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(S)-(+)-Ibuprofen

(S)-(+)-Ibuprofen

Catalog No. BCC4042
Size Price Stock
100mg $50.00 In stock
200mg $80.00 In stock
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Quality Control of (S)-(+)-Ibuprofen

Chemical structure

(S)-(+)-Ibuprofen

Biological Activity of (S)-(+)-Ibuprofen

Non-steroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenase 1 and cyclooxygenase 2 (IC50 values are 12 and 80 μM respectively). Active isomer of ibuprofen.

(S)-(+)-Ibuprofen Dilution Calculator

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Chemical Properties of (S)-(+)-Ibuprofen

Cas No. 51146-56-6 SDF Download SDF
Chemical Name (S)-α-Methyl-4-(2-methylpropyl)benzeneacetic acid
SMILES CC(C)Cc1ccc(cc1)[C@H](C)C(O)=O
Standard InChIKey HEFNNWSXXWATRW-JTQLQIEISA-N
Standard InChI InChI=1S/C13H18O2/c1-9(2)8-11-4-6-12(7-5-11)10(3)13(14)15/h4-7,9-10H,8H2,1-3H3,(H,14,15)/t10-/m0/s1
Formula C13H18O2 M.Wt 206.28
Solubility Soluble to 100 mM in DMSO and to 100 mM in ethanol
Storage Store at RT
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.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of (S)-(+)-Ibuprofen

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.8478 mL 24.2389 mL 48.4778 mL 96.9556 mL 121.1945 mL
5 mM 0.9696 mL 4.8478 mL 9.6956 mL 19.3911 mL 24.2389 mL
10 mM 0.4848 mL 2.4239 mL 4.8478 mL 9.6956 mL 12.1194 mL
50 mM 0.097 mL 0.4848 mL 0.9696 mL 1.9391 mL 2.4239 mL
100 mM 0.0485 mL 0.2424 mL 0.4848 mL 0.9696 mL 1.2119 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.

Background on (S)-(+)-Ibuprofen

S(+)-Ibuprofen is capable of inhibiting cyclooxygenase (COX) at clinically relevant concentrations, R(-)-ibuprofen is not a COX inhibitor.

References on (S)-(+)-Ibuprofen

Impact of patent ductus arteriosus and subsequent therapy with ibuprofen on the release of S-100B and oxidative stress index in preterm infants.[Pubmed: 25542161]


Hemodynamically significant patent ductus arteriosus (hsPDA) leads to injury in tissues/organs by reducing perfusion of organs and causing oxidative stress. The purpose of this study was to evaluate the oxidant/antioxidant status in preterm infants with hsPDA by measuring the total antioxidant capacity and total oxidant status and to assess neuronal damage due to oxidant stress related to hsPDA.

Two Enzyme Cooperatively Catalyzed Tandem Polymerization for the Synthesis of Polyester Containing Chiral (R)- or (S)-Ibuprofen Pendants.[Pubmed: 25200738]


An interesting cooperation between Candida antarctica Lipase B (CAL-B) and alkaline protease from Bacillus subtilis (BSP) in the copolymerization of bulky ibuprofen-containing hydroxyacid methyl ester (HAEP) and ε-caprolactone (ε-CL) is observed. This cooperation improved the M¯n of the polymers from 3130 (CAL-B) to 9200 g mol-1 (CAL-B/BSP). Experimental results clearly indicate that CAL-B mainly catalyzes the ring-opening polymerization (ROP) of ε-CL under the initiation of HAEP to form the homopolymer of ε-CL, while BSP catalyzes the subsequent polycondensation of the ROP product to yield the copolymer with increased molecular weight. Furthermore, using suitable chemo-enzymatic methods, valuable polyesters with chiral (R)- or (S)-ibuprofen pendants can be tailor-made.

S(+)-ibuprofen destabilizes MYC/MYCN and AKT, increases p53 expression, and induces unfolded protein response and favorable phenotype in neuroblastoma cell lines.[Pubmed: 24173829]


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.

In vitro evaluation of S-(+)-ibuprofen as drug candidate for intra-articular drug delivery system.[Pubmed: 24168233]


Intra-articular drug delivery systems (DDSs) are envisaged as interesting alternative to locally release non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen to reduce pain in patients with osteoarthritis. The present study examines the efficacy of S-(+)-ibuprofen on cartilage degradation as drug candidate for DDS loading. Humeral cartilage and joint capsule explants were collected from healthy sheep shoulder joints and they were cultured in mono- or in co-culture for 13 days with LPS in combination with S-(+)-ibuprofen at 50 µM and 1 mM. S-(+)-ibuprofen (50 µM) blocked prostaglandins production in LPS-activated explants but did not reduce cartilage degradation. By contrast, 1 mM S-(+)-ibuprofen treatment of cartilage explants reduced nitric oxide synthesis by 51% (p = 0.0072), proteoglycans degradation by 35% (p = 0.0114) and expression of serum amyloid protein - the main protein induced upon LPS challenge - by 44% (p < 0.0001). On contrary, in presence of synovial membrane, the protective effects of S-(+)-ibuprofen on cartilage damages were significantly diminished. At 1mM, S-(+)-ibuprofen reduced the cell lysis during culture of cartilage and joint capsule either in mono- or in co-culture. This study performed on sheep explants shows that 1 mM S-(+)-ibuprofen inhibited cartilage degradation via a mechanism independent of cyclooxygenase inhibition. Reduction of prostaglandins synthesis at 50 µM in all treatment groups and reduction of cartilage degradation observed at 1 mM suggest that S-(+)-ibuprofen could be considered as a promising drug candidate for the loading of intra-articular DDS.

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(S)-(+)-Ibuprofen,51146-56-6,Neuroscience,COX, supplier, inhibitor,Antagonist,Blocker,Modulator,Agonist, activators, activates, potent, BioCrick

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