PrednisoneCAS# 53-03-2 |
- BMY 14802 hydrochloride
Catalog No.:BCC5759
CAS No.:105565-55-7
- BD 1008 dihydrobromide
Catalog No.:BCC6674
CAS No.:138356-09-9
- BD 1047 dihydrobromide
Catalog No.:BCC6863
CAS No.:138356-21-5
- Siramesine
Catalog No.:BCC4304
CAS No.:147817-50-3
- BD 1063 dihydrochloride
Catalog No.:BCC6832
CAS No.:206996-13-6
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
| Cas No. | 53-03-2 | SDF | Download SDF |
| PubChem ID | 5865 | Appearance | Powder |
| Formula | C21H26O5 | M.Wt | 358.43 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | Dehydrocortisone | ||
| Solubility | DMSO : 100 mg/mL (278.99 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
| Chemical Name | (8S,9S,10R,13S,14S,17R)-17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,9,12,14,15,16-octahydrocyclopenta[a]phenanthrene-3,11-dione | ||
| SMILES | CC12CC(=O)C3C(C1CCC2(C(=O)CO)O)CCC4=CC(=O)C=CC34C | ||
| Standard InChIKey | XOFYZVNMUHMLCC-ZPOLXVRWSA-N | ||
| Standard InChI | InChI=1S/C21H26O5/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/h5,7,9,14-15,18,22,26H,3-4,6,8,10-11H2,1-2H3/t14-,15-,18+,19-,20-,21-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
||
| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
||
| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Prednisone (Adasone) is a synthetic corticosteroid agent that is particularly effective as an immunosuppressant compound.
Target: Others
Prednisone is a synthetic corticosteroid drug that is particularly effective as an immunosuppressant drug. It is used to treat certain inflammatory diseases (such as moderate allergic reactions) and (at higher doses) some types of cancer, but has significant adverse effects. Because it suppresses the immune system, it leaves patients more susceptible to infections.
Prednisone can also be used in the treatment of decompensated heart failure to potentiate renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large dose of loop diuretics. The mechanism is prednisone, as a glucocorticoid, can improve renal responsiveness to atrial natriuretic peptide by increasing the density of natriuretic peptide receptor type A in the renal inner medullary collecting duct, inducing a potent diuresis. References: | |||||
Prednisone Dilution Calculator
Prednisone Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.7899 mL | 13.9497 mL | 27.8995 mL | 55.7989 mL | 69.7486 mL |
| 5 mM | 0.558 mL | 2.7899 mL | 5.5799 mL | 11.1598 mL | 13.9497 mL |
| 10 mM | 0.279 mL | 1.395 mL | 2.7899 mL | 5.5799 mL | 6.9749 mL |
| 50 mM | 0.0558 mL | 0.279 mL | 0.558 mL | 1.116 mL | 1.395 mL |
| 100 mM | 0.0279 mL | 0.1395 mL | 0.279 mL | 0.558 mL | 0.6975 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
Prednisone (Adasone) is a synthetic corticosteroid agent that is particularly effective as an immunosuppressant compound.
- Acetylisocupressic acid
Catalog No.:BCN5695
CAS No.:52992-82-2
- Ajugol
Catalog No.:BCN2883
CAS No.:52949-83-4
- Genz-644282
Catalog No.:BCC1592
CAS No.:529488-28-6
- N-(2,6-Diphenylmethyl)-1-piperazine acetylamine
Catalog No.:BCC9052
CAS No.:5294-61-1
- Nanaomycin A
Catalog No.:BCC3611
CAS No.:52934-83-5
- Neosophoramine
Catalog No.:BCN5690
CAS No.:52932-74-8
- Dammaradienyl acetate
Catalog No.:BCN5689
CAS No.:52914-31-5
- PRIMA-1MET
Catalog No.:BCC2414
CAS No.:5291-32-7
- Motilin (human, porcine)
Catalog No.:BCC5894
CAS No.:52906-92-0
- 6,7-Dihydroxy-4-Methylcoumarin
Catalog No.:BCC8287
CAS No.:529-84-0
- Euxanthone
Catalog No.:BCN5694
CAS No.:529-61-3
- Genistin
Catalog No.:BCN2396
CAS No.:529-59-9
- Estrone
Catalog No.:BCN2201
CAS No.:53-16-7
- Mitotane (Lsodren)
Catalog No.:BCC3815
CAS No.:53-19-0
- Cocaine hydrochloride
Catalog No.:BCC5943
CAS No.:53-21-4
- Methylprednisolone acetate
Catalog No.:BCC9043
CAS No.:53-36-1
- Oxandrolone
Catalog No.:BCC5242
CAS No.:53-39-4
- Dehydroepiandrosterone
Catalog No.:BCN2202
CAS No.:53-43-0
- Indomethacin
Catalog No.:BCC3794
CAS No.:53-86-1
- L-Picein
Catalog No.:BCC8336
CAS No.:530-14-3
- Deoxyvasicinone
Catalog No.:BCN5697
CAS No.:530-53-0
- 2,6-Dimethoxy-1,4-benzoquinone
Catalog No.:BCN5698
CAS No.:530-55-2
- Syringic acid
Catalog No.:BCN5699
CAS No.:530-57-4
- Sinapic acid
Catalog No.:BCN3539
CAS No.:530-59-6
Old But Good: Modified-Release Prednisone in Rheumatoid Arthritis.[Pubmed:28356031]
Rev Recent Clin Trials. 2017;12(2):124-128.
BACKGROUND: Since more than 50 years glucocorticoids represent the milestone in the treatment of inflammatory diseases, including rheumatoid arthritis (RA). However, many patients with RA present a circadian rhythm in symptoms severity with a significant worsening in the morning, that correlates with cyclic changes in circulating hormones and cytokines. Classical steroid therapy given in the morning fails to intercept this pathophysiological phenomenon. In the last years, a novel formulation of Prednisone has been developed in order to better fit these variations, improve efficacy and minimize adverse events (chronotherapy). This modified-release (MR) Prednisone is administered in the evening at 10.00 p.m. and absorbed after about 4 hours. METHODS: In this article, we reviewed the recent clinical trials evaluating the efficacy of MR Prednisone in RA patients, including two randomized controlled double-blind clinical trials Circadian Administration of Prednisone in Rheumatoid Arthritis - 1 (CAPRA-1) and CAPRA-2 and other nonrandomized observational studies. RESULTS: According to the available evidence, MR Prednisone seems effective in ameliorating morning stiffness in RA patients. CONCLUSION: In conclusion, the use of MR Prednisone in the treatment regimen could be a costeffective choice in a significant proportion of RA patients, particularly in those with a clinical phenotype characterized by morning stiffness or morning recrudescence of pain. With regards to the safety, MR Prednisone adverse events profile does not differ from that of IR glucocorticoids.
Rapid Discontinuation of Prednisone in Kidney Transplant Recipients: 15-Year Outcomes From the University of Minnesota.[Pubmed:28376034]
Transplantation. 2017 Oct;101(10):2590-2598.
BACKGROUND: Short- and intermediate-term results have been reported after rapid discontinuation of Prednisone (RDP) in kidney transplant recipients. Yet there has been residual concern about late graft failure in the absence of maintenance Prednisone. METHODS: From October 1, 1999, through June 1, 2015, we performed a total of 1553 adult first and second kidney transplants-1021 with a living donor, 532 with a deceased donor-under our RDP protocol. We analyzed the 15-year actuarial overall patient survival (PS), graft survival (GS), death-censored GS (DCGS), and acute rejection-free survival (ARFS) rates for RDP compared with historical controls on maintenance Prednisone. RESULTS: For living donor recipients, the actuarial 15-year PS rates were similar between groups. But RDP was associated with increased GS (P = 0.02) and DCGS (P = 0.01). For deceased donor recipients, RDP was associated with significantly better PS (P < 0.01), GS (P < 0.01) and DCGS (P < 0.01). There was no difference between groups in the rate of acute or chronic rejection, or in the mean estimated glomerular filtration rate at 15 years. However, RDP-treated recipients had significantly lower rates of avascular necrosis, cytomegalovirus, cataracts, new-onset diabetes after transplant, and cardiac complications. Importantly, for recipients with GS longer than 5 years, there was no difference between groups in subsequent actuarial PS, GS, and DCGS. CONCLUSIONS: In summary, at 15 years postkidney transplant, RDP did not lead to decreased in PS or GS, or an increase in graft dysfunction but as associated with reduced complication rates.
Infection rates in tacrolimus versus cyclosporine-treated pediatric kidney transplant recipients on a rapid discontinuation of prednisone protocol: 1-year analysis.[Pubmed:28371243]
Pediatr Transplant. 2017 Jun;21(4).
AR is lower in pKTx recipients on Tac vs CsA. Data comparing infection outcomes for children treated with these agents are limited. We retrospectively studied infection outcomes in 96 pKTx recipients on a RDP. PS, DCGS, AR, and infection-free survival were assessed using Kaplan-Meier/log-rank tests and proportional hazards models. There were no differences in 1-year PS, DCGS, or AR between Tac and CsA recipients. After adjusting for AR, the hazard of CMV viremia was 4.0 times higher (95%CI: 1.04, 15.5; P = .044) and that of BK viremia was 3.8 times higher (95%CI: 1.5, 10.2; P = .007) in Tac recipients. The incidence of EBV viremia was similar between the groups (P = .56). PostTx lymphoproliferative disease was only observed in Tac recipients (3%). There was no difference in the incidence of pneumonia, urinary tract, or Clostridium difficile infections between Tac and CsA recipients. Among KTx recipients on RDP, the hazards of CMV and BK viremia within 1 year post-KTx were significantly higher in Tac recipients compared to CsA. Regular assessment for infections and lower Tac trough levels may be warranted in Tac recipients.
Induction of T-Cell Infiltration and Programmed Death Ligand 2 Expression by Adeno-Associated Virus in Rhesus Macaque Skeletal Muscle and Modulation by Prednisone.[Pubmed:28345428]
Hum Gene Ther. 2017 Jun;28(6):493-509.
Use of adeno-associated virus (AAV) to transduce genes into skeletal muscles can be associated with T-cell responses to viral capsid and/or to transgenic protein. Intramuscular mononuclear cell infiltrates primarily consisting of CD8+ T cells and also containing FOXP3+ regulatory T cells were present in rhesus macaque skeletal muscle treated with rAAVrh74.MCK.GALGT2 by vascular delivery. Administration of oral Prednisone prior to AAV gene delivery and throughout the study reduced such infiltrates by 60% at 24 weeks post AAV delivery compared with AAV-treated animals not receiving Prednisone, regardless of the presence of pre-existing AAV serum antibodies at the time of treatment. The majority of CD8+ T cells in AAV-treated muscles expressed activated caspase 3 and programmed cell death protein 1 (PD1), suggesting ongoing programmed cell death. AAV-transduced skeletal muscles also had elevated expression of programmed death ligand 2 (PDL2) on skeletal myofibers, and this increase in expression extended to muscles where transgene was not overexpressed. These data demonstrate that Prednisone can reduce the extent of intramuscular T-cell infiltrates in AAV-treated muscles, which may aid in achieving long-term transgene expression, as may the induction of PDL2 expression on skeletal myofibers to promote PD1-mediated programmed T-cell death.
