Overview on Clinical Data of Dexibuprofen

Phleps, W.

doi:10.1007/bf03342663

Cited by 34 publications

(26 citation statements)

References 10 publications

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“…S(+)-ibuprofen, also known as Dexibuprofen, is the active stereoisomer of ibuprofen racemate and it is shown to be equally efficacious to Diclofenac as an NSAID (20). It has been shown that neuroblastoma cell lines and primary tumor specimens express COX-2 and that COX inhibitors, Diclofenac and Celecoxib exhibit a growth suppressive effect on neuroblastoma cells.…”

Section: Discussionmentioning

confidence: 99%

S(+)-ibuprofen destabilizes MYC/MYCN and AKT, increases p53 expression, and induces unfolded protein response and favorable phenotype in neuroblastoma cell lines

Ikegaki

Hicks

Regan

et al. 2013

International Journal of Oncology

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Neuroblastoma is a common pediatric solid tumor that exhibits a striking clinical bipolarity favorable and unfavorable. The survival rate of children with unfavorable neuroblastoma remains low among all childhood cancers. MYCN and MYC play a crucial role in determining the malignancy of unfavorable neuroblastomas, whereas high-level expression of the favorable neuroblastoma genes is associated with a good disease outcome and confers growth suppression of neuroblastoma cells. A small fraction of neuroblastomas harbors TP53 mutations at diagnosis, but a higher proportion of the relapse cases acquire TP53 mutations. In this study, we investigated the effect of S(+)-ibuprofen on neuroblastoma cell lines, focusing on the expression of the MYCN, MYC, AKT, p53 proteins and the favorable neuroblastoma genes in vitro as biomarkers of malignancy. Treatment of neuroblastoma cell lines with S(+)-ibuprofen resulted in a significant growth suppression. This growth effect was accompanied by a marked decrease in the expression of MYC, MYCN, AKT and an increase in p53 expression in neuroblastoma cell lines without TP53 mutation. In addition, S(+)-ibuprofen enhanced the expression of some favorable neuroblastoma genes (EPHB6, CD44) and genes involved in growth suppression and differentiation (EGR1, EPHA2, NRG1 and SEL1L). Gene expression profile and Ingenuity pathway analyses using TP53-mutated SKNAS cells further revealed that S(+)-ibuprofen suppressed molecular pathways associated with cell growth and conversely enhanced those of cell cycle arrest and the unfolded protein response. Collectively, these results suggest that S(+)-ibuprofen or its related compounds may have the potential for therapeutic and/or palliative use for unfavorable neuroblastoma.

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Section: Discussionmentioning

confidence: 99%

S(+)-ibuprofen destabilizes MYC/MYCN and AKT, increases p53 expression, and induces unfolded protein response and favorable phenotype in neuroblastoma cell lines

Ikegaki

Hicks

Regan

et al. 2013

International Journal of Oncology

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“…Racemic ibuprofen and dexibuprofen showed a 30% and diclofenac a 90% higher incidence of adverse drug reactions. 2 Proton pump inhibitors and NSAIDs have been coadministered in an attempt to improve gastrointestinal safety. Prolongation of wound healing can be worrisome as well.…”

Section: Side Effects Of Traditional Nsaidsmentioning

confidence: 99%

Cyclooxygenase-2 Inhibitors in Gynecologic Practice

Connolly¹

2003

Clinical Medicine & Research

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Treatment of pain and inflammation associated with dysmenorrhea, endometriosis, ovarian cancers and operative procedures is an ongoing challenge in gynecology. Understanding the roles of prostanoids and estrogen in these conditions and appropriate treatment approaches have advanced beyond traditional nonsteroidal anti-inflammatory drugs. In this article, the author describes some of the basic mechanisms of nonspecific nonsteroidal anti-inflammatory drugs and newer cyclooxygenase-2 inhibitors, especially as they are used in the obstetrics/gynecology practice.

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“…The administration of enantiomerically pure preparations of the S(+)-enantiomer possesses advantages compared to the racemic drugs such as: reduced metabolic load, diminished probability of the pharmacokinetic interactions with other drugs, no interference with lipid metabolism, lower doses, neither inversion nor interaction with COX that typically causes variability in the pharmacokinetic (Evans, 2001). In fact, clinical trials with over 1463 patients (with osteoarthritis of the knee and hip, chronic inflammatory and degenerative rheumatic diseases and dysmenorrhea) and post-marketing surveillance of over 7133 outpatients performed by Gebro Pharma (Austria) proved the higher efficiency and gastrointestinal tolerability, and lower adverse side effects of the S(+)-ibuprofen versus racemic ibuprofen and diclofenac (Phleps, 2001).…”

Section: Introductionmentioning

confidence: 96%

Enzymatic kinetic resolution of racemic ibuprofen: past, present and future

José

Toledo

Briand

2015

Critical Reviews in Biotechnology

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This review is a journey concerning the investigations of the kinetic resolution of racemic ibuprofen for the last 20 years. The relevancy of the pharmacological uses of the S( + ) enantiomer along with its higher cost compared with racemic profen are the driving forces of a variety of scientific research studies addressing the enzymatic resolution of ibuprofen through enantiomeric esterification using lipases as biocatalysts. Lipases of fungal sources such as Candida rugosa, Rhizomucor miehei and the lipase B of Candida antarctica have been extensively studied both in homogeneous and heterogeneous (immobilized on solid supports) processes. In this context, the various alcohols and organic co-solvents frequently used in the esterification of racemic ibuprofen are summarized and discussed in this review. Moreover, recent investigations using membranes as reactors coupled with the separation of the desired product and microfluidic devices are presented. Finally, some guidelines about future perspectives regarding the technology of the kinetic resolution of profens and research niches are given.

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Overview on Clinical Data of Dexibuprofen

Cited by 34 publications

References 10 publications

S(+)-ibuprofen destabilizes MYC/MYCN and AKT, increases p53 expression, and induces unfolded protein response and favorable phenotype in neuroblastoma cell lines

S(+)-ibuprofen destabilizes MYC/MYCN and AKT, increases p53 expression, and induces unfolded protein response and favorable phenotype in neuroblastoma cell lines

Cyclooxygenase-2 Inhibitors in Gynecologic Practice

Enzymatic kinetic resolution of racemic ibuprofen: past, present and future

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