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Prednisolone

Alias:
Cat No.:V1698 Purity: ≥98%
Prednisolone (AKOS-016010152; AK-115681; Predsol; Pediapred) is an approved medication acting as a potent and synthetic glucocorticoid with anti-inflammatory and immunomodulatory properties.
Prednisolone
Prednisolone Chemical Structure CAS No.: 50-24-8
Product category: Calcium Channel
This product is for research use only, not for human use. We do not sell to patients.
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5g
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Other Forms of Prednisolone:

  • Prednisolone hemisuccinate
  • Prednisolone Acetate (Omnipred)
  • Prednisolone sodium metazoate
  • Prednisolone valerate acetate
  • Prednisolone Phosphate Sodium
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Top Publications Citing lnvivochem Products
Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Prednisolone (AKOS-016010152; AK-115681; Predsol; Pediapred) is an approved medication acting as a potent and synthetic glucocorticoid with anti-inflammatory and immunomodulatory properties. Prednisolone (50 mg/kg, im) given 15 min before LPS-attenuated production of NO2- and NO3- by neutrophils and suppresses LPS-stimulated mRNA for NOS II in rat neutrophils. Prednisolone reduces joint swelling through a mechanism associated with a reduction in IL-1beta and IL-6 protein and mRNA expression levels in SCW-induced arthritis rats.

Biological Activity I Assay Protocols (From Reference)
Targets
Glucocorticoid receptor
ln Vitro
Resistance or sensitivity to glucocorticoids is considered to be of crucial importance for disease prognosis in childhood acute lymphoblastic leukemia. Prednisolone exerted a delayed biphasic effect on the resistant CCRF-CEM leukemic cell line, necrotic at low doses and apoptotic at higher doses. At low doses, prednisolone exerted a pre-dominant mitogenic effect despite its induction on total cell death, while at higher doses, prednisolone's mitogenic and cell death effects were counterbalanced. Early gene microarray analysis revealed notable differences in 40 genes. The mitogenic/biphasic effects of prednisolone are of clinical importance in the case of resistant leukemic cells. This approach might lead to the identification of gene candidates for future molecular drug targets in combination therapy with glucocorticoids, along with early markers for glucocorticoid resistance [1].
Prednisolone (0.002-10 μg/mL; 3 days) suppresses human leukocyte mitosis.[5]
ln Vivo
Nitric oxide is believed to participate in nonspecific cellular immunity. Gram negative bacterial endotoxins increase the production of reactive nitrogen intermediates (RNI) in phagocytic cells by inducing the enzyme nitric oxide synthase II (NOS II). Anti-inflammatory glucocorticoids attenuate endotoxin-induced increases in RNI. This study evaluated the effect of in vivo administration of prednisolone on Escherichia coli lipopolysaccharide endotoxin (LPS)-induced increases in plasma RNI and neutrophil mRNA for NOS II and production of RNI in the rat. We show that LPS rapidly induces mRNA for NOS II and production of RNI (NO2- and NO3- anion) in rat neutrophils within 2 hr after in vivo administration of a sublethal dose of 0.5 mg/kg, i.v. A pharmacologic dose of prednisolone (50 micrograms/kg, im) given 15 min before LPS-attenuated production of NO2- and NO3- by neutrophils and suppressed LPS-stimulated mRNA for NOS II. 3-Amino, 1,2,4-triazine inhibited NO2- and NO3- production without affecting gene expression for NOS II. These data demonstrate that LPS rapidly induces functional gene expression for NOS II and prednisolone prevents induction of NOS II activity by inhibiting transcription of its mRNA [2].
Diaphragm atrophy and weakness occur after administration of massive doses of corticosteroids for short periods. In the present study the effects of prolonged administration of moderate doses of fluorinated and nonfluorinated steroids were investigated on contractile properties and histopathology of rat diaphragm. 60 rats received saline, 1.0 mg/kg triamcinolone, or 1.25 or 5 mg/kg i.m. prednisolone daily for 4 wk. Respiratory and peripheral muscle mass increased similarly in control and both prednisolone groups, whereas triamcinolone caused severe muscle wasting. Maximal tetanic tension averaged 2.23 +/- 0.54 kg/cm2 (SD) in the control group. An increased number of diaphragmatic bundles in the 5-mg/kg prednisolone group generated maximal tetanic tensions < 2.0 kg/cm2 (P < 0.05). In addition, fatigability during the force-frequency protocol was most pronounced in this group (P < 0.05). In contrast, triamcinolone caused a prolonged half-relaxation time and a leftward shift of the force-frequency curve (P < 0.05). Histological examination of the diaphragm showed a normal pattern in the control and 1.25-mg/kg prednisolone group. Myogenic changes, however, were found in the 5-mg/kg prednisolone group and, more pronounced, in the triamcinolone group. Selective type IIb fiber atrophy was found in the latter group, but not in the prednisolone groups. In conclusion, triamcinolone induced type IIb fiber atrophy, resulting in reduced respiratory muscle strength and a leftward shift of the force-frequency curve. In contrast, 5 mg/kg prednisolone caused alterations in diaphragmatic contractile properties and histological changes without fiber atrophy [3].
Since NZB/NZW mice develop an immune nephritis similar to that of systemic lupus erythematosus in man, a study was designed in these mice to compare the clinical and immunologic effects of three immunosuppressive drug regimens. For 72 weeks, groups of 20 mice received daily oral therapy with a) no drugs, b) azathioprine, c) prednisolone or d) combined azathioprine-prednisolone. The combined regimen was superior to either drug used alone in preventing deaths from renal disease. Prednisolone alone also prolonged life significantly, but not as effectively as combination therapy. Azathioprine alone was not effective. All drugs suppressed the antibody response to an exogenous antigen (Vi polysaccharide) equally well. None of the drug regimens prevented the appearance of proteinuria, antinuclear antibodies, Coombs' antibody, or γ-globulin deposits in glomeruli. However, the ability of a therapeutic regimen to suppress antibodies to native DNA correlated well with its ability to suppress renal disease. No malignancies were found among 73 animals autopsied, but significant hepatic damage occurred in the groups receiving prednisolone. Thus, combined therapy was superior to either drug used alone, and the immunosuppressive effect of greatest clinical importance seemed to be the ability to prevent formation of anti-DNA antibodies.[4]
Cell Assay
Prednisolone treatment [1]
Concentrations of Prednisolone were selected on the basis of the average in vivo dosage administrated intravenously to children at ages between 1 month and 12 years old (details in supplementary data, file: CCRFCEM Cytotoxixity Assay.xls). Also, bioactivity in cortisol equivalents is estimated to be in the range of 40–200 nM. To ensure that the study covers these ranges, prednisolone was diluted to the following 12 concentrations: control, 10 nM, 100 nM, 1 μM, 5.5 μM, 11 μM, 22 μM, 44 μM, 88 μM, 175 μM, 350 μM, and 700 μM.
Cell proliferation assay Cell population counts were determined with the use of a NIHON KOHDEN CellTaq-α hematology analyzer. Cells were counted at the −24 h time point as well as 0 h, 4 h, 24 h, 48 h, and 72 h after initiation of exposure to prednisolone. For this purpose, 200 μl of cell suspensions were obtained from each flask and counted directly with the analyzer.
Protein extraction and Western blotting [1]
Cells were harvested after 1 h and 4 h exposure to different concentrations of Prednisolone. Protein extraction and Western blotting were performed as previously described. Total protein content was determined by the Bradford method using bovine serum albumin as a standard. Proteins were separated by SDS-PAGE and Western blotting was carried out, with anti-p65 antibodies
Microarray analysis [1]
cDNA microarray chips (1200 genes) were obtained from TAKARA (Human Cancer Chip v.40). Hybridization was performed with the CyScribe Post-Labeling kit as described by the manufacturer, utilizing the Cy3 and Cy5 fluorescent dyes. Slides were scanned with a microarray scanner. Images were generated with ScanArray microarray acquisition software. cDNAs from three experimental setups were used, each one consisting of three independent experiments. The experimental setups consisted of the three following pairs: control vs. 10 nM Prednisolone (designated as 0vs1), 10 nM prednisolone vs. 700 μM prednisolone (designated as 1vs3), control vs. 700 μM prednisolone (designated as 0vs3). This is a ‘simple loop’ experimental design, taking into account all possible combinations between samples, as previously described. Raw microarray data are available as supplementary data.
Real-time reverse transcription PCR (qRT-PCR) [1]
The GRIM19 (NDUFA13) gene was tested from three samples control, 10 nM and 700 μM Prednisolone at 4 h and 48 h treatment, using the one-step Plexor™ qRT-PCR kit. The set of primers was designed using the on-line tool Plexor™ Primer Design System v1.2 by Promega
Animal Protocol
Study design, animals, and treatment [3]
60 adult male Wistar rats, aged 14 wk, weighing 350-400 g, were randomized in quadruplets, into one of four treatment groups: control (C), saline, 0.05 ml/d i.m.; low dose prednisolone (LD), 1.25 mg/kg per d i.m.; high dose prednisolone (HD), 5 mg/kg per d i.m.; or triamcinolone-diacetate (TR), 1 mg/kg per d i.m. Dilution of medication was performed such that with each injection all animals received a similar volume (0.05 ml). During 4 wk the animals were injected daily in the left hindlimb. They were fed ad libitum and weighed twice weekly. After the treatment period, contractile properties, histological, and histochemical characteristics of the diaphragm were examined.[3]
Animal/Disease Models: NZB/NZW mice, immune nephritis model[4]
Doses: 5 mg/ kg/day
Route of Administration: po (oral gavage) 6 days a week for 72 weeks
Experimental Results: Dramatically lowered mortality rate and prolonged life Dramatically.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Oral prednisolone reaches a Cmax of 113-1343ng/mL with a Tmax of 1.0-2.6 hours. Oral prednisolone is approximately 70% bioavailable.
Prednisolone is over 98% eliminated in urine.
A 0.15mg/kg dose of prednisolone has a volume of distribution of 29.3L, while a 0.30mg/kg dose has a volume of distribution of 44.2L.
A 0.15mg/kg dose of prednisolone has a clearance of 0.09L/kg/h, while a 0.30mg/kg dose has a clearance of 0.12L/kg/h.
A randomized crossover study was conducted to compare the pharmacokinetics and pharmacodynamics of 30 mg prednisolone in a plain oral tablet (Precortisyl) with those of an enteric coated tablet (Deltacortril) in 8 patients (ages 63-81 yr) with chronic obstructive pulmonary disease and in 8 healthy males (ages 22-44 yr). Although drug absorption was considerably slower from the enteric coated tablet, peak plasma levels and total area under the concn-time curve were equivalent for the formulations. Adrenal suppression was significantly less in volunteers after enteric coated than after plain tablets. This difference was not significant in patients. Plasma cortisol levels declined more slowly after enteric coated tablets in both groups. Blood glucose levels increased over 8 hr in both groups. It was concluded that in patients with chronic obstructive pulmonary disease, peak plasma levels and total area under the concn-time curve of plain and enteric coated prednisolone tablets are equivalent; enteric coated tablets result in a lag in the decline of plasma cortisol and, in volunteers, a less marked suppression of cortisol.
The transfer of prednisolone to breast milk was studied in 3 nursing women (ages 28-37 yr) who received an intravenous injection of 50 mg prednisolone sodium phosphate (Hydeltrasol). Concn of prednisolone in milk declined more rapidly than in serum, but were similar to expected unbound serum levels. Milk levels ranged from about 15% to 40% of serum levels. The exchange between unbound drug in serum and breast milk appeared to be relatively rapid and bidirectional. An average of 0.025% (0.01-0.49%) of the prednisolone dose was recovered in milk. It was concluded that the transfer of prednisolone to breast milk does not appear to pose a clinically significant risk.
The pharmacokinetics of prednisolone after oral and intravenous administration of 10 and 20 mg have been studied. Serum protein binding of prednisolone was also measured after the iv injections. The bioavailability after oral administration was 84.5% after 10 mg and 77.6% after 20 mg (p>0.05). Dose dependent pharmacokinetics were found, the VDss and Clt being significantly larger (p<0.01) after 20 mg iv than after 10 mg iv. The protein binding of prednisolone in all subjects was non-linear, and is the most likely cause of the dose dependent pharmacokinetics, as there was no dose dependent variation in elimination half-time.
Doses of 16, 32, 48 and 64 mg prednisolone were administered intravenously to normal volunteers who also received 100 prednisolone orally. Plasma prednisolone concentrations were estimated by quantitative thin layer chromatography. The bioavailability fraction was 1.063 +/- 0.154 (s.d.) indicating complete availability of prednisolone following oral administration. The mean T 1/2 over all doses were 4.11 +/- 0.97 (s.d.) hr and there was no evidence of a dose-related change in its value. The mean systemic clearance over all doses was 0.104 +/- 0.034 (s.d) L/hr/kg. There was no evidence of a dose-related change in clearance or in the apparent volume of distribution (overall mean 0.588 +/- 0.152 L/kg). The area under the plasma concentration-time curve was linearly related to dose. Plasma concentration-time curves normalised for dose were superimposable. It was concluded that over the dose range investigated, non-linear pharmacokinetic behavior had not been demonstrated in this group of normal volunteers.
For more Absorption, Distribution and Excretion (Complete) data for PREDNISOLONE (13 total), please visit the HSDB record page.
Metabolism / Metabolites
Prednisolone can be reversibly metabolized to [prednisone] which is then metabolized to 17α,21-dihydroxy-pregnan-1,4,6-trien-3,11,30-trione (M-XVII), 20α-dihydro-prednisone (M-V), 6βhydroxy-prednisone (M-XII), 6α-hydroxy-prednisone (M-XIII), or 20β-dihydro-prednisone (M-IV). 20β-dihydro-prednisone is metabolized to 17α,20ξ,21-trihydroxy-5ξ-pregn-1-en-3,11-dione(M-XVIII). Prednisolone is metabolized to Δ6-prednisolone (M-XI), 20α-dihydro-prednisolone (M-III), 20β-dihydro-prednisolone (M-II), 6αhydroxy-prednisolone (M-VII), or 6βhydroxy-prednisolone(M-VI). 6αhydroxy-prednisolone is metabolized to 6α,11β,17α,20β,21-pentahydroxypregnan-1,4-diene-3-one (M-X). 6βhydroxy-prednisolone is metabolized to 6β,11β,17α,20β,21-pentahydroxypregnan-1,4-diene-3-one (M-VIII), 6β,11β,17α,20α,21-pentahydroxypregnan-1,4-diene-3-one (M-IX), and 6β,11β,17α,21-tetrahydroxy-5ξ-pregn-1-en-3,20-dione (M-XIV). MVIII is metabolized to 6β,11β,17α,20β,21-pentahydroxy-5ξ-pregn-1-en-3-one (M-XV) and then to MXIV, while MIX is metabolized to 6β,11β,17α,20α,21-pentahydroxy-5ξ-pregn-1-en-3-one (M-XVI) and then to MXIV. These metabolites and their glucuronide conjugates are excreted predominantly in the urine.
Reduction of the 4,5 double bond can occur at both hepatic and extrahepatic sites and yields an inactive substance. Subsequent reduction of the 3-ketone substituent to a 3-hydroxyl to form tetrahydrocortisol has been demonstrated only in liver. Most of the ring a - reduced metabolites are enzymatically coupled through the 3-hydroxyl with sulfate or with glucuronic acid to form water soluble sulfate esters or glucuronides, and they are excreted as such.
Conjugated mostly in liver but also in kidney. /Human, oral/
In the present study the metabolism of prednisolone in the isolated, perfused, dual recirculating human placental lobule was reexamined, using a perfusate based on tissue culture medium 199. Four metabolites were identified in both the maternal and fetal compartments in 6 hr perfusions by comparison of relative retention times measured by HPLC and capillary GC and of mass spectra recorded by capillary GC/MS with those of authentic reference standards. The steroids were derivatized as the MO-TMS ethers for mass spectral measurements. Analysis of samples from five perfusion experiments resulted in the following percentage conversions after 6 hr perfusion (mean + or - standard deviation, maternal and fetal perfusate, respectively): prednisone (49.1 + or - 7.8, 49.1 + or - 6.6), 20 alpha-dihydroprednisone (0.84 + or - 0.29, 0.81 + or - 0.35), 20 beta-dihydroprednisone (39.1 + or - 6.7, 39.2 + or - 5.9), 20 beta-dihydroprednisolone (6.8 + or - 2.7, 6.3 + or - 1.6) and unmetabolized prednisolone (4.1 + or - 1.8, 4.6 + or - 2.1). No evidence was found for metabolites formed by 6 beta-hydroxylation or cleavage of the C17-C20 bond.
A randomized, four-way cross-over study was conducted in eight healthy male volunteers to determine the relative and absolute bioavailability of prednisone (PN) and prednisolone (PL). PN and PL were administered as single, oral 10-mg tablet doses and as 10-mg zero-order 0.5-hour intravenous infusions. Comparable mean PN and PL maximum plasma concentrations (Cmax), times for Cmax, areas under the plasma concentration-time curves (AUC), and apparent elimination rate constants between tablet treatments demonstrated that PN and PL tablets were bioequivalent. Absolute bioavailability (F) determinations based on plasma PL concentrations were independent of which IV treatment was used as reference and indicated complete systemic availability of PL from both PN and PL tablets. However, F based on plasma PN data was contradictory. Using IV PN as reference, approximately 70% systemic availability was observed from both tablets, whereas using IV PL as reference, systemic availability was greater than unity. PN and PL are model compounds that exemplify the difficulties involved in accurately determining the relative and absolute bioavailability of substances that undergo reversible metabolism.
Prednisone, prednisolone, and methylprednisolone are currently administered in association with cyclosporin A in the postoperative treatment of transplant patients. The aim of this work was to evaluate the effects of these corticosteroids on the expression of several forms of cytochromes p450, including p450 1A2, 2D6, 2E1, and 3A, and on cyclosporin A oxidase activity in human liver. For this purpose, human hepatocytes prepared from lobectomies were maintained in culture in a serum-free medium, in collagen-coated dishes, for 96-144 hr, in the absence or presence of 50-100 uM corticosteroids, rifampicin, or dexamethasone. To mimic more closely the current clinical protocol, hepatocyte cultures were also co-treated with corticosteroids and cyclosporin A or ketoconazole (a selective inhibitor of cytochromes p450 3A). Cyclosporin A oxidase activity, intracellular retention of cyclosporin A oxidized metabolites within hepatocytes, accumulation of cytochromes p450 proteins and corresponding messages, and de novo synthesis and half-lives of these cytochromes p450 were measured in parallel in these cultures. Our results, obtained from seven different hepatocyte cultures, showed that 1) dexamethasone and prednisone, but not prednisolone or methylprednisolone, were inducers of cytochrome p450 3A, at the level of protein and mRNA accumulation, as well as of cyclosporin A oxidase activity, known to be predominantly catalyzed by these cytochromes p450; 2) although corticosteroids are known to be metabolized in human liver, notably by cytochrome p450 3A, partial or total inhibition of this cytochromes p450 by cyclosporin or ketoconazole, respectively, did not affect the inducing efficiency of these molecules; 3) corticosteroids did not affect the half-life of cytochrome p450 3A or the accumulation of other forms of cytochromes p450, including 1A2, 2D6, and 2E1; 4) chronic treatment of cells with cyclosporin did not affect cytochrome p450 3A accumulation; 5) corticosteroids were all competitive inhibitors of cyclosporin A oxidase in human liver microsomes, with Ki values of 61 + or - 12, 125 + or - 25, 190 + or - 38, and 210 + or - 42 uM for dexamethasone, prednisolone, prednisone, and methylprednisolone, respectively; and 6) chronic treatment of cells with corticosteroids did not influence the excretion of oxidized metabolites of cyclosporin from the cells.
Biological Half-Life
Prednisolone has a plasma half life of 2.1-3.5 hours. This half life is shorter in children and longer in those with liver disease.
...Prednisolone (60 mg/sq m/day in three divided doses) was administered both orally and intravenously /to 23 children with acute lymphoblastic leukemia (ALL) (aged 2-15 years)/, and samples were obtained on several days during the initial 5 weeks of remission induction therapy. ...The median unbound clearance (32 L/hr/sq m) was lower, and the half-life (3.6 hr) longer than previously reported in childhood ALL.
Doses of 16, 32, 48 and 64 mg prednisolone were administered intravenously to normal volunteers who also received 100 prednisolone orally. ...The mean T 1/2 over all doses were 4.11 +/- 0.97 (s.d.) hr and there was no evidence of a dose-related change in its value.
Toxicity/Toxicokinetics
Interactions
Seizures have been observed in patients receiving cyclosporine and high doses of methylprednisolone. /Methylprednisolone
In one study, women taking oral contraceptives or postmenopausal estrogen therapy were given prednisolone concurrently. Alterations in metabolism of prednisolone, including incr half-life, were consistent with a potential for enhanced pharmacologic effect or toxicity when prednisolone was added to an estrogen regimen.
Ketoconazole inhibits the deposition of ... prednisolone by inhibiting 6beta-hydroxylase, thereby prolonging the adrenal suppressive effect of ... /prednisolone/.
Drugs reported to increase blood levels of cyclosporine include ... prednisolone.
For more Interactions (Complete) data for PREDNISOLONE (26 total), please visit the HSDB record page.
Non-Human Toxicity Values
LD50 Mouse ip > 1000 mg/kg body weight /Prednisolone acetate/
LD Mouse ip 767 mg/kg body weight
LD50 Swiss mouse oral 1680 mg/kg body weight
LD50 Sherman rat (male) sc 147 mg/kg body weight
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation

Amounts of prednisolone in breastmilk are very low. No adverse effect have been reported in breastfed infants with maternal use of any corticosteroid during breastfeeding. Although it is often recommended to avoid breastfeeding for 4 hours after a dose this maneuver is not necessary because prednisolone milk levels are very low. Medium to large doses of corticosteroids given systemically or injected into joints or the breast have been reported to cause temporary reduction of lactation.
Because absorption from the eye is limited, ophthalmic prednisolone would not be expected to cause any adverse effects in breastfed infants. To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue.

◉ Effects in Breastfed Infants
None reported with prednisolone or any other corticosteroid. In a prospective follow-up study, 6 nursing mothers reported taking prednisone (dosage unspecified) with no adverse infant effects. There are several reports of mothers breastfeeding during long-term use of corticosteroids with no adverse infant effects: prednisone 10 mg daily (2 infants) and prednisolone 5 to 7.5 mg daily (14 infants).
A woman who was nursing (extent not stated) her newborn infant was treated for pemphigus with oral prednisolone 25 mg daily, with the dosage increased over 2 weeks to 60 mg daily. She was also taking cetirizine 10 mg daily and topical betamethasone 0.1% twice daily to the lesions. Because of a poor response, the betamethasone was changed to clobetasol propionate ointment 0.05%. She continued breastfeeding throughout treatment and her infant was developing normally at 8 weeks of age and beyond.
A woman with pemphigoid gestationis was treated with prednisolone in a dosage tapering from 0.7 mg/kg daily to 1 mg daily during breastfeeding. She also received courses of intravenous immune globulin 2 grams/kg over 3 days at 4, 9 and 13 weeks postpartum. She breastfed her infant (extent not stated) for 3 months with no problems noted.
Two mothers with systemic lupus erythematosus were reported who took prednisolone 30 or 40 mg daily during pregnancy and lactation as well as tacrolimus 3 mg daily. Three years after birth, both children were healthy. The durations of lactation were not stated.
A woman with rheumatoid arthritis refractory to etanercept took sarilumab 200 mg every two weeks during pregnancy until 37 weeks of gestation. She was also taking prednisolone 10 mg and tacrolimus 3 mg daily. She delivered a healthy infant at 38 weeks of gestation and breastfed her infant. Prednisolone was continued postpartum, tacrolimus was restarted at 7 days postpartum, and sarilumab was restarted at 28 days postpartum. The mother continued to breastfeed until 6 months postpartum. The infant was vaccinated with multiple live vaccines after reaching six months old, including the Bacille-Calmette-Guerin vaccine, with no adverse effects.

◉ Effects on Lactation and Breastmilk
Published information on the effects of prednisolone on serum prolactin or on lactation in nursing mothers was not found as of the revision date. Medium to large doses of corticosteroids given systemically or injected into joints or the breast have been reported to cause temporary reduction of lactation.
A study of 46 women who delivered an infant before 34 weeks of gestation found that a course of another corticosteroid (betamethasone, 2 intramuscular injections of 11.4 mg of betamethasone 24 hours apart) given between 3 and 9 days before delivery resulted in delayed lactogenesis II and lower average milk volumes during the 10 days after delivery. Milk volume was not affected if the infant was delivered less than 3 days or more than 10 days after the mother received the corticosteroid. An equivalent dosage regimen of prednisolone might have the same effect.
A study of 87 pregnant women found that betamethasone given as above during pregnancy caused a premature stimulation of lactose secretion during pregnancy. Although the increase was statistically significant, the clinical importance appears to be minimal. An equivalent dosage regimen of prednisolone might have the same effect.
5755 man TDLo oral 9 mg/kg/2W-I BEHAVIORAL: TOXIC PSYCHOSIS Drug Intelligence and Clinical Pharmacy., 18(603), 1984 [PMID:6745088]
5755 women TDLo oral 14 mg/kg/13D-I BEHAVIORAL: TOXIC PSYCHOSIS Drug Intelligence and Clinical Pharmacy., 18(603), 1984 [PMID:6745088]
5755 rat LD50 intraperitoneal 2 gm/kg Advances in Teratology., 3(181), 1968
5755 rat LD50 subcutaneous 147 mg/kg Toxicology and Applied Pharmacology., 8(250), 1966 [PMID:5956877]
5755 rat LD50 intravenous 120 mg/kg Pharmaceutical Chemistry Journal, 16(63), 1982
Protein Binding
Prednisolone's protein binding is highly variable, ranging from 65-91% in healthy patients.
References

[1]. Prednisolone exerts late mitogenic and biphasic effects on resistant acute lymphoblastic leukemia cells: Relation to early gene expression. Leuk Res, 2009. 33(12): p. 1684-95.

[2]. Rapid induction of messenger RNA for nitric oxide synthase II in rat neutrophils in vivo by endotoxin and its suppression by prednisolone. Proc Soc Exp Biol Med. 1994 Mar;205(3):220-9.

[3]. Triamcinolone and prednisolone affect contractile properties and histopathology of rat diaphragm differently. J Clin Invest. 1993 Sep;92(3):1534-42.

[4]. Comparison of therapeutic and immunosuppressive effects of azathioprine, prednisolone and combined therapy in nzp/nzw mice. Arthritis & Rheumatism: Official Journal of the American College of Rheumatology, 1973, 16(2): 163-170.

[5]. Inhibition of human leukocyte mitosis by prednisolone in vitro. Cancer Res. 1961 Dec;21:1518-21.

Additional Infomation
Therapeutic Uses
Anti-Inflammatory Agents, Steroidal; Antineoplastic Agents, Hormonal; Glucocorticoids, Synthetic
Ophthalmic corticosteroids are indicated in the treatment of corticosteroid-responsive allergic and inflammatory conditions of the palpebral and bulbar conjunctiva, cornea, and anterior segment of the globe. /Corticosteroids (Ophthalmic); Included in US product labeling/
VET: Hormonal therapy for neoplasia commonly involves the use of glucocorticoids. Direct antitumor effects are related to their lympholytic properties; glucocorticoids can inhibit mitosis, RNA synthesis, and protein synthesis in sensitive lymphocytes. Glucocorticoids are considered cell-cycle nonspecific and are often used in chemotherapeutic protocols after induction by another agent. Prednisolone /is/ commonly used to treat lymphoreticular neoplasms in combination with other drugs. Because /it/ readily enters the CSF, ... prednisolone /is/ especially useful in treatment of leukemias and lymphomas of the CNS.
Indicated in a wide range of endocrine, rheumatic, allergic, dermatologic, respiratory, hematologic, neoplastic, and other disorders.
For more Therapeutic Uses (Complete) data for PREDNISOLONE (28 total), please visit the HSDB record page.
Drug Warnings
VET: IT OFTEN MAY BE CONTRAINDICATED IN CONGESTIVE HEART FAILURE, DIABETES OR OSTEOPOROSIS. EXCEPT FOR EMERGENCY LIFE SAVING USE, IT SHOULD BE OMITTED IN TUBERCULOSIS, CHRONIC NEPHRITIS, CUSHINGOID SYNDROMES, & PEPTIC ULCER CASES.
Side effects and compliance were examined in 63 pediatric patients (ages 10 mo-14 yr) with acute asthma who received an oral dose of 1-2 mg/kg prednisolone (Solone; Panafcortelone) as a whole or crushed tablet or in liquid form for 7 days. Up to 44% of patients either refused to take or vomited the drug on the first day. Improved acceptability of prednisolone occurred with time, but prescribing practices indicated short-term treatment of 1 to 4 days was common. Abdominal pain and mood changes occurred in 19% and 80% of patients, respectively, at some stage of the study period. It was concluded that oral prednisolone is poorly tolerated in pediatric patients and its use may lead to suboptimal therapy.
Glucocorticoid use in children is not only associated with the side effects which are seen in adults, but also with severe adverse effects on statural growth. As little as 2.5-5.0 mg prednisolone/day can cause a retardation in statural growth. A direct relationship exists between the dose of glucocorticoid used and statural growth. The use of knemometry, a sensitive technique for measuring the growth of long bones in children has increased the accuracy of growth rate measurements. Many factors, such as disease process, sex, daily vs alternate day therapy, ethnic variations or whether the patient has been immobilized must be considered when evaluating the effects on stature of a particular glucocorticoid.
RESULTS FROM CONTROLLED TRIAL, INDICATE THAT PREDNISOLONE TREATMENT IS NOT BENEFICIAL & CAN BE DETRIMENTAL IN ACUTE NEUROPATHY OF UNDETERMINED ETIOLOGY.
For more Drug Warnings (Complete) data for PREDNISOLONE (48 total), please visit the HSDB record page.
Pharmacodynamics
Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Prednisolone has a short duration of action as the half life is 2.1-3.5 hours. Corticosteroids have a wide therapeutic window as patients make require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C21H28O5
Molecular Weight
360.44
Exact Mass
360.193
Elemental Analysis
C, 69.98; H, 7.83; O, 22.19
CAS #
50-24-8
Related CAS #
Prednisolone;50-24-8; Prednisolone;50-24-8;Prednisolone hemisuccinate;2920-86-7;Prednisolone acetate;52-21-1; 630-67-1 (sodium metazoate); 72064-79-0 (valerate acetate); 125-02-0 (Na+ phosphate)
PubChem CID
5755
Appearance
White to off-white solid powder
Density
1.3±0.1 g/cm3
Boiling Point
570.6±50.0 °C at 760 mmHg
Melting Point
240 °C (dec.)(lit.)
Flash Point
313.0±26.6 °C
Vapour Pressure
0.0±3.6 mmHg at 25°C
Index of Refraction
1.612
LogP
1.5
Hydrogen Bond Donor Count
3
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
2
Heavy Atom Count
26
Complexity
724
Defined Atom Stereocenter Count
7
SMILES
C[C@]12C[C@@H]([C@H]3[C@H]([C@@H]1CC[C@@]2(C(=O)CO)O)CCC4=CC(=O)C=C[C@]34C)O
InChi Key
OIGNJSKKLXVSLS-VWUMJDOOSA-N
InChi Code
InChI=1S/C21H28O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h5,7,9,14-16,18,22,24,26H,3-4,6,8,10-11H2,1-2H3/t14-,15-,16-,18+,19-,20-,21-/m0/s1
Chemical Name
(8S,9S,10R,11S,13S,14S,17R)-11,17-Dihydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-7,8,9,11,12,14,15,16-octahydro-6H-cyclopenta[a]phenanthren-3-one
Synonyms

prednisolone; 50-24-8; Metacortandralone; Hydroretrocortine; Delta-Cortef; Deltacortril; Deltahydrocortisone; Codelcortone; sodium phosphate Predsol; Pediapred

HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 72 mg/mL (199.7 mM)
Water:<1 mg/mL
Ethanol: 10 mg/mL (27.7 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.77 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.08 mg/mL (5.77 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (5.77 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.7744 mL 13.8719 mL 27.7439 mL
5 mM 0.5549 mL 2.7744 mL 5.5488 mL
10 mM 0.2774 mL 1.3872 mL 2.7744 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

Calculator

Molarity Calculator allows you to calculate the mass, volume, and/or concentration required for a solution, as detailed below:

  • Calculate the Mass of a compound required to prepare a solution of known volume and concentration
  • Calculate the Volume of solution required to dissolve a compound of known mass to a desired concentration
  • Calculate the Concentration of a solution resulting from a known mass of compound in a specific volume
An example of molarity calculation using the molarity calculator is shown below:
What is the mass of compound required to make a 10 mM stock solution in 5 ml of DMSO given that the molecular weight of the compound is 350.26 g/mol?
  • Enter 350.26 in the Molecular Weight (MW) box
  • Enter 10 in the Concentration box and choose the correct unit (mM)
  • Enter 5 in the Volume box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 17.513 mg appears in the Mass box. In a similar way, you may calculate the volume and concentration.

Dilution Calculator allows you to calculate how to dilute a stock solution of known concentrations. For example, you may Enter C1, C2 & V2 to calculate V1, as detailed below:

What volume of a given 10 mM stock solution is required to make 25 ml of a 25 μM solution?
Using the equation C1V1 = C2V2, where C1=10 mM, C2=25 μM, V2=25 ml and V1 is the unknown:
  • Enter 10 into the Concentration (Start) box and choose the correct unit (mM)
  • Enter 25 into the Concentration (End) box and select the correct unit (mM)
  • Enter 25 into the Volume (End) box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 62.5 μL (0.1 ml) appears in the Volume (Start) box
g/mol

Molecular Weight Calculator allows you to calculate the molar mass and elemental composition of a compound, as detailed below:

Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
Instructions to calculate molar mass (molecular weight) of a chemical compound:
  • To calculate molar mass of a chemical compound, please enter the chemical/molecular formula and click the “Calculate’ button.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
  • Molecular mass (or molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
  • Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
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Reconstitution Calculator allows you to calculate the volume of solvent required to reconstitute your vial.

  • Enter the mass of the reagent and the desired reconstitution concentration as well as the correct units
  • Click the “Calculate” button
  • The answer appears in the Volume (to add to vial) box
In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
Step 2: Enter in vivo formulation (This is only a calculator, not the exact formulation for a specific product. Please contact us first if there is no in vivo formulation in the solubility section.)
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Clinical Trial Information
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CTID: NCT05412394
Phase: Phase 4    Status: Recruiting
Date: 2023-09-18
Study of Ipatasertib or Apitolisib With Abiraterone Acetate Versus Abiraterone Acetate in Participants With Castration-Resistant Prostate Cancer Previously Treated With Docetaxel Chemotherapy
CTID: NCT01485861
Phase: Phase 1/Phase 2    Status: Completed
Date: 2023-09-14
A Study of the Drug IMGN632 in Children With Leukemia That Has Come Back After Treatment or is Difficult to Treat
CTID: NCT05320380
Phase: Phase 1/Phase 2    Status: Withdrawn
Date: 2023-09-01
Safety and Efficacy of Prednisolone in Adrenal Insufficiency Disease (PRED-AID Study)
CTID: NCT03936517
Phase: Phase 3    Status: Active, not recruiting
Date: 2023-09-01
Efficacy and Safety of Infliximab for Immune Checkpoint Inhibitor Induced Colitis
CTID: NCT05947669
Phase: Phase 3    Status: Recruiting
Date: 2023-08-24
A Placebo-controlled Phase 2 Trial to Investigate the Safety and Efficacy of Secukinumab in Giant Cell Arteritis
CTID: NCT03765788
Phase: Phase 2    Status: Completed
Date: 2023-08-21
The Efficacy and Safety of the RCMOP Sequential Therapy as a First-line Treatment for Patients With Intermediate-to-high Risk Diffuse Large B-cell Lymphoma Who Had Incomplete Remission.
CTID: NCT05990985
Phase: N/A    Status: Not yet recruiting
Date: 2023-08-18
The Glucocorticoid Low-dose Outcome in RheumatoId Arthritis Study
CTID: NCT02585258
Phase: Phase 4    Status: Completed
Date: 2023-07-18
Barretts oEsophageal Resection With Steroid Therapy Trial
CTID: NCT02004782
Phase: Phase 4    Status: Withdrawn
Date: 2023-07-03
DEXTENZA for the Treatment of Postoperative Pain and Inflammation Following Vitreo-retinal Surgery
CTID: NCT04462523
Phase: Phase 4    Status: Completed
Date: 2023-06-15
Preparation and Characterization Intranasal Film Loaded With Steroid as a Local Treatment of Anosmia in Compare to Insulin Intranasal Film
CTID: NCT05328414
Phase: Phase 1/Phase 2    Status: Completed
Date: 2023-06-01
A Randomized, Multicenter Open Label Study Comparing Early Administration of Azathioprine Plus IFX to Steroids Plus Azathioprine for Acute Severe Colitis
CTID: NCT02425852
Phase: Phase 4    Status: Completed
Date: 2023-05-31
Applying Shear Wave Elastography for Adjunct Steroid on Tuberculous Lymphadenitis
CTID: NCT05861440
Phase: N/A    Status: Recruiting
Date: 2023-05-19
EFFECTIVENESS OF SINGLE DOSE ORAL DEXAMETHASONE VERSUS MULTIDOSE PREDNISOLONE FOR TREATMENT OF ACUTE EXACERBATIONS OF ASTHMA AMONG CHILDREN ATTENDING THE EMERGENCY DEPARTMENT OF CHILDREN HOSPITAL, ISLAMABAD
CTID: NCT05850143
Phase: N/A    Status: Enrolling by invitation
Date: 2023-05-09
Systemic Therapy in Advancing or Metastatic Prostate Cancer: Evaluation of Drug Efficacy
CTID: NCT00268476
Phase: Phase 2/Phase 3    Status: Active, not recruiting
Date: 2023-04-18
Baricitinib Plus Glucocorticoid for Eosinophilia in IgG4-RD
CTID: NCT05781516
Phase: N/A    Status: Recruiting
Date: 2023-03-27
A Study of Polatuzumab Vedotin in Combination With Rituximab or Obinutuzumab, Cyclophosphamide, Doxorubicin, and Prednisone in Participants With B-Cell Non-Hodgkin's Lymphoma
CTID: NCT01992653
Phase: Phase 1/Phase 2    Status: Completed
Date: 2023-03-14
Methotrexate and Prednisolone Study in Erythema Nodosum Leprosum
CTID: NCT03775460
Phase: N/A    Status: Recruiting
Date: 2023-03-13
Comparison of Tofacitinib and Prednisolone in the Treatment of Active Takayasu's Arteritis
CTID: NCT05749666
Phase: Phase 3    Status: Recruiting
Date: 2023-03-01
Intraorbital Injection Versus Oral Steroid in Anterior Idiopathic Orbital Inflammation
CTID: NCT03958344
Phase: Phase 3    Status: Recruiting
Date: 2023-02-16
Prevention of Glucocorticoid Induced Impairment of Bone Metabolism
CTID: NCT04767711
Phase: N/A    Status: Completed
Date: 2023-02-06
Tacrolimus Plus Glucocorticoid for Severe Thrombocytopenia in SS
CTID: NCT05694130
Phase: Phase 2/Phase 3    Status: Not yet recruiting
Date: 2023-01-23
Efficacy and Safety of Two Glucocorticoid Regimens in the Treatment of Sarcoidosis
CTID: NCT03265405
Phase: Phase 4    Status: Completed
Date: 2023-01-11
A Trial of CHOP-R Therapy, With or Without Acalabrutinib, in Patients With Newly Diagnosed Richter's Syndrome
CTID: NCT03899337
Phase: Phase 2    Status: Recruiting
Date: 2023-01-09
A Trial to Learn How BAY1834845 and BAY1830839 Affect Inflammation When Taken by Mouth Twice a Day for 7 Days in a Row in Healthy Male Participants
CTID: NCT05003089
Phase: Phase 1    Status: Completed
Date: 2022-12-16
The Treatment of Adrenal Crisis With Inhaled Prednisolone
CTID: NCT05639127
PhaseEarly Phase 1    Status: Unknown status
Date: 2022-12-06
Miracle Mouthwash Plus Hydrocortisone vs Prednisolone Mouth Rinse for Mouth Sores Caused by Everolimus
CTID: NCT02229136
Phase: Phase 2    Status: Completed
Date: 2022-12-01
An RCT of Mycophenolate Mofetil (MMF) in Fibrotic Hypersensitivity Pneumonitis
CTID: NCT05626387
Phase: Phase 4    Status: Recruiting
Date: 2022-11-30
Radiotherapy Versus Radiotherapy Plus Chemotherapy in Early Stage Follicular Lymphoma
CTID: NCT00115700
Phase: Phase 3    Status: Completed
Date: 2022-11-18
Impact of Tapering Immunosuppressants on Maintaining Minimal Disease Activity in Adult Subjects With Psoriatic Arthritis
CTID: NCT04610476
Phase: Phase 3    Status: Recruiting
Date: 2022-11-14
Newly Diagnosed Immune Thrombocytopenia Testing the Standard Steroid Treatment Against Combined Steroid & Mycophenolate
CTID: NCT03156452
Phase: Phase 3    Status: Completed
Date: 2022-10-26
Paediatric Arteriopathy Steroid Aspirin Project
CTID: NCT03249844
Phase: Phase 3    Status: Withdrawn
Date: 2022-10-19
ASIA Down Syndrome Acute Lymphoblastic Leukemia 2016
CTID: NCT03286634
Phase: Phase 2    Status: Recruiting
Date: 2022-09-28
Timed Release Tablet Prednisone in Polymyalgia Rheumatica
CTID: NCT00836810
Phase: Phase 2/Phase 3    Status: Completed
Date: 2022-09-13
Intravenous Immunoglobulin and Prednisolone for RPL After ART.
CTID: NCT04701034
Phase: Phase 2    Status: Unknown status
Date: 2022-09-10
German Multicenter Trial for Treatment of Newly Diagnosed Acute Lymphoblastic Leukemia in Adults (07/2003)
CTID: NCT00198991
Phase: Phase 4    Status: Completed
Date: 2022-08-18
Vedolizumab for Immune Mediated Colitis
CTID: NCT04797325
Phase: Phase 2    Status: Recruiting
Date: 2022-08-17
Neoadjuvant Intense Endocrine Therapy for High Risk and Locally Advanced Prostate Cancer
CTID: NCT05406999
Phase: Phase 2    Status: Recruiting
Date: 2022-08-16
The Norwegian Prednisolone in Early Psychosis Study
CTID: NCT03340909
Phase: Phase 2    Status: Terminated
Date: 2022-08-01
The Role of Budesonide Intrapolyp Injection in CRSwNP
CTID: NCT05474924
Phase: Phase 4    Status: Unknown status
Date: 2022-07-26
AAVCAGsCD59 for the Treatment of Wet AMD
CTID: NCT03585556
Phase: Phase 1    Status: Completed
Date: 2022-05-25
Treatment of Patients With Diffuse Large B Cell Lymphoma Who Are Not Suitable for Anthracycline Containing Chemotherapy
CTID: NCT01679119
Phase: Phase 2    Status: Completed
Date: 2022-05-18
Roflumilust in Chronic Rhinosinusitis With Nasal Polyposis.
CTID: NCT05369039
Phase: Phase 2    Status: Unknown status
Date: 2022-05-11
Comparison of Two Corticosteroid Regimens for Post COVID-19 Diffuse Lung Disease
CTID: NCT04657484
Phase: N/A    Status: Completed
Date: 2022-04-26
Budesonide Multimatrix(MMX) Versus Prednisolone in Management of Mild to Moderate Ulcerative Colitis
CTID: NCT05341401
Phase: Phase 2/Phase 3    Status: Unknown status
Date: 2022-04-22
Sirolimus Versus Sirolimus Plus Prednisolone for Kaposiform Hemangioendothelioma
CTID: NCT03188068
Phase: Phase 2    Status: Completed
Date: 2022-04-21
Bioequivalence Study of Prednisolone and Dexamethasone
CTID: NCT04733144
Phase: Phase 1    Status: Unknown status
Date: 2022-04-12
The Effect of Curcumin on the Development of Prednisolone-induced Hepatic Insulin Resistance
CTID: NCT04315350
Phase: N/A    Status: Terminated
Date: 2022-04-12
Pilocarpine After Combined Cataract/Trabectome Surgery
CTID: NCT04005079
Phase: Phase 3    Status: Withdrawn
Date: 2022-04-07
Pre-phase Treatment Before R-CHOP Chemotherapy in Elderly Patients With Newly Diagnosed DLBCL
CTID: NCT03465527
Phase: Phase 2    Status: Completed
Date: 2022-04-01
Role of Montelukast in the Management of Chronic Rhinosinusitis With Nasal Polyps.
CTID: NCT05143502
Phase: Phase 1/Phase 2    Status: Unknown status
Date: 2022-03-18
Exclusion Diet vs corticosteroIds in patientS With activE Crohn's Disease
CTID: NCT05284136
Phase: Phase 2/Phase 3    Status: Not yet recruiting
Date: 2022-03-17
Rituximab and Belimumab Combination Therapy in PR3 Vasculitis
CTID: NCT03967925
Phase: Phase 2    Status: Unknown status
Date: 2022-03-08
Rituximab, Combination Chemotherapy, and Yttrium Y 90 Ibritumomab Tiuxetan in Treating Patients With Relapsed Follicular Non-Hodgkin Lymphoma
CTID: NCT00637832
Phase: Phase 2    Status: Terminated
Date: 2022-01-06
A Study of Abemaciclib (LY2835219) in Combination With Other Anti-Cancer Therapies in Japanese Participants With Advanced Cancer
CTID: NCT04071262
Phase: Phase 1    Status: Completed
Date: 2021-09-21
Acute Unilateral Vestibulopathy and Corticosteroid Treatment
CTID: NCT02912182
Phase: Phase 4    Status: Terminated
Date: 2021-09-10
Evaluation of HepQuant SHUNT to Assess Liver Disease; Substudy Within GS-US-416-2124
CTID: NCT03087968
PhaseEarly Phase 1    Status: Withdrawn
Date: 2021-08-30
In Clinic Optometrist Insertion of Dextenza Prior to Cataract Surgery
CTID: NCT05023304
Phase: Phase 4    Status: Not yet recruiting
Date: 2021-08-26
Prednisolone in Early Diffuse Systemic Sclerosis
CTID: NCT03708718
Phase: Phase 2    Status: Completed
Date: 2021-07-30
Comparison of Disease Modifying Antirheumatic Drugs Therapy in Patients With RA Failing Methotrexate Monoth e.querySelector("font strong").innerText = 'View More' } else if(up_display === 'none' || up_display === '') { icon_angle_down.

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