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NO-prednisolone Sale

(Synonyms: NO-泼尼松龙; NCX-1015) 目录号 : GC36757

NO-prednisolone 是释放一氧化氮 (NO) 的 Prednisolone 衍生物。NO-prednisolone 有效刺激体内 IL-10 产生。

NO-prednisolone Chemical Structure

Cas No.:327610-87-7

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实验参考方法

Kinase experiment:

Peripheral blood mononuclear cells (PBMCs) are isolated from heparinized human whole venous blood using Ficoll-Hypaque (d=1.077?g). PBMCs are then washed three times with HEPES buffered RPMI 1640 containing 0.05% gentamycin and 10% donor serum. Cells (1×106, ~20% monocytes, the remainder having been lymphocytes) are transferred to a 48 well plate and pre-incubated for 1?h with Prednisolone, NO-prednisolone (10 μM-0.1 nM) or vehicle, followed by activation with LPS (1?μg/mL) for 24?h at 37°C and 5% CO2. Supernatants are removed and IL-1β production measured using a commercially available human IL-1β ELISA[2].

Animal experiment:

Mice[1]BALB/c and male Swiss Albino mice (6-8 weeks old) are used. Mice (12 per group) are injected intrarectally with 50% ethanol or 1, 1.5, 2, or 2.5 mg per mouse of TNBS. TNBS-treated mice then are treated s.c. with 5 mg/kg/day Prednisolone or NO-prednisolone for 7 days. Surviving mice are killed 8 days after TNBS administration, colonic inflammation is scored, and myeloperoxidase (MPO) activity is measured. After instillation of 1.5 mg per mouse of TNBS, animals are allocated randomly into one of three treatment groups [placebo, NO-prednisolone (5 or 0.5 mg/kg/day s.c.), or Prednisolone (10 or 5 mg/kg/day s.c.)] and followed for 7 days. Mice are monitored for the appearance of diarrhea, loss of body weight, and overall mortality. At the end of the experiment, surviving mice are killed, blood samples are collected by cardiac puncture, and a 7 cm segment of the colon is excised for macroscopic and microscopic damage evaluation. Colonic IL-2, IL-10, IFN-γ, and tumor necrosis factor-α (ELISA and RT-PCR) and MPO activity are assessed according to published methods. In duplicate experiments, the colons of surviving mice are excised for LPMC preparation.

References:

[1]. Fiorucci S, et al. NCX-1015, a nitric-oxide derivative of prednisolone, enhances regulatory T cells in the lamina propria and protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis in mice. Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15770-5.
[2]. Paul-Clark M, et al. 21-NO-prednisolone is a novel nitric oxide-releasing derivative of prednisolone with enhanced anti-inflammatory properties. Br J Pharmacol. 2000 Dec;131(7):1345-54.

产品描述

NO-prednisolone is a nitric oxide (NO)-releasing derivative of Prednisolone. NO-prednisolone potently stimulates IL-10 production in vivo. IL-10[1]

NO-prednisolone (NCX-1015), an NO-releasing derivative of Prednisolone, is demonstrated to be more effective than Prednisolone in reducing inflammation, inhibiting cytokine and chemokine generation, and up-regulating the expression of the steroid-sensitive cell-surface marker CD163 in human peripheral blood mononuclear cells[1] Incubation of PBMCs with NO-prednisolone (NCX-1015) and Prednisolone produces a concentration-dependent activation of CD163. NO-prednisolone is more potent than Prednisolone at inducing CD163 cell surface expression. The increased efficacy of NO-prednisolone, compared with the parent molecule Prednisolone, is also observed when assessing inhibition of LPS induced IL-1β production[2].

In vivo treatment with NO-prednisolone (NCX-1015) potently stimulates IL-10 production, suggesting that the NO steroid induces a regulatory subset of T cells that negatively modulates intestinal inflammation. The two doses of NO-prednisolone tested, 0.5 and 5 mg/kg/day (equivalent to 0.33 and 3.3 mg/kg/day prednisone, respectively) effectively attenuates the severity of the wasting syndrome, ameliorates the colitis score, and reduces the colonic myeloperoxidase (MPO) activity. NO-prednisolone administration also reduces the colonic mRNA and protein content of tumor necrosis factor-α, IL-12, and IFN-γ. NO-prednisolone also reduces the expression of inducible NO synthase and cyclooxygenase-2 but in contrast does not inhibit colonic expression of IL-10 mRNA or protein. In fact, IL-10 expression is enhanced in mice treated with NO-prednisolone[1].

[1]. Fiorucci S, et al. NCX-1015, a nitric-oxide derivative of prednisolone, enhances regulatory T cells in the lamina propria and protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis in mice. Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15770-5. [2]. Paul-Clark M, et al. 21-NO-prednisolone is a novel nitric oxide-releasing derivative of prednisolone with enhanced anti-inflammatory properties. Br J Pharmacol. 2000 Dec;131(7):1345-54.

Chemical Properties

Cas No. 327610-87-7 SDF
别名 NO-泼尼松龙; NCX-1015
Canonical SMILES C[C@@]12[C@](C(COC(C3=CC=C(CO[N+]([O-])=O)C=C3)=O)=O)(O)CC[C@@]1([H])[C@]4([H])CCC5=CC(C=C[C@]5(C)[C@@]4([H])[C@@H](O)C2)=O
分子式 C29H33NO9 分子量 539.57
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mM 1.8533 mL 9.2666 mL 18.5333 mL
5 mM 0.3707 mL 1.8533 mL 3.7067 mL
10 mM 0.1853 mL 0.9267 mL 1.8533 mL
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Research Update

Low-dose prednisolone in addition to the initial disease-modifying antirheumatic drug in patients with early active rheumatoid arthritis reduces joint destruction and increases the remission rate: a two-year randomized trial

Arthritis Rheum 2005 Nov;52(11):3360-70.PMID:16255010DOI:10.1002/art.21298.

Objective: To assess the efficacy of low-dose prednisolone on joint damage and disease activity in patients with early rheumatoid arthritis (RA). Methods: At the start of their initial treatment with a disease-modifying antirheumatic drug (DMARD), patients with early (duration < or =1 year) active RA were randomly assigned to receive either 7.5 mg/day prednisolone or no prednisolone for 2 years. Radiographs of the hands and feet were obtained at baseline and after 1 and 2 years and scored according to the Sharp score as modified by van der Heijde. Remission was defined as a Disease Activity Score in 28 joints of <2.6. Bone mineral density was measured by dual x-ray absorptiometry at baseline and after 2 years. Results: Of the 250 patients included, 242 completed the study and 225 had radiographs available both at baseline and at 2 years. At 2 years, the median and interquartile range (IQR) change in total Sharp score was lower in the prednisolone group than in the NO-prednisolone group (1.8 [IQR 0.5-6.0] versus 3.5 [IQR 0.5-10]; P = 0.019). In the prednisolone group, there were fewer newly eroded joints per patient after 2 years (median 0.5 [IQR 0-2] versus 1.25 [IQR 0-3.25]; P = 0.007). In the prednisolone group, 25.9% of patients had radiographic progression beyond the smallest detectable difference compared with 39.3% of patients in the NO-prednisolone group (P = 0.033). At 2 years, 55.5% of patients in the prednisolone group had achieved disease remission, compared with 32.8% of patients in the NO-prednisolone group (P = 0.0005). There were few adverse events that led to withdrawal. Bone loss during the 2-year study was similar in the 2 treatment groups. Conclusion: Prednisolone at 7.5 mg/day added to the initial DMARD retarded the progression of radiographic damage after 2 years in patients with early RA, provided a high remission rate, and was well tolerated. Therefore, the data support the use of low-dose prednisolone as an adjunct to DMARDs in early active RA.

Prednisolone does not prevent hypersensitivity reactions in antiretroviral drug regimens containing abacavir with or without nevirapine

AIDS 2001 Dec 7;15(18):2423-9.PMID:11740193DOI:10.1097/00002030-200112070-00010.

Objectives: To determine the effect of adjuvant prednisolone use on the development of abacavir (ABC)- and nevirapine (NVP)-associated hypersensitivity reactions (HSR). Methods: Randomized open-label study in antiretroviral-naive adult HIV-1 infected patients using a factorial design in which NVP and/or hydroxyurea (HU) and/or prednisolone are added to a regimen of ABC, zidovudine and lamivudine. Prednisolone (40 mg once daily) was added for the first 2 weeks of treatment. As it was difficult to distinguish ABC-associated HSR from NVP-associated HSR, these events were treated as a composite endpoint. The odds ratio (OR) of developing HSR for prednisolone-use was calculated with and without stratification by NVP and/or HU. Logistic regression was performed to identify risk factors for developing HSR. Results: Of the 229 patients 115 were randomized to prednisolone and 114 to NO-prednisolone; 19 (17%) and 11 (10%) patients, respectively, developed HSR. The expected prevention of HSR by prednisolone use was not observed. In fact use of prednisolone showed an increased risk for HSR although this did not reach statistical significance [OR, 1.82; 95% confidence interval (CI), 0.82-4.03]. There was a higher incidence of HSR in the NVP group than in the non-NVP group (20% versus 6%; P = 0.002). An additional risk factor identified in a multivariate logistic model was a high baseline CD4 cell count (OR, 1.26 per 100 x 10(6) cells/l increase; 95% CI, 1.06-1.51). Conclusions: The simultaneous start of ABC and NVP in first-line antiretroviral regimens should be avoided because of a high (20%) incidence of HSR. Short-term therapy with prednisolone did not prevent HSR in patients using ABC with or without NVP.

The effect of study design and analysis methods on recovery rates in Bell's palsy

Laryngoscope 2009 Oct;119(10):2046-50.PMID:19653268DOI:10.1002/lary.20626.

Objectives/hypothesis: We investigated how study design affects the rate of recovery in Bell's palsy. Study design: Prospective, randomized, double-blind, placebo-controlled, multicenter trial. Methods: Data were extracted from the Scandinavian Bell's palsy study, which included 829 patients. The study design was factorial; 416 patients given prednisolone, 413 not given prednisolone, 413 patients given valacyclovir, 416 not given valacyclovir. Data were analyzed with intention-to-treat principle and complete-case analysis methods and recovery was defined as Sunnybrook score 100, House-Brackmann grade I or < or =grade II at 12 months. Results: With the intention-to-treat principle and last-observation-carried-forward method (n = 829) and recovery defined as Sunnybrook 100, 300 of the 416 patients (72%) receiving prednisolone had recovered compared with 237 of the 413 (57%) who did not receive prednisolone (P < .0001). With recovery defined as House-Brackmann grade I, the corresponding recovery rates were 324 of 416 (78%) and 266 of 413 (64%) (P < .0001). With complete-case analysis and recovery defined House-Brackmann grade I (n = 782), 335 of 389 patients (86%) given prednisolone recovered compared with 277 of 393 (70%) in the group not given prednisolone (P < .0001). With recovery defined as House-Brackmann < or =grade II (n = 797), the corresponding recovery rates were 380 of 396 (96%) and 353 of 401 (88%) (P < .0001). The analysis method affected the recovery rates in the valacyclovir and no-valacyclovir groups in a similar way as in the prednisolone and NO-prednisolone groups. Conclusions: Recovery rates in a Bell's palsy study are substantially affected by the choice of analysis method and definition of recovery.