with ouabain enhances the vascular reactivity to vasopressor agents, increases the release of norepinephrine from the perivascular adrenergic nerve endings and promotes increases in the activity of endothelial angiotensin-converting enzyme and the local synthesis of angiotensin II in the tail vascular bed. Additionally, the hypertension induced by ouabain has been associated with central mechanisms that increase sympathetic tone, subsequent to the activation of the cerebral renin-angiotensin system. Thus, the association with peripheral mechanisms and central mechanisms, mainly involving the renin-angiotensin system, may contribute to the acute effects of ouabain-induced elevation of arterial blood pressure.
PMID:21956536 Padilha AS et al; Braz J Med Biol Res 44 (9): 933-8 (2011)
The migratory capability of cancer cells is one of the most important hallmarks reflecting metastatic potential. Ouabain, an endogenous cardiac glycoside produced by the adrenal gland, has been previously reported to have anti-tumor activities; however, its role in the regulation of cancer cell migration remains unknown. The present study has revealed that treatment with ouabain at physiological concentrations is able to inhibit the migratory activities of human lung cancer H292 cells. The negative effects of ouabain were found to be mediated through the suppression of migration regulatory proteins, such as focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (Akt), and cell division cycle 42 (Cdc42). We found that the observed actions of ouabain were mediated via a reactive oxygen species (ROS)-dependent mechanism because the addition of ROS scavengers (N-acetylcysteine and glutathione) could reverse the effect of ouabain on cell migration. Furthermore, ouabain was shown to inhibit the spheroidal tumor growth and decrease the cancer cell adhesion to endothelial cells. However, the compound had no significant effect on anoikis of the cells. ...
PMID:23874694 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3707866 Pongrakhananon V et al; PLoS One 8 (7): e68623 (2013)
The steroid Na(+)/K(+) ATPase (NKA) blocker ouabain has been shown to exhibit pro-apoptotic effects in various cell systems; however, the mechanism involved in those effects is unclear. Here, we have demonstrated that incubation of HeLa cells during 24 hr with nanomolar concentrations of ouabain or digoxin causes apoptotic death of 30-50% of the cells. Ouabain caused the activation of caspases-3/7 and -9; however, caspase-8 was unaffected. The fact that compound Z-LEHD-FMK reduced both apoptosis and caspase-9 activation elicited by ouabain, suggest a mitochondrially-mediated pathway. This was strengthened by the fact that ouabain caused ATP depletion and the release of mitochondrial cytochrome c into the cytosol. Furthermore, upon ouabain treatment mitochondrial disruption and redistribution into the cytosol were observed. A mitochondrial site of action for ouabain was further corroborated by tight co-localization of fluorescent ouabain with mitochondria. Finally, in ouabain-treated cells the histamine-elicited elevation of cytosolic Ca(2+) concentration ([Ca(2+)]c) suggests an additional effect on the endoplasmic reticulum (ER) leading to Ca(2+) store depletion. We conclude that fluorescent ouabain is taken up and tightly co-localizes with mitochondria of HeLa cells. This indicates that apoptosis may be triggered by a direct action of ouabain on mitochondria.
PMID:23933121 Alonso E et al; Steroids 78 (11): 1110-8 (2013)
Ouabain, a potent inhibitor of the Na(+), K(+)-ATPase, was identified as an endogenous substance. Recently, ouabain was shown to affect various immunological processes. We have previously demonstrated the ability of ouabain to modulate inflammation, but little is known about the mechanisms involved. Thus, the aim of the present work is to evaluate the immune modulatory role of ouabain on zymosan-induced peritonitis in mice. Our results show that ouabain decreased plasma exudation (33%). After induction of inflammation, OUA treatment led to a 46% reduction in the total number of cells, as a reflex of a decrease of polymorphonuclear leukocytes, which does not appear to be due to cell death. Furthermore, OUA decreased TNF-alpha (57%) and IL-1beta (58%) levels, without interfering with IL-6 and IL-10. Also, in vitro experiments show that ouabain did not affect endocytic capacity. Moreover, electrophoretic mobility shift assay (EMSA) shows that zymosan treatment increased (85%) NF-kappaB binding activity and that ouabain reduced (30%) NF-kappaB binding activity induced by zymosan. Therefore, our data suggest that ouabain modulated acute inflammatory response, reducing the number of cells and cytokines levels in the peritoneal cavity, as well as NFkappaB activation, suggesting a new mode of action of this substance.
PMID:26078492 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4442290 Leite JA et al; Mediators Inflamm 2015: 265798 doi: 10.1155/2015/265798 (2015)
For more Mechanism of Action (Complete) data for Ouabain (9 total), please visit the HSDB record page.
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