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fludrocortisone

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Description

Fludrocortisone is a synthetic mineralocorticoid that is a potent and long-acting agonist of the mineralocorticoid receptor. It is used to treat primary adrenal insufficiency (Addison’s disease) and to prevent the development of hypokalemia in patients receiving diuretics. Fludrocortisone has been studied extensively for its effects on blood pressure, electrolyte balance, and cardiovascular function. It is synthesized from deoxycorticosterone by the introduction of a fluorine atom at the 9α position. The introduction of the fluorine atom enhances the potency and duration of action of the molecule. Fludrocortisone increases sodium retention and potassium excretion by the kidneys, leading to an increase in blood volume and blood pressure. It is also important in the treatment of orthostatic hypotension. It is important to note that fludrocortisone can have significant side effects, including hypertension, hypokalemia, and fluid retention. It is therefore important to use this medication under the close supervision of a physician.'

Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID31378
CHEMBL ID1201388
CHEBI ID50885
SCHEMBL ID4545
MeSH IDM0008577

Synonyms (123)

Synonym
CHEMBL1201388
gtpl2873
9alpha-flourocortisol
(11beta)-9-fluoro-11,17,21-trihydroxypregn-4-ene-3,20-dione
9alpha-fluoro-11beta,17alpha,21-trihydroxy-pregn-4-ene-3,20-dione
LMST02030103 ,
9.alpha.-fluorocortisol
corticosterone, 9-fluoro-17-hydroxy-
pregn-4-ene-3, 9-fluoro-11.beta.,17,21-trihydroxy-
9.alpha.-fluorohydrocortisone
fludrone
alflorone
fluohydrocortisone
f-col
9.alpha.-fluoro-17-hydroxycorticosterone
9 .alpha. ff
astonin-h
nsc11318
nsc-11318
fluorocortisol
fluodrocortisone
9-afh
9-fluoro-11.beta.,21-trihydroxypregn-4-ene-3,20-dione
fluorocortisone
f-cortef
wln: l e5 b666 ov mutj a1 bf cq e1 fv1q fq
9-fluorocortisol
pregn-4-ene-3, 9-fluoro-11,17,21-trihydroxy-, (11.beta.)-
fluohydrisone
cortisol, 9-fluoro-
fludrocortone
fludronef
9-fluorohydrocortisone
u 5963
9.alpha.-fluoro-11.beta.,21-trihydroxy-4-pregnene-3,20-dione
stc 1400
9-af
PRESTWICK_648
NCGC00181081-01
9-fluoro-11beta,17,21-trihydroxypregn-4-ene-3,20-dione
brn 3014278
9-alpha-fluorohydrocortisone
9alpha-fluoro-hydrocortisone
einecs 204-833-2
9 alpha fludrohydrocortisone
9 alpha-fluorohydrocortisone
9 alpha ff
pregn-4-ene-3,20-dione, 9-fluoro-11-beta,17,21-trihydroxy-
9-alpha-fluorocortisol
9-fluoro-11-beta,17,21-trihydroxypregn-4-ene-3,20-dione
pregn-4-ene-3,20-dione, 9-fluoro-11beta,17,21-trihydroxy-
9alpha-fluoro-11beta,17alpha,21-trihydroxy-4-pregnene-3,20-dione
9alpha-fludrocortisone
pregn-4-ene-3,20-dione, 9-fluoro-11,17,21-trihydroxy-, (11beta)-
nsc 11318
9-fluoro-17-hydroxycortisone
fludrocortisona [inn-spanish]
9 alpha-fluoro-17-hydroxycorticosterone
9-alpha-fluoro-17-hydroxycorticosterone
fludrocortisone [inn:ban]
hsdb 3332
9-alpha-fludrocortisone
9alpha-fluoro-17-hydroxycorticosterone
fludrocortisonum [inn-latin]
CHEBI:50885 ,
fludrocortisona
fludrocortisonum
127-31-1
fludrocortisone
C07004
ZK5 ,
9alpha-fluorocortisol
DB00687
fludrocortisone (inn)
D07967
astonin-h (tn)
(8s,9r,10s,11s,13s,14s,17r)-9-fluoro-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-1,2,6,7,8,11,12,14,15,16-decahydrocyclopenta[a]phenanthren-3-one
9 alpha fluorohydrocortisone
9 fluorohydrocortisone
9 alpha fluoro 17 hydroxycorticosterone
9 fluoro 17 hydroxycortisone
9 fluorocortisol
dtxcid503061
cas-127-31-1
dtxsid7023061 ,
tox21_113344
tox21_112700
BMSE000987
BMSE001009
4-08-00-03427 (beilstein handbook reference)
hydrocortisone-9alpha-fluoro
u0476m545b ,
unii-u0476m545b
9-fluoro-11.beta.,17,21-trihydroxypregn-4-ene-3,20-dione
fludrocortisone [inn]
fludrocortisone [who-dd]
fludrocortisone [hsdb]
fludrocortisone [mi]
fludrocortisone [vandf]
SCHEMBL4545
tox21_113344_1
NCGC00274078-01
CS-4832
pregn-4-ene-3,20-dione, 9-fluoro-11.beta.,17,21-trihydroxy-
9-fluoro-11,17,21-trihydroxypregn-4-ene-3,20-dione, (11.beta.)- #
9.alpha.-fluoro-11.beta.,17.alpha.,21-trihydroxy-4-pregnene-3,20-dione
9.alpha.-fluorcortisol
(11.beta.)-9-fluoro-11,17,21-trihydroxypregn-4-ene-3,20-dione
W-108386
HY-B1203
pregn-4-ene-3,20-dione,9-fluoro-11,17,21-trihydroxy-,(11|a)-
(11alpha)-9-fluoro-11,17,21-trihydroxypregn-4-ene-3,20-dione
Q2697578
(8s,9r,10s,11s,13s,14s,17r)-9-fluoro-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,9,10,11,12,13,14,15,16,17-dodecahydro-1h-cyclopenta[a]phenanthren-3(2h)-one
127-31-1 (free)
9-fludrocortisone;9-fluorcortisol
EN300-19737599
(1r,3as,3bs,9as,9br,10s,11as)-9b-fluoro-1,10-dihydroxy-1-(2-hydroxyacetyl)-9a,11a-dimethyl-1h,2h,3h,3ah,3bh,4h,5h,7h,8h,9h,9ah,9bh,10h,11h,11ah-cyclopenta[a]phenanthren-7-one
AKOS040742512
fludrocortisona (inn-spanish)
fludrocortisonum (inn-latin)
9alpha-fluorohydrocortisone
fludrocortison

Research Excerpts

Overview

Fludrocortisone acetate is a drug used to treat adrenal insufficiencies which can be prescribed to hospitalized orambulatory pediatric patients at dosages not commercially available. It is the first-line drug for treatment of orthostatic hypotension.

ExcerptReferenceRelevance
"Fludrocortisone acetate is a drug used to treat adrenal insufficiencies which can be prescribed to hospitalized or ambulatory pediatric patients at dosages not commercially available. "( Stability Studies of Fludrocortisone Acetate Capsules and Fludrocortisone Acetate Titrated Powders (Powder Triturates).
Bertault-Peres, P; Bouguergour, C; Brandin, T; Curti, C; Jean, C; Lamy, E; Panuccio, C; Primas, N; Rathelot, P; Vanelle, P; Wasilewski, M,
)
1.89
"Fludrocortisone is a mineralocorticoid that facilitates retention of sodium and water."( Fludrocortisone evaluation in aneurysmal subarachnoid hemorrhage patients with cerebral salt wasting (Flush Salt).
Blunck, JR; Elledge, SR; Shewmaker, JW; Yang, S, 2023
)
3.07
"Fludrocortisone is a mineralocorticoid that increases blood volume and blood pressure."( Fludrocortisone for orthostatic hypotension.
Ansari, Y; Chung, KA; Gibbons, CH; Helfand, M; Peterson, K; Raj, SR; Veazie, S, 2021
)
2.79
"Fludrocortisone is a potent mineralocorticoid, which has no known direct vasoactive properties, and is the first-line drug for treatment of orthostatic hypotension. "( Fludrocortisone in the treatment of systemic hypotension in primary open-angle glaucoma patients.
Dubler, B; Flammer, J; Gugleta, K; Orgül, S; Stümpfig, D, 1999
)
3.19
"Fludrocortisone acetate is an effective and safe drug for the treatment of severe and otherwise intractable postural hypotension secondary to therapy with levodopa."( Levodopa-induced postural hypotension. Treatment with fludrocortisone.
Hoehn, MM, 1975
)
1.22

Effects

Fludrocortisone has been a mainstay of therapy for orthostatic hypotension for many years. It has been shown to reduce natriuresis, which may help maintain plasma volume in patients with SAH.

ExcerptReferenceRelevance
"Fludrocortisone has been beneficial in addressing tubulopathies in adult studies, with limited paediatric data available."( Fludrocortisone-a treatment for tubulopathy post-paediatric renal transplantation: A national paediatric nephrology unit experience.
Ali, SR; Athavale, D; Hughes, DA; Maxwell, H; Ramage, I; Shaheen, I; Shaikh, MG; Young, D, 2018
)
2.64
"Fludrocortisone has been evaluated in open-label trials and has long-established usage in clinical practice."( Pharmacological options in the management of orthostatic hypotension in older adults.
Kearney, F; Moore, A, 2009
)
1.07
"Fludrocortisone has been a mainstay of therapy for orthostatic hypotension for many years. "( A sensitive radioimmunoassay for fludrocortisone in human plasma.
Mitsky, VP; Nicholson, WE; Robertson, D; Robertson, RM; Vernikos, J; Workman, RJ, 1994
)
2.01
"Fludrocortisone has been shown to reduce natriuresis, which may help maintain plasma volume in patients with SAH."( Fludrocortisone in the treatment of subarachnoid hemorrhage-induced hyponatremia.
Kale-Pradhan, PB; Woo, MH, 1997
)
2.46
"Fludrocortisone has been used in management of orthostatic hypotension."( Ambulatory 24-hour blood pressure recordings in patients with Parkinson's disease with or without fludrocortisone.
Hakamäki, T; Lehtonen, A; Rajala, T, 1998
)
1.24
"Fludrocortisone acetate has maintained all dogs in good health."( Adrenocortical insufficiency in the dog.
Bath, ML; Hill, FW, 1978
)
0.98

Actions

Fludrocortisone promotes potassium excretion by its direct actions on the renal distal tubules. Spironolactone decreased body weight and increased plasma potassium concentration. Fludroc Cortisone does not suppress urinary aldosterone excretion in cats with PHA.

ExcerptReferenceRelevance
"Fludrocortisone did not increase angiotensinogen in these mice, implying that the rise in angiotensinogen in the siRNA-treated rats must have depended on the liver, most likely reflecting diminished cleavage by renin."( Conventional Vasopressor and Vasopressor-Sparing Strategies to Counteract the Blood Pressure-Lowering Effect of Small Interfering RNA Targeting Angiotensinogen.
Danser, AHJ; Daugherty, A; Foster, D; Garrelds, IM; Hoorn, EJ; Lu, HS; Mirabito Colafella, KM; Nioi, P; Ren, L; Uijl, E; van Veghel, R; Ye, D, 2022
)
1.44
"Fludrocortisone does not suppress urinary aldosterone excretion in cats with PHA, but does so in cats with arterial hypertension because of other causes."( Evaluation of the oral fludrocortisone suppression test for diagnosing primary hyperaldosteronism in cats.
Boevé, MH; Boroffka, SA; Djajadiningrat-Laanen, SC; IJzer, J; Kooistra, HS; Naan, EC,
)
1.88
"Fludrocortisone caused an increase in body weight and no significant reduction in serum potassium concentration, while spironolactone decreased body weight and increased plasma potassium concentration."( Effect of mineralocorticoid activity on transtubular potassium gradient, urinary [K]/[Na] ratio, and fractional excretion of potassium.
Chacko, M; Emmett, M; Fordtran, JS, 1998
)
1.02
"Fludrocortisone promotes potassium excretion by its direct actions on the renal distal tubules."( Fludrocortisone for the treatment of heparin-induced hyperkalemia.
Fish, DN; Kass, CL; Sherman, DS, 2000
)
2.47

Treatment

Fludrocortisone treatment rescues otherwise potentially life-threatening hyponatremia due to RSW and the secondary mineralocorticoid deficiency. Treatment is associated with a rapid catch-up growth and control of electrolyte imbalances in ASD.

ExcerptReferenceRelevance
"Fludrocortisone treatment rescues otherwise potentially life-threatening hyponatremia due to RSW and the secondary mineralocorticoid deficiency driven by elevated ANP and/or BNP, caused by sudden volume expansion following DDAVP initiation."( Lessons from Wolfram Syndrome: Initiation of DDAVP Therapy Causes Renal Salt Wasting Due to Elevated ANP/BNP Levels, Rescued by Fludrocortisone Treatment.
Dermitzaki, E; Kleanthous, K; Maratou, E; Mastorakos, G; Moutsatsou, P; Papadimitriou, A; Papadimitriou, DT; Spyropoulou, D; Urano, F; Zoupanos, G, 2021
)
1.55
"Fludrocortisone treatment is associated with a rapid catch-up growth and control of electrolyte imbalances in ASD. "( Catch-up Growth and Discontinuation of Fludrocortisone Treatment in Aldosterone Synthase Deficiency.
Aghayev, A; Altincik, SA; Bayramoglu, E; Bereket, A; Cayir, A; Doger, E; Guran, T; Gurpinar Tosun, B; Kaygusuz, SB; Kendir Demirkol, Y; Mammadova, J; Nalbantoglu, O; Ozbek, MN; Seven Menevse, T; Turan, S; Yesiltepe Mutlu, G, 2022
)
2.43
"The fludrocortisone treatments also were effective at low doses in preventing or reversing the autoimmune mouse hearing loss."( Low dose combination steroids control autoimmune mouse hearing loss.
Kempton, JB; Trune, DR, 2010
)
0.84
"The fludrocortisone-treated patient cohort was compared to the nontreated patient cohort with respect to overall survival and event-free survival for crisis frequency, worsening gait, frequent fractures, spine curvature, renal insufficiency, and pacemaker insertion."( Fludrocortisone in patients with familial dysautonomia--assessing effect on clinical parameters and gene expression.
Axelrod, FB; Berlin, D; Gold von Simson, G; Goldberg, JD; Mann, SP; Mull, J; Rolnitzky, L; Slaugenhaupt, SA, 2005
)
2.25
"4 Fludrocortisone treatment increased the pressor sensitivity to intravenous saralasin but not to angiotensin-II."( The pressor actions of noradrenaline, angiotensin II and saralasin in chronic autonomic failure treated with fludrocortisone.
Bannester, R; Davies, B; Sever, P; Wilcox, C, 1979
)
1.03
"Treatment with fludrocortisone in an affected 10-year-old child resulted in an increase in blood pressure and estimated glomerular filtration rate."( Clinical and molecular characterization of a family with a dominant renin gene mutation and response to treatment with fludrocortisone.
Adams, JN; Bleyer, AJ; Cornell, LD; Elleder, M; Hart, PS; Hart, TC; Haws, R; Hodanová, K; Hulková, H; Kapp, K; Kmoch, S; Sikora, J; Sovová, J; Vyletal, P; Zivná, M; Zivný, J, 2010
)
0.91
"Treatment with fludrocortisone improved renal function in an affected child."( Clinical and molecular characterization of a family with a dominant renin gene mutation and response to treatment with fludrocortisone.
Adams, JN; Bleyer, AJ; Cornell, LD; Elleder, M; Hart, PS; Hart, TC; Haws, R; Hodanová, K; Hulková, H; Kapp, K; Kmoch, S; Sikora, J; Sovová, J; Vyletal, P; Zivná, M; Zivný, J, 2010
)
0.91
"Treatment with fludrocortisone and sodium chloride was begun, but the hypertension worsened."( Hypertension in a patient with aldosterone deficiency.
Hasan, KS; Joseph, M; Touger, L,
)
0.47
"Treatment with fludrocortisone resulted in sodium and fluid homeostasis."( Cerebral salt wasting in tuberculous meningitis: treatment with fludrocortisone.
Alabaz, D; Alhan, E; Celik, US; Kocabas, E; Ulutan, S; Yildizdas, D, 2005
)
0.91
"Treatment with fludrocortisone resulted in resolution of these episodes and allowed performance of a Glenn shunt at 3 half months of age."( Fludrocortisone in the management of an infant with a single ventricle and an overly tightened pulmonary artery band.
Balfour, I; Dempsher, D; Jureidini, SB; Ponciroli, KM,
)
1.91
"Treatment with fludrocortisone effectively reversed the OH in four of the five patients."( Orthostatic hypotension in human immunodeficiency virus infection may be the result of generalized autonomic nervous system dysfunction.
Cohen, JA; Miller, L; Polish, L, 1991
)
0.62
"Treatment with fludrocortisone and ephedrine was initiated with a good haemodynamic and symptomatic result."( Hypotension during exercise caused by venodilatation.
Rohold, A; Svanegaard, J; Thayssen, P, 1990
)
0.62

Toxicity

Fludrocortisone had to be withdrawn in 2 patients because of severe adverse effects. These adverse reactions necessitated discontinuation of fludroc Cortisone in two patients.

ExcerptReferenceRelevance
"The primary end point was the time needed to correct serum sodium levels; secondary end points were in-hospital deaths, disability at 3 months, disability at 6 months, occurence of stroke, and serious adverse reactions."( Safety and Efficacy of Fludrocortisone in the Treatment of Cerebral Salt Wasting in Patients With Tuberculous Meningitis: A Randomized Clinical Trial.
Kalita, J; Kumar, M; Misra, UK, 2018
)
0.79
" These adverse reactions necessitated discontinuation of fludrocortisone in 2 patients."( Safety and Efficacy of Fludrocortisone in the Treatment of Cerebral Salt Wasting in Patients With Tuberculous Meningitis: A Randomized Clinical Trial.
Kalita, J; Kumar, M; Misra, UK, 2018
)
1.04
" Fludrocortisone had to be withdrawn in 2 patients because of severe adverse effects."( Safety and Efficacy of Fludrocortisone in the Treatment of Cerebral Salt Wasting in Patients With Tuberculous Meningitis: A Randomized Clinical Trial.
Kalita, J; Kumar, M; Misra, UK, 2018
)
1.7
"Ambulatory FST is safe and accurate and can be performed with significantly less healthcare costs compared to FSTin."( Ambulatory fludrocortisone suppression test in the diagnosis of primary aldosteronism: Safety, accuracy and cost-effectiveness.
Avander, K; Calissendorff, J; Carasel, A; Falhammar, H; Shabo, I; Volpe, C, 2022
)
1.11
" Adverse events (AEs) were reported from the first dose of FCA until the end-of-study visit."( Phase 1B study of the safety and tolerability of the mineralocorticoid fludrocortisone acetate in patients with geographical atrophy.
Chang, A; Hong, T; Maddess, T; Penfold, P; Provis, J, 2022
)
0.95
"IVT FCA is clinically safe and well tolerated and did not increase IOP."( Phase 1B study of the safety and tolerability of the mineralocorticoid fludrocortisone acetate in patients with geographical atrophy.
Chang, A; Hong, T; Maddess, T; Penfold, P; Provis, J, 2022
)
0.95

Pharmacokinetics

ExcerptReferenceRelevance
"1 The pharmacodynamic profile of single oral doses of prorenoate potassium (40 mg) and spironolactone (100 mg), as judged by reversal of the effects of fludrocostisone on the urinary electrolyte composition, was compared to that of placebo in a double-blind crossover study in six healthy subjects."( The pharmacodynamics of single doses of prorenoate potasssium and spironolactone in fludrocortisone treated normal subjects.
Ramsay, LE; Shelton, JR; Tidd, MJ, 1976
)
0.48
" The proposed method was successfully applied to pharmacokinetic studies in humans."( A highly sensitive method for the quantification of fludrocortisone in human plasma using ultra-high-performance liquid chromatography tandem mass spectrometry and its pharmacokinetic application.
Banda, J; Gudla, SP; Lakshmanan, R; Prudhivi, R; Vvs, SP, 2015
)
0.67
" Fludrocortisone PK showed a short plasma elimination half-life and a large inter-individual variability."( Pharmacokinetics of oral fludrocortisone in septic shock.
Alvarez, JC; Annane, D; Bellissant, E; Hamitouche, N; Laviolle, B; Polito, A; Ribot, M, 2016
)
1.65

Compound-Compound Interactions

ExcerptReferenceRelevance
"We studied the effect of sleeping in the head-up tilt (HUT) position, alone and in combination with fludrocortisone, on orthostatic tolerance and blood pressure (BP) in six patients with hypoadrenergic orthostatic hypotension."( Treatment of orthostatic hypotension with sleeping in the head-up tilt position, alone and in combination with fludrocortisone.
Ten Harkel, AD; Van Lieshout, JJ; Wieling, W, 1992
)
0.71

Bioavailability

ExcerptReferenceRelevance
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

Fludrocortisone acetate is given at very low dosage (50 μg) to patients suffering from septic shock. After one week the dosage will be up-titrated to midodrine 30 mg/day and fludroc Cortisone 0.5mg/day.

ExcerptRelevanceReference
" This may have been mediated by vascular alpha-adrenoceptors because log dose-response curves of saralasin-induced increases in systolic pressure were shifted to the right in a parallel fashion after phentolamine."( The pressor actions of noradrenaline, angiotensin II and saralasin in chronic autonomic failure treated with fludrocortisone.
Bannester, R; Davies, B; Sever, P; Wilcox, C, 1979
)
0.47
" This reduced size permits use of smaller volumes of dissolution medium, allowing most very low dose oral solid dosage forms to be handled."( Semiautomated system for high-pressure liquid chromatographic determination of dissolution rate of fludrocortisone acetate tablets.
Abdou, HM; Ast, TM; Cioffi, FJ, 1978
)
0.47
" Although fludrocortisone has glucocorticoid activity, the "hydrocortisone equivalent" effect of the small dosage used was unlikely to inhibit either pituitary corticotrophin or growth hormone production."( Hypoaldosteronism in three sibs due to 18-dehydrogenase deficiency.
Gray, CE; Hamilton, W; Ireland, JT; McCandless, AE, 1976
)
0.66
" Severe orthostatic light-headedness and frequent syncope had previously been alleviated only be reducing the dosage of levodopa to levels producing less than optimal antiparkinsonian benefits."( Levodopa-induced postural hypotension. Treatment with fludrocortisone.
Hoehn, MM, 1975
)
0.5
" The glucocorticoid effect on motoneuron outlasts the dosing period, suggesting an underlying alteration in the neuron."( Glucocorticoids and mammalian motor nerve excitability.
Baker, T; Okamoto, M; Riker, WF, 1975
)
0.25
" The substitution treatment was gradually reduced to the original (pre-pregnancy) dosage during the first three post-partum days."( [Pregnancy in Addison's disease].
Alexopoulos, A; Breckwoldt, M; DeGregorio, G; Wieacker, P, 1989
)
0.28
"A patient with Addison's disease required increased corticosteroid dosage whilst receiving rifampicin."( Changes in cortisol metabolism following rifampicin therapy.
Courtenay-Evans, RJ; Edwards, OM; Galley, JM; Hunter, J; Tait, AD, 1974
)
0.25
" The dosage was reduced to 30 mg four times daily because of the development of complex ventricular premature beats."( Effect of prenalterol on orthostatic hypotension in the Shy-Drager syndrome.
Fagard, R; Goovaerts, J; Knockaert, D; Verfaillie, C, 1984
)
0.27
"2-200 mug/d) concurrently suppressed plasma ir-ACTH and ir-betaEP, with a near maximal effect at 20 mug, and a half-maximal effect between 2 and 6 mug; similar dose-response characteristics were found for thymolysis."( Glucocorticoid and mineralocorticoid effects on adrenocorticotropin and beta-endorphin in the adrenalectomized rat.
Clements, J; Funder, JW; Khalid, BA; Lim, AT, 1982
)
0.26
" Log fludrocortisone dose-response relationships in the presence or absence of antagonists did not differ from linearity and parallelism, supporting the theoretical basis of the method."( Steady-state relative potency of aldosterone antagonists: spironolactone and prorenoate.
Harrison, IR; McInnes, GT; Shelton, JR, 1981
)
0.78
" The toxicity profile of taxol is still evolving as changes in the dosing and scheduling of the drug are instituted."( Incapacitating autonomic neuropathy precipitated by taxol.
Fingert, HJ; Jerian, SM; Kohn, EC; Link, CJ; Reed, E; Sarosy, GA, 1993
)
0.29
" No differences between males and females were noted throughout this time with regard to: (a) A or 17-OHP levels (neither of which were suppressed to 'control values'); (b) the dosage of cortisone received (13."( Growth pattern during the first 36 months of life in congenital adrenal hyperplasia (21-hydroxylase deficiency).
Argenziano, A; Di Maio, S; Franzese, A; Gasparini, N; Salerno, M; Tenore, A, 1997
)
0.3
" All patients with AD have been studied under basal conditions and nine of them also after 2 weeks on oral corticosteroid therapy (individual cortisol dosage ranging from 25 to 37."( High plasma levels of endothelin-1 in untreated Addison's disease.
Canettieri, G; Centanni, M; Cerci, S; D'Ambrosio, C; De Ciocchis, A; Letizia, C; Scavo, D; Scuro, L, 1996
)
0.29
" Since Shy-Drager syndrome is often treated with antiparkinsonian drugs, neuroleptic malignant syndrome can possibly develop after the change in dosage of catecholaminergic drugs."( [A case of impending neuroleptic malignant syndrome associated with Shy-Drager syndrome].
Egi, N; Harada, T; Kumagai, R; Kurokawa, K; Nakamura, S; Okazaki, M; Shimote, K, 1998
)
0.3
" To confirm these facts, we analyzed the clinical data and the biological markers of control of therapy in two groups of patients with salt-losing CAH aged from 2 to 12 years: group I: before (time 0) and 6 months after the increase in 9 alpha-F dosage (time +6); group II: at time 0 and time +6 but without change in 9 alpha-F dosage."( Should we monitor more closely the dosage of 9 alpha-fluorohydrocortisone in salt-losing congenital adrenal hyperplasia?
Dubuis, JM; Lopes, LA; Sizonenko, PC; Vallotton, MB,
)
0.13
" Thus, the development of sustained-release forms, as microparticle suspensions, is interesting in order to improve patient compliance by reducing dosing frequencies and side effects."( Poly(epsilon-caprolactone) and Eudragit microparticles containing fludrocortisone acetate.
Astier, A; Ducki, C; Gibaud, S; Jabir Al Awwadi, N, 2004
)
0.56
"Plasma ACTH was measured before (0830 h) and 120 min after morning dosing with hydrocortisone (HC)."( Ineffectiveness of rosiglitazone therapy in Nelson's syndrome.
Ince, P; Munir, A; Newell-Price, J; Ross, R; Song, F; Walters, SJ, 2007
)
0.34
" Correlations between blood pressures and serum renin levels, and the dosage of fludrocortisone were calculated."( Blood pressure in the first year of life in children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency: a pilot study.
Claahsen-van der Grinten, HL; Kapusta, L; Mooij, CF; Otten, BJ, 2010
)
0.59
" No significant correlations between blood pressure and serum renin, androstenedione and 17-OHP levels and fludrocortisone dosage were found."( Blood pressure in the first year of life in children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency: a pilot study.
Claahsen-van der Grinten, HL; Kapusta, L; Mooij, CF; Otten, BJ, 2010
)
0.57
" In conclusion, the steroid substitution in Addison's disease requires individually tailored dosage and adequate monitoring."( [Metabolic assessment of hydrocortisone replacement therapy in patients with primary adrenocortical insufficiency].
Fichna, M; Gryczyńska, M; Sowińska, A; Sowiński, J, 2011
)
0.37
" Since there continues to be disagreement about the utility of fludrocortisone in septic shock, we assessed the effects of a single administration of low doses of hydrocortisone (50 mg intravenously) and fludrocortisone (50 μg orally), given either alone or in combination, on phenylephrine mean arterial pressure and cardiac systolic and diastolic function dose-response relationships in 12 healthy male volunteers with hypo-aldosteronism induced by intravenous sodium loading."( Low doses of fludrocortisone and hydrocortisone, alone or in combination, on vascular responsiveness to phenylephrine in healthy volunteers.
Bellissant, E; Donal, E; Lainé, F; Laviolle, B; Le Maguet, P, 2013
)
1
"Fludrocortisone acetate is given at very low dosage (50 μg) to patients suffering from septic shock with controversial clinical results."( Human plasma quantification of fludrocortisone using liquid chromatography coupled with atmospheric pressure chemical ionization mass spectrometry after low-dosage administration.
Alvarez, JC; Annane, D; Grassin-Delyle, S; Polito, A; Ribot, M, 2013
)
2.12
"This method allows fludrocortisone pharmacokinetic/pharmacodynamic studies when given at low dosage in an intensive care unit in case of adrenal insufficiency during a septic shock."( Human plasma quantification of fludrocortisone using liquid chromatography coupled with atmospheric pressure chemical ionization mass spectrometry after low-dosage administration.
Alvarez, JC; Annane, D; Grassin-Delyle, S; Polito, A; Ribot, M, 2013
)
1
" Therefore, elevation of the bed of the head and dosing of short-acting antihypertensive agents at bedtime is often indicated."( Orthostatic hypotension associated with baroreceptor dysfunction: treatment approaches.
Bakris, GL; Briasoulis, A; Silver, A; Yano, Y, 2014
)
0.4
" In the current study, we sought to determine if blood sampling and a shorter dosing period would provide a possible means to test for primary hyperaldosteronism."( Serum aldosterone and cortisol concentrations before and after suppression with fludrocortisone in cats: a pilot study.
Behrend, EN; Johnson, A; Kemppainen, R; Lee, H; Matsuda, M; Refsal, K, 2015
)
0.64
" Heterogeneity was related in part to the dosing strategy."( Corticosteroids for treating sepsis.
Annane, D; Bellissant, E; Bollaert, PE; Briegel, J; Keh, D; Kupfer, Y, 2015
)
0.42
"The objective of this retrospective study was to examine factors that may have affected the stabilisation times of 50 dogs with spontaneous hypoadrenocorticism that were being treated with fludrocortisone acetate, with particular emphasis on dosing frequency and the concurrent use of prednisolone."( Factors that affect stabilisation times of canine spontaneous hypoadrenocorticism.
Boden, LA; Ramsey, IK; Roberts, E, 2016
)
0.62
"We evaluated rates of illnesses and associated factors in patients with CAH followed prospectively and receiving repeated glucocorticoid stress dosing education."( Longitudinal Assessment of Illnesses, Stress Dosing, and Illness Sequelae in Patients With Congenital Adrenal Hyperplasia.
El-Maouche, D; Hargreaves, CJ; Mallappa, A; Merke, DP; Sinaii, N; Veeraraghavan, P, 2018
)
0.48
"Repeated stress-related glucocorticoid dosing teaching is essential, but revised age-appropriate guidelines for the management of infectious illnesses are needed for patients with adrenal insufficiency that aim to reduce adrenal crises and prevent hypoglycemia, particularly in children."( Longitudinal Assessment of Illnesses, Stress Dosing, and Illness Sequelae in Patients With Congenital Adrenal Hyperplasia.
El-Maouche, D; Hargreaves, CJ; Mallappa, A; Merke, DP; Sinaii, N; Veeraraghavan, P, 2018
)
0.48
" Although current guidelines exist for dose adjustments in these situations, there is no accepted dosing regimen for patients with PAI participating in intensive endurance exercise."( Stress-Dosed Glucocorticoids and Mineralocorticoids Before Intensive Endurance Exercise in Primary Adrenal Insufficiency.
Bonnecaze, AK; Burns, CA; Reynolds, P, 2019
)
0.51
" Patients can be managed successfully by monitoring for recurrence of Addison's symptoms and adjusting medication dosing as needed."( Addison's disease in pregnancy: Case report, management, and review of the literature.
Bathgate, S; Corrigan, K; Macri, C; Margulies, SL, 2020
)
0.56
"Appropriate management of adrenal insufficiency (AI) in pregnancy can be challenging due to the rarity of the disease and lack of evidence-based recommendations to guide glucocorticoid and mineralocorticoid dosage adjustment."( Current Management and Outcome of Pregnancies in Women With Adrenal Insufficiency: Experience from a Multicenter Survey.
Anand, G; Badenhoop, K; Bancos, I; Bensing, S; Bergthorsdottir, R; Beuschlein, F; Bothou, C; Corsello, SM; Drake, W; Ebbehoj, A; Esposito, D; Etzrodt-Walter, G; Falhammar, H; Ferrigno, R; Hahner, S; Husebye, E; Isidori, AM; Kienitz, T; Li, D; Meyer, G; Murray, R; Oksnes, M; Paragliola, RM; Pearce, S; Pivonello, R; Quinkler, M; Reisch, N; Seejore, K; Simeoli, C; Sævik, ÅB; Thalmann, SP; Trainer, P; Wahlberg, J; Ward, EG, 2020
)
0.56
" Glucocorticoid dosage was increased at any time during pregnancy in 73/128 (57%) of cases."( Current Management and Outcome of Pregnancies in Women With Adrenal Insufficiency: Experience from a Multicenter Survey.
Anand, G; Badenhoop, K; Bancos, I; Bensing, S; Bergthorsdottir, R; Beuschlein, F; Bothou, C; Corsello, SM; Drake, W; Ebbehoj, A; Esposito, D; Etzrodt-Walter, G; Falhammar, H; Ferrigno, R; Hahner, S; Husebye, E; Isidori, AM; Kienitz, T; Li, D; Meyer, G; Murray, R; Oksnes, M; Paragliola, RM; Pearce, S; Pivonello, R; Quinkler, M; Reisch, N; Seejore, K; Simeoli, C; Sævik, ÅB; Thalmann, SP; Trainer, P; Wahlberg, J; Ward, EG, 2020
)
0.56
" Aims of this study were to assess the influence of sex and body weight on GC dosing and to describe the choice of GC in AI of different etiologies."( What factors have impact on glucocorticoid replacement in adrenal insufficiency: a real-life study.
Borretta, G; Cannavò, S; Dughera, F; Ferrau', F; Latina, A; Parisi, A; Pellegrino, M; Pia, A; Puglisi, S; Ragonese, M; Reimondo, G; Rossini, A; Tabaro, I; Terzolo, M, 2021
)
0.62
"To investigate the current use of salt supplementation, fludrocortisone (FC) and hydrocortisone (HC) dosage as well as weight, height, BMI and blood pressure (BP) in CAH children aged 0-3 years."( Treatment of congenital adrenal hyperplasia in children aged 0-3 years: a retrospective multicenter analysis of salt supplementation, glucocorticoid and mineralocorticoid medication, growth and blood pressure.
Ahmed, SF; Atapattu, N; Bachega, TASS; Balsamo, A; Birkebaek, N; Blankenstein, O; Bonfig, W; Bryce, J; Claahsen-van der Grinten, HL; Cools, M; Costa, EC; Darendeliler, F; de Vries, L; Elsedfy, H; Guaragna-Filho, G; Güran, T; Güven, A; Hannema, SE; Korbonits, M; Krone, NP; Krone, RE; Milenkovic, T; Mohnike, K; Neumann, U; Poyrazoglu, S; Thankamony, A; van der Linde, A; Vieites, A; Voet, B, 2022
)
0.97
" First, a stability-indicating fludrocortisone acetate dosing method was validated."( Stability Studies of Fludrocortisone Acetate Capsules and Fludrocortisone Acetate Titrated Powders (Powder Triturates).
Bertault-Peres, P; Bouguergour, C; Brandin, T; Curti, C; Jean, C; Lamy, E; Panuccio, C; Primas, N; Rathelot, P; Vanelle, P; Wasilewski, M,
)
0.74
" Two subsequent participants were then dosed with the same dose."( Phase 1B study of the safety and tolerability of the mineralocorticoid fludrocortisone acetate in patients with geographical atrophy.
Chang, A; Hong, T; Maddess, T; Penfold, P; Provis, J, 2022
)
0.95
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
adrenergic agentAny agent that acts on an adrenergic receptor or affects the life cycle of an adrenergic transmitter.
anti-inflammatory drugA substance that reduces or suppresses inflammation.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (8)

ClassDescription
mineralocorticoidMineralocorticoids are a class of steroid hormones that regulate water and electrolyte metabolism.
17alpha-hydroxy steroidThe alpha-stereoisomer of 17-hydroxy steroid.
11beta-hydroxy steroidAny 11-hydroxy steroid in which the hydroxy group at position 11 has beta- configuration.
C21-steroidA steroid that has a structure based on a 21-carbon (pregnane) skeleton. Note that individual examples may have ring substituents at other positions and/or contain double bonds, aromatic A-rings, expanded/contracted rings etc., so the formula and mass may vary from that given for the generic structure.
3-oxo-Delta(4) steroidA 3-oxo steroid conjugated to a C=C double bond at the alpha,beta position.
20-oxo steroidAn oxo steroid carrying an oxo group at position 20.
21-hydroxy steroid
fluorinated steroidA steroid which is substituted with one or more fluorine atoms in any position.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (10)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
GALC proteinHomo sapiens (human)Potency0.707928.183828.183828.1838AID1159614
TDP1 proteinHomo sapiens (human)Potency28.23200.000811.382244.6684AID686978; AID686979
AR proteinHomo sapiens (human)Potency0.04370.000221.22318,912.5098AID1259243; AID1259247; AID1259381; AID743036; AID743040; AID743042; AID743053; AID743054
progesterone receptorHomo sapiens (human)Potency1.89580.000417.946075.1148AID1346784; AID1347036
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency0.06830.000214.376460.0339AID720691; AID720692; AID720719
estrogen nuclear receptor alphaHomo sapiens (human)Potency2.05040.000229.305416,493.5996AID743069; AID743075; AID743078; AID743079; AID743080; AID743091
aryl hydrocarbon receptorHomo sapiens (human)Potency16.78550.000723.06741,258.9301AID743085
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_aHomo sapiens (human)Potency0.03130.001723.839378.1014AID743083
nuclear receptor subfamily 1, group I, member 2Rattus norvegicus (Norway rat)Potency14.12540.10009.191631.6228AID1346983
Interferon betaHomo sapiens (human)Potency0.04190.00339.158239.8107AID1347407
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (30)

Processvia Protein(s)Taxonomy
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (5)

Processvia Protein(s)Taxonomy
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (2)

Processvia Protein(s)Taxonomy
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (74)

Assay IDTitleYearJournalArticle
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347412qHTS assay to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: Counter screen cell viability and HiBit confirmation2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347125qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347111qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347123qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347128qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347119qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347110qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347116qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347115qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347414qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: Secondary screen by immunofluorescence2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347129qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347118qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347114qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347124qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347109qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347127qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347113qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347122qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1132664Glucocorticoid activity in sc dosed bilaterally adrenalectomized rat assessed as glycogen deposition in liver administered for 5 days relative to cortisol1978Journal of medicinal chemistry, May, Volume: 21, Issue:5
A Fujita--Ban structure--activity analysis of 44 steroids.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1346902Human Mineralocorticoid receptor (3C. 3-Ketosteroid receptors)1993European journal of pharmacology, Oct-15, Volume: 247, Issue:2
Pharmacological and functional characterization of human mineralocorticoid and glucocorticoid receptor ligands.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,568)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990833 (53.13)18.7374
1990's187 (11.93)18.2507
2000's224 (14.29)29.6817
2010's254 (16.20)24.3611
2020's70 (4.46)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 96.32

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index96.32 (24.57)
Research Supply Index7.49 (2.92)
Research Growth Index4.49 (4.65)
Search Engine Demand Index177.62 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (96.32)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials120 (7.16%)5.53%
Reviews141 (8.41%)6.00%
Case Studies393 (23.43%)4.05%
Observational1 (0.06%)0.25%
Other1,022 (60.94%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (36)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Mineralocorticoid Treatment for Sudden Sensorineural Hearing Loss [NCT01186185]Early Phase 15 participants (Actual)Interventional2012-08-31Terminated(stopped due to PI moved to new institution, unable to complete study)
Effects of Fludrocortisone on Norepinephrine-mean Arterial Pressure Dose-response, Gastric Mucosal Perfusion and Arterial Stiffness in Septic Shock [NCT02069288]Phase 30 participants (Actual)InterventionalWithdrawn(stopped due to Problems of drugs supply by the manufacturer)
A Randomized Clinical Trial of Fludrocortisone for Vasovagal Syncope: The Second Prevention of Syncope Trial (POST II) [NCT00118482]Phase 4213 participants (Actual)Interventional2005-05-31Completed
Evaluation of the Role of Hydrocortisone Either Alone or Combined With Fludrocortisone in the Outcome of Septic Shock in Adults [NCT04492280]Phase 466 participants (Actual)Interventional2018-09-01Completed
A Phase 1-2 Multi-Center Study to Assess the Efficacy and Safety of Abiraterone Acetate as Adjunctive Therapy in Pre-Pubescent Children With Classic 21-Hydroxylase Deficiency [NCT03548246]Phase 20 participants (Actual)Interventional2023-01-31Withdrawn(stopped due to This study plan has halted and was withdrawn from the IRB.)
Case Detection and Confirmation, Subtype Classification of Patients With Primary Aldosteronism [NCT03500120]200 participants (Actual)Observational2017-09-01Completed
A Phase II Open Label Randomised Controlled Clinical Trial of Different Dosing Regimens of Fludrocortisone in Septic Shock With Assessment of Temporal Changes in Hormonal, Inflammatory, and Genetic Markers of Vascular Responsiveness [NCT04494789]Phase 2300 participants (Anticipated)Interventional2021-02-11Recruiting
Effekte Von Fludrocortison Auf Soziale Kognition Und Gedächtnis Unter Berücksichtigung Von Geschlechtereffekten [NCT02478034]80 participants (Actual)Interventional2015-05-31Completed
Effects of Mineralocorticoid Receptor Stimulation on Cognitive Bias and Social Cognition in Patients With Major Depression and Healthy Controls: What's the Role of NMDA Receptors? [NCT03062150]232 participants (Actual)Interventional2016-09-27Completed
A Phase 1 Clinical Study to Investigate the Safety and Pharmacokinetics of MK-5684 in China Participants With Metastatic Castration-Resistant Prostate Cancer [NCT06136598]Phase 114 participants (Anticipated)Interventional2023-12-25Not yet recruiting
Evaluation of the Hemodynamics Effects of Fludrocortisone on the Pressor Response to Noradrenaline in Septic Shock Patients [NCT05001854]Phase 2/Phase 340 participants (Anticipated)Interventional2022-03-31Suspended(stopped due to study suspended until new therapeutic units are available)
Phase 3 Study of Hydrocortisone and Fludrocortisone in Glucocorticoid Insufficiency Related to Traumatic Brain Injury [NCT01093261]Phase 3336 participants (Actual)Interventional2010-08-31Completed
Hemodynamic and Biological Effects of 3 Increasing Doses of Fludrocortisone in Healthy Volunteers [NCT02140918]Phase 216 participants (Actual)Interventional2014-07-01Completed
Evaluation of Efficacy and Tolerance of Fludrocortisone (Flucortac) in the Treatment of Orthostatic Neurogenic Hypotension [NCT04128137]Phase 490 participants (Anticipated)Interventional2020-07-09Recruiting
A Phase 3 Randomized, Open-label Study of MK-5684 Versus Alternative Abiraterone Acetate or Enzalutamide in Participants With Metastatic Castration-resistant Prostate Cancer (mCRPC) Previously Treated With Next-generation Hormonal Agent (NHA) and Taxane-b [NCT06136624]Phase 31,200 participants (Anticipated)Interventional2023-12-22Not yet recruiting
A Phase 1 Clinical Study to Investigate the Safety and Pharmacokinetics of MK-5684 in Japanese Participants With Metastatic Castration-resistant Prostate Cancer (mCRPC) [NCT06104449]Phase 16 participants (Anticipated)Interventional2023-11-14Recruiting
A Multi-Center Phase II Study to Evaluate Tumor Response to Ipilimumab (BMS-734016) Monotherapy in Subjects With Melanoma Brain Metastases [NCT00623766]Phase 299 participants (Actual)Interventional2008-07-31Completed
A Monocentric Randomized, Controlled, Double Blind, Crossover Phase II Trial to Show Non-inferiority of the Effect of Pyridostigmine Bromide vs. Fludrocortisone on Symptoms of Autonomic Dysregulation in Parkinson's Disease [NCT01993680]Phase 218 participants (Actual)Interventional2012-06-30Completed
Hypoglycemia Associated Autonomic Failure in Type 1 DM, Question 1 [NCT00608101]0 participants (Actual)Interventional2010-09-30Withdrawn
A Phase 3, Randomized, Open-label Study of MK-5684 Versus Alternative Abiraterone Acetate or Enzalutamide in Participants With Metastatic Castration-resistant Prostate Cancer (mCRPC) That Progressed On or After Prior Treatment With One Next-generation Hor [NCT06136650]Phase 31,500 participants (Anticipated)Interventional2023-12-18Recruiting
Comparison of Outcomes With Midodrine and Fludrocortisone for Objective Recurrence in Treating Syncope (COMFORTS Trial) [NCT04595942]Phase 31,375 participants (Anticipated)Interventional2020-11-19Recruiting
An Open, Randomized, Long-Term Clinical Trial of Flutamide, Testolactone, and Reduced Hydrocortisone Dose vs. Conventional Treatment of Children With Congenital Adrenal Hyperplasia [NCT00001521]Phase 462 participants (Actual)Interventional1995-06-08Active, not recruiting
The Role of Minerelocorticoid Receptor on Modulating Aldosterone Production [NCT02871648]Phase 123 participants (Actual)Interventional2016-01-31Completed
Hemodynamic and Biological Effects of Fludrocortisone and Hydrocortisone, in Healthy Volunteers With Aldosterone Induced Suppression [NCT00673270]Phase 1/Phase 213 participants (Actual)Interventional2008-05-31Terminated
Pathophysiology and Nature of Ovarian Hyperstimulation Syndrome (OHSS) as a Clinical Entity Could be Fully Explained and Effectively Managed as a State of Defective Mineralocorticoid Response [NCT04351126]Phase 2107 participants (Actual)Interventional2019-04-01Completed
Phase III of Recombinant Human Activated Protein C and Low Dose of Hydrocortisone and Fludrocortisone in Adult Septic Shock [NCT00625209]Phase 31,241 participants (Actual)Interventional2008-03-31Completed
Efficacy of Therapeutic Interventions for Orthostatic Hypotension in Parkinson's Disease and Multiple System Atrophy [NCT00103597]Phase 150 participants Interventional2005-01-31Completed
Safety and Efficacy of Fludrocortisone Addition to Dexamethasone in the Management of Hospitalised COVID-19 Patients [NCT05453214]Phase 310 participants (Actual)Interventional2021-12-04Completed
Mineralocorticoid Receptor in the Treatment of Severe Depression: A Randomized, Double Blind, and Placebo Controlled Trial [NCT00295347]65 participants (Anticipated)Interventional2005-12-31Completed
The Effects of Fludrocortisone on Information Processing in Healthy Female Volunteers [NCT01648998]Phase 140 participants (Actual)Interventional2012-05-31Completed
Comparison of Furosemide/Fludrocortisone With Ammonium Chloride Loading Test in the Diagnosis of Incomplete dRTA in Kidney Stone Formers [NCT01690039]170 participants (Actual)Observational2012-09-30Completed
Fludrocortisone's Test in the Identification of Salt Sensitivity [NCT01453959]Phase 440 participants (Anticipated)Interventional2011-07-31Recruiting
Impact of the Administration of Fludrocortisone on Fluid and Electrolyte Balance in Very Premature Infants: Pilot Study [NCT03001089]Phase 266 participants (Actual)Interventional2017-06-01Completed
"Fight-or-flight Versus Tend-and-befriend Response to Behavioral and Pharmacological Interventions in Patients With Borderline Personality Disorder (Part II)" [NCT05310253]240 participants (Anticipated)Interventional2022-02-01Recruiting
Phase 3 Study of Corticotherapy (Hydrocortisone Alone Versus Hydrocortisone Plus Fludrocortisone) Versus Corticotherapy Plus Intensive Insulin Therapy for Septic Shock [NCT00320099]Phase 3508 participants (Actual)Interventional2006-01-31Completed
A Phase I, Randomized, Single-Blind, Crossover Study to Assess the Pharmacodynamics of AZD9977 Following Single-Dose Administration to Healthy Male Subjects [NCT02532998]Phase 140 participants (Actual)Interventional2015-09-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00118482 (3) [back to overview]Quality of Life Will be the Third Secondary Outcome Measure. The Investigators Will Compare the Quality of Life in Treated and Untreated Patients.
NCT00118482 (3) [back to overview]The Frequency of Syncope Will be the First Secondary Outcome Measure.
NCT00118482 (3) [back to overview]The Primary Outcome Measure Will be the Recurrence of Syncope in Follow up Period.
NCT00623766 (9) [back to overview]Overall Survival (OS)
NCT00623766 (9) [back to overview]Best Overall Response Rate (BORR) by Modified World Health Organization (mWHO) Criteria and by Immune-relate Response Criteria (irRC)
NCT00623766 (9) [back to overview]Disease Control Rate by Immune-related Response Criteria (irRC)
NCT00623766 (9) [back to overview]Disease Control Rate by Modified World Health Organization (mWHO) Tumor Assessment Criteria
NCT00623766 (9) [back to overview]Duration of Response (DOR) by Modified World Health Organization (mWHO) Criteria and by Immune-related Response Criteria (irRC)
NCT00623766 (9) [back to overview]Number of Participants Surviving at 6, 12, 18, 24, and 36 Months (Overall Survival [OS] Rate)
NCT00623766 (9) [back to overview]Number of Participants Who Died or Had a Treatment-related Adverse Event (AE), Immune-related AE, Immune-related Serious Adverse Event (SAE), Nervous System Disorder, Treatment-related Nervous System Disorder, SAE, and AE Leading to Discontinuation
NCT00623766 (9) [back to overview]Onset of Response by Modified World Health Organization (mWHO) Criteria and Immune-related Response Criteria (irRC)
NCT00623766 (9) [back to overview]Progression-free Survival (PFS) by Modified World Health Organization (mWHO) Criteria and by Immune-related Response Criteria (irRC)
NCT02532998 (27) [back to overview]Apparent Clearance (CL/F) of AZD9977.
NCT02532998 (27) [back to overview]Apparent Clearance (CL/F) of Eplerenone.
NCT02532998 (27) [back to overview]Apparent Volume of Distribution at Terminal Phase (Vz/F) of AZD9977.
NCT02532998 (27) [back to overview]Apparent Volume of Distribution at Terminal Phase (Vz/F) of Eplerenone.
NCT02532998 (27) [back to overview]Area Under Plasma Concentration-time Curve From Zero Extrapolated to Infinity (AUC) of AZD9977.
NCT02532998 (27) [back to overview]Area Under Plasma Concentration-time Curve From Zero Extrapolated to Infinity (AUC) of Eplerenone.
NCT02532998 (27) [back to overview]Area Under the Plasma Concentration-time Curve From Time Zero to t Hours After Dosing (AUC(0-t)) of Eplerenone.
NCT02532998 (27) [back to overview]Area Under the Plasma Concentration-time Curve From Time Zero to t Hours After Dosing (AUC[0-t]) of AZD9977.
NCT02532998 (27) [back to overview]Number of Participants With Clinically Significant Blood Pressure Values.
NCT02532998 (27) [back to overview]Number of Participants With Clinically Significant Electrocardiogram.
NCT02532998 (27) [back to overview]Number of Participants With Clinically Significant Physical Examination Values.
NCT02532998 (27) [back to overview]Number of Participants With Clinically Significant Pulse Rate.
NCT02532998 (27) [back to overview]Number of Participants With Clinically Significant Safety Laboratory Tests Values.
NCT02532998 (27) [back to overview]Observed Maximum Concentration (Cmax) of AZD9977
NCT02532998 (27) [back to overview]Observed Maximum Concentration (Cmax) of Eplerenone.
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 Assessed Per Sodium/Potassium Ratio in Urine in AZD9977 Treatment With Placebo Versus Treatment With AZD9977.
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 Assessed Per Sodium/Potassium Ratio in Urine in Eplerenone Treatment Versus a Combination Treatment of Eplerenone and AZD9977.
NCT02532998 (27) [back to overview]Terminal Half-life (t½λz) of AZD9977.
NCT02532998 (27) [back to overview]Terminal Half-life (t½λz) of Eplerenone.
NCT02532998 (27) [back to overview]Time to Reach Maximum Concentration (Tmax) of AZD9977.
NCT02532998 (27) [back to overview]Time to Reach Maximum Concentration (Tmax) of Eplerenone.
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 Assessed by Estimating the Fractional Sodium Excretion in Urine for Each Urine Collection Time Interval.
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 Assessed Per Fractional Potassium Excretion in Urine for Each Urine Collection Time Interval.
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 Assessed Per Total Sodium Excreted Cumulatively and During Each of the Urine Collection Intervals.
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 Assessed Per Urine Production for Each Urine Collection Time Interval.
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 by Assessment of Total Potassium Excreted Cumulatively and During Each of the Urine Collection Intervals
NCT02532998 (27) [back to overview]Pharmacodynamics of AZD9977 by Assessment of Total Urine Volume Excreted Cumulatively and During Each of the Urine Collection Intervals

Quality of Life Will be the Third Secondary Outcome Measure. The Investigators Will Compare the Quality of Life in Treated and Untreated Patients.

Quality of life will be the third secondary outcome measure. The investigators will compare the quality of life in patients on fludrocortisone vs placebo. Reported as RAND36 (Research ANd Development) score. The RAND 36-Item Health Survey taps eight health concepts: physical functioning, bodily pain, role limitations due to physical health problems, role limitations due to personal or emotional problems, emotional well-being, social functioning, energy/fatigue, and general health perceptions. It also includes a single item that provides an indication of perceived change in health. Min value = 0 , Maximum value = 100. The lower the score the more disability. The higher the score the less disability i.e., a score of zero is equivalent to maximum disability and a score of 100 is equivalent to no disability. (NCT00118482)
Timeframe: 12 months

Interventionscore on a scale (Mean)
Fludrocortisone Acetate69
Placebo84

[back to top]

The Frequency of Syncope Will be the First Secondary Outcome Measure.

Frequency will be reported as 12- month syncope event rates (%) (NCT00118482)
Timeframe: Within 12 months

Interventionrate % (Mean)
Fludrocortisone Acetate44.0
Placebo60.5

[back to top]

The Primary Outcome Measure Will be the Recurrence of Syncope in Follow up Period.

This will be measured in terms of number of patients that had at least 1 syncopal spell in the 12 month follow up period. (NCT00118482)
Timeframe: Within 12 months

InterventionParticipants (Count of Participants)
Fludrocortisone Acetate42
Placebo54

[back to top]

Overall Survival (OS)

OS is defined as the time from date of first dose of study drug until the date of death. For those patients who did not die, OS was censored at the recorded last date of patient contact, and those missing a recorded last date of contact will be censored at the last date the patient was known to be alive. (NCT00623766)
Timeframe: From first dose to 24 months

InterventionMonths (Median)
Ipilimumab, 10 mg/kg, IV in Corticosteroid-free Patients6.97
Ipilimumab, 10 mg/kg, IV in Corticosteroid-dependent Patients3.75

[back to top]

Best Overall Response Rate (BORR) by Modified World Health Organization (mWHO) Criteria and by Immune-relate Response Criteria (irRC)

BORR is defined as the number of patients whose global best overall response (BOR) was complete (CR) or partial response (PR), divided by the total number of participants who received treatment. CR=complete disappearance of all index lesions. PR=decrease, relative to baseline, of 50% or greater in the sum of the products of the 2 largest perpendicular diameters of all index lesions. The global BOR is the best overall response (OR) designation over the study as a whole for an individual in the study based on overall tumor burden. Both central nervous system (CNS) (brain lesions) and non-CNS compartments (lesions outside the brain) are considered for the global BOR. For the analysis of global BOR of CR or PR (by both modified WHO criteria and immune-related response criteria [irRC]), the OR assessment must be confirmed by a second (confirmatory) evaluation meeting the criteria for response and must be performed no less than 4 weeks after the criteria for response are first met. (NCT00623766)
Timeframe: From Day 1, first dose until the last tumor assessment, Week 12

,
InterventionPercentage of participants (Number)
Global BORR (mWHO criteria)BORR in brain (mWHO criteria)BORR in non-CNS compartment (mWHO criteria)Global BORR (irRC)BORR in brain (irRC)BORR in non-CNS compartment (irRC criteria )
Ipilimumab, 10 mg/kg IV, in Corticosteroid-dependent Patients4.84.84.84.84.84.8
Ipilimumab, 10 mg/kg IV, in Corticosteroid-free Patients9.815.713.79.815.713.7

[back to top] [back to top]

Disease Control Rate by Modified World Health Organization (mWHO) Tumor Assessment Criteria

Disease control rate is defined as the number of patients with a best overall response of complete response (CR), partial response (PR), or stable disease (SD) (global, in brain, or outside of brain) based on mWHO criteria divided by the number of patients who received treatment. By mWHO criteria: CR=complete disappearance of all index lesions. PR=decrease, relative to baseline, of 50% or greater in the sum of the 2 largest perpendicular diameters of all index lesions. SD=does not meet criteria for CR or PR, in the absence of progressive disease (PD). Patients with PR or CR not confirmed after at least 4 weeks are scored as SD unless they have new primary lesions. PD=at least 25% increase in the sum of the diameters of all index lesions (taking as reference the smallest sum recorded at or following baseline) and/or the appearance of any new lesions. CNS=central nervous system. (NCT00623766)
Timeframe: From Day 1, first dose to end of Week 12

,
InterventionPercentage of participants (Number)
Global disease control rateDisease control rate in brain
Ipilimumab, 10 mg/kg IV, in Corticosteroid-dependent Patients4.89.5
Ipilimumab, 10 mg/kg IV, in Corticosteroid-free Patients17.623.5

[back to top] [back to top]

Number of Participants Surviving at 6, 12, 18, 24, and 36 Months (Overall Survival [OS] Rate)

OS is defined as the time from the first dose of study drug until the date of death. Overall survival rate is the percentage of participants known to be alive at a timepoint. For those patients who did not die, OS was censored at the recorded last date of patient contact, and those with a missing recorded last date of contact will be censored at the last date the patient was known to be alive. The survival rate at a specified time-point is the probability that a patient is alive at that time following randomization. The rate is calculated for each treatment group using the Kaplan-Meier product-limit method. A corresponding 2-sided 95% bootstrap confidence interval will be calculated. (NCT00623766)
Timeframe: From first dose to Months 6, 12, 18, 24, and 36 months

,
InterventionProbability of being alive (Number)
At 6 monthsAt 12 monthsAt 18 monthsAt 24 monthsAt 36 months
Ipilimumab, 10 mg/kg IV, in Corticosteroid-dependent Patients0.380.190.190.100.10
Ipilimumab, 10 mg/kg IV, in Corticosteroid-free Patients0.550.310.260.260.26

[back to top] [back to top] [back to top] [back to top]

Apparent Clearance (CL/F) of AZD9977.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

InterventionL/h (Geometric Mean)
Treatment D23.78
Treatment B26.20

[back to top]

Apparent Clearance (CL/F) of Eplerenone.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

InterventionL/h (Geometric Mean)
Treatment C10.87
Treatment D9.360

[back to top]

Apparent Volume of Distribution at Terminal Phase (Vz/F) of AZD9977.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

InterventionL (Geometric Mean)
Treatment B246.7
Treatment D220.4

[back to top]

Apparent Volume of Distribution at Terminal Phase (Vz/F) of Eplerenone.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

InterventionL (Geometric Mean)
Treatment C49.11
Treatment D44.77

[back to top]

Area Under Plasma Concentration-time Curve From Zero Extrapolated to Infinity (AUC) of AZD9977.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh*nmol/L (Geometric Mean)
Treatment D21060
Treatment B19120

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Area Under Plasma Concentration-time Curve From Zero Extrapolated to Infinity (AUC) of Eplerenone.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh*ng/mL (Geometric Mean)
Treatment C9199
Treatment D10680

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Area Under the Plasma Concentration-time Curve From Time Zero to t Hours After Dosing (AUC(0-t)) of Eplerenone.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh*ng/mL (Geometric Mean)
Treatment C9035
Treatment D10510

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Area Under the Plasma Concentration-time Curve From Time Zero to t Hours After Dosing (AUC[0-t]) of AZD9977.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh*nmol/L (Geometric Mean)
Treatment D19970
Treatment B18520

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Number of Participants With Clinically Significant Blood Pressure Values.

"Clinically significant blood pressure values (if available) were recorded for all participants.~The systolic blood pressure (mmHg) and diastolic BP (mmHg) was obtained after each subject had rested in the supine position for at least 5 minutes and was performed in accordance with the Schedule of Assessments of study protocol.~Abnormal findings in blood pressure after 10 minutes resting in the supine position was defined as following:~Systolic blood pressure (SBP) < 90 mmHg or ≥ 140 mmHg~Diastolic blood pressure (DBP) < 50 mmHg or ≥ 90 mmHg." (NCT02532998)
Timeframe: From screening to post-study visit, up to 10 weeks

InterventionParticipants (Number)
Treatment A0
Treatment D0
Treatment B0
Treatment C0

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Number of Participants With Clinically Significant Electrocardiogram.

"Clinically significant electrocardiogram values were recorded for all participants in the study.~A 12-lead ECG was obtained after each subject had rested in the supine position for at least 10 minutes and was performed in accordance with the Schedule of Assessments of study protocol.~The investigator judged the overall interpretation as normal or abnormal. If abnormal, it would have been decided as to whether or not the abnormality was clinically significant and the reason for the abnormality would have been recorded. The investigator could add extra 12-lead resting ECG safety assessments if there were any abnormal findings of if the investigator considered it was necessary for any other safety reason. These assessments would have been entered as an unscheduled assessment." (NCT02532998)
Timeframe: From screening to post-study visit, up to 10 weeks

InterventionParticipants (Number)
Treatment A0
Treatment D0
Treatment B0
Treatment C0

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Number of Participants With Clinically Significant Physical Examination Values.

"Number of participants with clinically significant physical examination values.~The complete physical examinations included an assessment of the general appearance, respiratory, cardiovascular, abdomen, skin, head, and neck (including ears, eyes, nose, mouth and throat), lymph nodes, thyroid, musculoskeletal and neurological systems. The brief physical examinations included an assessment of the general appearance, skin, abdomen, cardiovascular and respiratory systems. The results of the physical examination were listed by body system for each subject. Body weight was listed by participant and time-point. Any new or aggravated clinically relevant abnormal medical finding at a physical examination as compared with the baseline assessment were reported as an adverse event (AE)." (NCT02532998)
Timeframe: From screening to post-study visit, up to 10 weeks

InterventionParticipants (Number)
Treatment A0
Treatment D0
Treatment B0
Treatment C0

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Number of Participants With Clinically Significant Pulse Rate.

"Clinically significant pulse rate (if available) was recorded for all participants in the study.~The pulse was obtained after each subject had rested in the supine position for at least 5 minutes and was performed in accordance with the Schedule of Assessments of study protocol.~Abnormal findings in pulse rate, after 10 minutes resting in the supine position, was defined as following:~• Pulse < 45 or > 85 beats per minute (bpm)" (NCT02532998)
Timeframe: From screening to post-study visit, up to 10 weeks

InterventionParticipants (Number)
Treatment A0
Treatment D0
Treatment B0
Treatment C0

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Number of Participants With Clinically Significant Safety Laboratory Tests Values.

Clinically significant safety laboratory test values included hematology, clinical chemistry, urinalysis and urine chemistry, including urine creatinine and uric acid measurements. Viral serology and urine drugs of abuse, alcohol and cotinine were assessed for eligibility. If deterioration in laboratory value was associated with clinical symptoms and/or signs, the symptom or sign were reported as an adverse event and the associated laboratory result was considered as additional information. Laboratory results were listed and summarized according to change from baseline and repeat/unscheduled measurements. Any out of range laboratory results were flagged in the individual listings. (NCT02532998)
Timeframe: From screening to post-study visit, up to 10 weeks

InterventionParticipants (Number)
Treatment A0
Treatment D0
Treatment B0
Treatment C0

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Observed Maximum Concentration (Cmax) of AZD9977

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionnmol/L (Geometric Mean)
Treatment D6238
Treatment B5816

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Observed Maximum Concentration (Cmax) of Eplerenone.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionng/mL (Geometric Mean)
Treatment C1557
Treatment D1729

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Pharmacodynamics of AZD9977 Assessed Per Sodium/Potassium Ratio in Urine in AZD9977 Treatment With Placebo Versus Treatment With AZD9977.

"The sum over the urine collection intervals of the logarithm of the urinary sodium/potassium ratio from two hours to eight hours post-dose.~NOTE: Note: Data are presented as the sum of the difference between ln(Na+) and ln(K+) over the collected intervals 2-4, 4-6 and 6-8 hours." (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionsodium/potassium ratio (Mean)
Treatment A-4.09
Treatment B-0.694

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Pharmacodynamics of AZD9977 Assessed Per Sodium/Potassium Ratio in Urine in Eplerenone Treatment Versus a Combination Treatment of Eplerenone and AZD9977.

"The sum over the urine collection intervals of the logarithm of the urinary sodium/potassium ratio from two hours to eight hours post-dose.~NOTE: Data are presented as the sum of the difference between ln(Na+) and ln(K+) over the collected intervals 2-4, 4-6 and 6-8 hours." (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionsodium/potassium ratio (Mean)
Treatment C-0.545
Treatment D0.694

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Terminal Half-life (t½λz) of AZD9977.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh (Mean)
Treatment D6.753
Treatment B6.726

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Terminal Half-life (t½λz) of Eplerenone.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh (Mean)
Treatment C3.232
Treatment D3.419

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Time to Reach Maximum Concentration (Tmax) of AZD9977.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh (Median)
Treatment D0.52
Treatment B0.50

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Time to Reach Maximum Concentration (Tmax) of Eplerenone.

Pre IMP dose and post IMP dose at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 12, 16 and 24 hours (NCT02532998)
Timeframe: From 2 hours post dose to 8 hours post dose

Interventionh (Median)
Treatment C1.98
Treatment D2.00

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Pharmacodynamics of AZD9977 Assessed by Estimating the Fractional Sodium Excretion in Urine for Each Urine Collection Time Interval.

"Pharmacodynamics of AZD9977 by assessment of fractional sodium excretion in urine for each urine collection time interval.~Pharmacodynamics of AZD9977 after single dosing of AZD9977 with fludrocortisone and/or eplerenone." (NCT02532998)
Timeframe: From 0 to 8 hours after dosing

,,,
Intervention% value (Mean)
0 to 2 hours2 to 4 hours4 to 6 hours6 to 8 hours
Treatment A0.340.220.150.16
Treatment B0.320.350.360.36
Treatment C0.330.370.380.48
Treatment D0.330.480.580.66

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Pharmacodynamics of AZD9977 Assessed Per Fractional Potassium Excretion in Urine for Each Urine Collection Time Interval.

"Pharmacodynamics of AZD9977 assessed per fractional potassium excretion in urine for each urine collection time interval.~Pharmacodynamics of AZD9977 after single dosing of AZD9977 with fludrocortisone and/or eplerenone" (NCT02532998)
Timeframe: From 0 to 8 hours post dosing

,,,
Intervention% value (Mean)
0 to 2 hours2 to 4 hours4 to 6 hours6 to 8 hours
Treatment A21.7222.2614.6018.08
Treatment B21.1418.9512.1213.34
Treatment C21.6621.1512.4813.48
Treatment D22.1920.3012.4913.35

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Pharmacodynamics of AZD9977 Assessed Per Total Sodium Excreted Cumulatively and During Each of the Urine Collection Intervals.

"Pharmacodynamics of AZD9977 by assessment of total sodium excreted cumulatively and during each of the urine collection intervals.~Pharmacodynamics of AZD9977 after single dosing of AZD9977 with fludrocortisone and/or eplerenone." (NCT02532998)
Timeframe: From 0 to 24 hours after dosing

,,,
Interventionmmol (Mean)
0 to 2 hours2 to 4 hours4 to 6 hours6 to 8 hours8 to 10 hours10 to 12 hours12 to 14 hours14 to 16 hours16 to 24 hours
Treatment A71215192328323646
Treatment B71523323946515466
Treatment C71523344755626779
Treatment D817314663748287103

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Pharmacodynamics of AZD9977 Assessed Per Urine Production for Each Urine Collection Time Interval.

"Pharmacodynamics of AZD9977 assessed per urine production for each urine collection time interval.~Pharmacodynamics of AZD9977 after single dosing of AZD9977 with fludrocortisone and/or eplerenone." (NCT02532998)
Timeframe: From 8 hours before dosing until 24 hours after dosing

,,,
InterventionmL (Mean)
-8 to -2 hours-2 to 0 hour0 to 2 hour2 to 4 hour4 to 6 hours6 to 8 hours8 to 10 hours10 to 12 hours12 to 14 hours14 to 16 hours16 to 24 hours
Treatment A321.4303.5307.4272.2178.8216.6266.0337.1280.2357.3296.0
Treatment B284.5274.3305.0245.6229.9273.6246.6309.0306.0326.5292.2
Treatment C294.9284.5298.8272.6202.2291.5300.2324.5306.3354.2290.6
Treatment D309.3288.6320.2236.1246.0115.7326.6361.9300.7345.9302.8

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Pharmacodynamics of AZD9977 by Assessment of Total Potassium Excreted Cumulatively and During Each of the Urine Collection Intervals

"Pharmacodynamics of AZD9977 by assessment of total potassium excreted cumulatively and during each of the urine collection intervals.~Pharmacodynamics of AZD9977 after single dosing of AZD9977 with fludrocortisone in comparison to AZD9977 placebo." (NCT02532998)
Timeframe: From 0 to 24 hours after dosing

,,,
Interventionmmol (Mean)
0 to 2 hours2 to 4 hours4 to 6 hours6 to 8 hours8 to 10 hours10 to 12 hours12 to 14 hours14 to 16 hours16 to 24 hours
Treatment A13.629.038.349.961.471.180.787.7101.8
Treatment B14.027.135.544.653.863.372.579.294.4
Treatment C13.727.435.945.154.964.073.579.795.4
Treatment D14.526.735.244.454.462.171.377.592.1

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Pharmacodynamics of AZD9977 by Assessment of Total Urine Volume Excreted Cumulatively and During Each of the Urine Collection Intervals

"Pharmacodynamics of AZD9977 by assessment of total urine volume excreted cumulatively and during each of the urine collection intervals.~Pharmacodynamics of AZD9977 after single dosing of AZD9977 with fludrocortisone and/or eplerenone" (NCT02532998)
Timeframe: From 8 hours before dosing until 24 hours after dosing

,,,
InterventionmL (Mean)
0 to 2 hour2 to 4 hour4 to 6 hours6 to 8 hours8 to 10 hours10 to 12 hours12 to 14 hours14 to 16 hours16 to 24 hours
Treatment A307.4579.5758.3974.91242.21574.41865.12221.02506.6
Treatment B305.0550.7780.61054.21300.81609.81915.82242.32534.5
Treatment C298.8571.4773.61065.11365.31689.81996.12350.32640.9
Treatment D320.2556.3802.21099.01425.21791.72091.72435.72741.2

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