体外活性：泼尼松可阻断细胞周期 G1 期的外周血淋巴细胞 (PBL) 生长，并抑制活化的人外周血 T 淋巴细胞中的 IL-2 受体 (IL-2R) 表达和 IL-2 分泌。泼尼松可增加 PHA 激活的人 PBL 的凋亡，且泼尼松对 CD8(+) T 淋巴细胞的凋亡作用强于对 CD4(+) T 淋巴细胞。

与对照组相比，泼尼松（肌肉注射，10 mg/kg，每日一次，第 4-13 天）降低了患有脑心肌炎病毒性心肌炎的 BALB/c 小鼠的存活率。此外，心肌病毒滴度在第4天达到峰值，但不存在抗体滴度。第8天，病毒和抗体滴度仍然升高。与对照相比，第 10 天抗体滴度仍显着升高，但病毒滴度显着降低[2]。在SLE小鼠（MRL/lpr）模型中，泼尼松（5 mg/kg，胃内给药，每日一次）可以改变FA的代谢[3]。

Animal/Disease Models: Female MRL/lpr mice[3]
Doses: 5 mg/kg
Route of Administration: intragastrically (po) administration, daily
Experimental Results: Elevated polyunsaturated FA, such as arachidonic acid and docosahexaenoic acid, and decreased the total level of n-6 polyunsaturated fatty acids in.

Absorption, Distribution and Excretion
Oral prednisone has a Tmax of 2 hours, while the delayed-release formulation has a Tmax of 6-6.5 hours. A 5mg dose of prednisone has an AUC of 572mL/min/1.73m2, a 20mg dose of prednisone has an AUC of 1034mL/min/1.73m2, and a 50mg dose of prednisone has an AUC of 2271mL/min/1.73m2. Data regarding the Cmax of prednisone is not readily available.
Prednisone is excreted mainly in the urine as sulfate and glucuronide conjugates.
Data regarding the volume of distribution for prednisone is not readily available. However, 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.
Data regarding the clearance of prednisone is not readily available. A 5.5µg/h/kg infusion of prednisolone has an average clearance of 0.066±0.12L/h/kg, while a 0.15±0.03L/h/kg infusion has an average clearance of 0.15L/h/kg.
Thirty minutes after iv administration of (3)H-prednisone to a monkey, the concentration of prednisone was highest in the kidney. The drug was also found in the liver, spleen, lung, small intestine, serum and bile. The concentration of prednisolone was highest in the liver. It was also found in the kidney, pancreas, spleen, lung, small intestine, serum and bile.
Prednisone is readily absorbed from the gut. Serum concentrations of prednisone and prednisolone, its active metabolite, have been found to be maximal 1 hour after oral administration of a 5-mg tablet of prednisone to beagle dogs. Following both ip and oral administration of prednisone to mice, serum levels of prednisone, prednisolone and other metabolites were maximal at 15 min. These levels were higher in mice given ip injections of prednisone than in those receiving the same doses by the oral route. Oral administration of prednisone to dogs and monkeys led to serum levels comparable with those following iv injections, but individual variations were relatively large.
Prednisone is readily absorbed from the gut. In a series of 22 normal subjects, the mean peak serum concentration was 930 ug/L (range, 508-1579) following oral administration of a 50 mg tablet.
The protein binding characteristics of prednisone and prednisolone, alone and together, in human and rabbit plasma and human serum albumin, are reported. The kinetics of prednisolone binding were nonlinear and those of prednisone were linear in both human and rabbit plasma; prednisone binding was linear with human serum albumin, although to a lesser degree. It is suggested that prednisone binds to proteins other than albumin in plasma. Binding of prednisone was not influenced by prednisolone. The results support the hypothesis that the protein binding characteristics of prednisone and prednisolone do not explain the reported nonlinear pharmacokinetics of prednisone.
Administration of physiologic doses unlikely to adversely affect infant. FDA Category: C (C = Studies in laboratory animals have revealed adverse effects on the fetus (teratogenic, embryocidal, etc.) but there are no controlled studies in pregnant women. The benefits from use of the drug in pregnant women may be acceptable despite its potential risks, or there are no laboratory animal studies or adequate studies in pregnant women.) /Adrenocorticosteroids/ /from table II/

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Metabolism / Metabolites
Prednisone is 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). Prednison is reversibly metabolized to [prednisolone]. 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.
In one study after an oral dose of prednisone, the plasma prednisolone concentration peaked between 60 and 120 min and then declined exponentially. After rapid iv injection of steroid, the plasma prednisolone concentration peaked within 10 to 20 min. An initial rapid distribution phase succeeded by a slower decay phase was expressed by a biphasic exponential disappearance curve of the plasma prednisolone concentration versus time. Plasma prednisolone concentrations achieved with an oral dose of prednisone were in the same range as those obtained during the second phase after iv administration.
Reduction of the 11-oxo to the 11alpha-hydroxyl group by the enzyme 11beta-hydroxydehydrogenase converts prednisone to prednisolone, its biologically active form. This reaction takes place mainly in the liver, and may proceed satisfactorily even in the presence of liver disease
In vitro, prednisone is converted to prednisolone by liver, lung and renal tissue. Conversely, prednisolone is converted to prednisone by renal tissue.
... 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.
Prednisone is completely converted to the active metabolite prednisolone by 11‘_-hydroxysteroid dehydrogenases. It is then further metabolized mainly in the liver. The exposure of prednisolone is 4-6 fold higher than that of prednisone.
Route of Elimination: Excreted in the urine as sulfate and glucuronide conjugates.
Half Life: Half life of both the immediate- and delayed- release formulation is 2 to 3 hours.

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Biological Half-Life
Prednisone and its active metabolite [prednisolone] have half lives of 2-3 hours from both immediate and delayed release preparations.
In a series of 22 normal subjects, the mean peak serum concentration was 930 ug/L (range, 508-1579) following oral administration of a 50 mg tablet. The overall mean serum half-life was 2.95 hours

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Amounts of prednisone 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 prednisone 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.
◉ Effects in Breastfed Infants
None reported with prednisone or any other corticosteroid. In a prospective follow-up study, six 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 with Crohn's disease used prednisone 60 mg daily in a tapering schedule immediately postpartum during breastfeeding (extent not stated). She also received sulfasalazine 4 grams daily and infliximab 5 mg/kg every 8 weeks during pregnancy and postpartum. At 6 months of age, the infant was asymptomatic with regular weight gain.
The National Transplantation Pregnancy Registry reports that as of December 2013, 124 women with transplants have taken prednisone while breastfeeding 169 infants for periods as long as 48 months, with no apparent infant harm.
◉ Effects on Lactation and Breastmilk
Published information on the effects of prednisone 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 prednisone 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 prednisone might have the same effect.

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Protein Binding
Corticosteroids are generally bound to corticosteroid binding globulin and serum albumin in plasma. Prednisone is <50% bound to protein in plasma.

[1]. RIEMER AD. Application of the newer corticosteroids to augment diuresis in congestive heart failure. Am J Cardiol. 1958 Apr;1(4):488-96.
[2]. [2]N Tomioka, et al. Effects of prednisolone on acute viral myocarditis in mice. J Am Coll Cardiol. 1986 Apr;7(4):868-72.
[3]. Qianqian Li, et al. Metabolic Profiling Reveals an Abnormal Pattern of Serum Fatty Acids in MRL/lpr Mice Under Treatment With Prednisone. Front Pharmacol. 2020 Feb 25;11:115.

Prednisone is an odorless white crystalline powder. (NTP, 1992)
Prednisone is a synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid. It has a role as a prodrug, an anti-inflammatory drug, an antineoplastic agent, an immunosuppressive agent and an adrenergic agent. It is a 20-oxo steroid, an 11-oxo steroid, a 21-hydroxy steroid, a 17alpha-hydroxy steroid, a glucocorticoid, a 3-oxo-Delta(1),Delta(4)-steroid, a primary alpha-hydroxy ketone, a tertiary alpha-hydroxy ketone and a C21-steroid.
A synthetic anti-inflammatory glucocorticoid derived from [cortisone]. It is biologically inert and converted to [prednisolone] in the liver. Prednisone was granted FDA approval on 21 February 1955.
Prednisone is a Corticosteroid. The mechanism of action of prednisone is as a Corticosteroid Hormone Receptor Agonist.
Prednisone is a synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. After cell surface receptor attachment and cell entry, prednisone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production. This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cell populations.
Prednisone is only found in individuals that have used or taken this drug. It is a synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. Prednisone is a glucocorticoid receptor agonist. It is first metabolized in the liver to its active form, prednisolone. Prednisolone crosses cell membranes and binds with high affinity to specific cytoplasmic receptors. The result includes inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.
A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.

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Drug Indication
Prednisone is indicated as an anti-inflammatory or immunosuppressive drug for allergic, dermatologic, gastrointestinal, hematologic, ophthalmologic, nervous system, renal, respiratory, rheumatologic, infectious, endocrine, or neoplastic conditions as well as in organ transplant.

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Mechanism of Action
Prednisone is first metabolized in the liver to its active form, prednisolone, a glucocorticoid agonist corticosteroid. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.
In physiologic doses, corticosteroids are administered to replace deficient endogenous hormones. In larger (pharmacologic) doses, glucocorticoids decrease inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes; inhibiting macrophage accumulation in inflamed areas; reducing leukocyte adhesion to capillary endothelium; reducing capillary wall permeability and edema formation; decreasing complement components; antagonizing histamine activity and release of kinin from substrates; reducing fibroblast proliferation, collagen deposition, and subsequent scar tissue formation; and possibly by other mechanisms as yet unknown. The drugs suppress the immune response by reducing activity and volume of the lymphatic system, producing lymphocytopenia, decreasing immunoglobulin and complement concentrations, decreasing passage of immune complexes through basement membranes, and possibly by depressing reactivity of tissue to antigen-antibody interactions. Glucocorticoids stimulate erythroid cells of bone marrow, prolong survival time of erythrocytes and platelets, and produce neutrophilia and eosinopenia. Glucocorticoids promote gluconeogenesis, redistribution of fat from peripheral to central areas of the body, and protein catabolism, which results in negative nitrogen balance. They reduce intestinal absorption and increase renal excretion of calcium. /Corticosteroids/
Glucocorticoids are capable of suppressing the inflammatory process through numerous pathways. They interact with specific intracellular receptor proteins in target tissues to alter the expression of corticosteroid-responsive genes. Glucocorticoid-specific receptors in the cell cytoplasm bind with steroid ligands to form hormone-receptor complexes that eventually translocate to the cell nucleus. There these complexes bind to specific DNA sequences and alter their expression. The complexes may induce the transcription of mRNA leading to synthesis of new proteins. Such proteins include lipocortin, a protein known to inhibit PLA2a and thereby block the synthesis of prostaglandins, leukotrienes, and PAF. Glucocorticoids also inhibit the production of other mediators including AA metabolites such as COX, cytokines, the interleukins, adhesion molecules, and enzymes such as collagenase. /Glucocorticoids/

C21H26O5

358.43

358.178

53-03-2

Prednisone-d8;Prednisone acetate;125-10-0

5865

Crystals
White to practically white, crystalline powder

1.3±0.1 g/cm3

573.7±50.0 °C at 760 mmHg

236-238 °C(lit.)

314.8±26.6 °C

0.0±3.6 mmHg at 25°C

1.604

1.57

91.67

2

5

2

26

764

6

O([H])[C@]1(C(C([H])([H])O[H])=O)C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])C([H])([H])C([H])([H])C4=C([H])C(C([H])=C([H])[C@]4(C([H])([H])[H])[C@@]3([H])C(C([H])([H])[C@@]21C([H])([H])[H])=O)=O

XOFYZVNMUHMLCC-ZPOLXVRWSA-N

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

(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

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: ≥ 2.08 mg/mL (5.80 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.08 mg/mL (5.80 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (5.80 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
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