Chemical Property of Dexibuprofen
Chemical Property:
- Appearance/Colour:colourless, crystalline solid
- Vapor Pressure:0.000139mmHg at 25°C
- Melting Point:49-53 °C(lit.)
- Refractive Index:59 ° (C=2, EtOH)
- Boiling Point:319.6 °C at 760 mmHg
- PKA:4.41±0.10(Predicted)
- Flash Point:216.7 °C
- PSA：37.30000
- Density:1.029 g/cm3
- LogP:3.07320
- Storage Temp.:Store at RT
- Solubility.:45% (w/v) aq 2-hydroxypropyl-β-cyclodextrin: 1.5 mg/mL
- Water Solubility.:insoluble
- XLogP3:3.5
- Hydrogen Bond Donor Count:1
- Hydrogen Bond Acceptor Count:2
- Rotatable Bond Count:4
- Exact Mass:206.130679813
- Heavy Atom Count:15
- Complexity:203
- Purity/Quality:
-
99% *data from raw suppliers
(S)-(+)-Ibuprofen *data from reagent suppliers
Safty Information:
- Pictogram(s):
Xn
- Hazard Codes:Xn
- Statements:
63-22
- Safety Statements:
45-36/37
- MSDS Files:
-
SDS file from LookChem
Total 1 MSDS from other Authors
Useful:
- Canonical SMILES:CC(C)CC1=CC=C(C=C1)C(C)C(=O)O
- Isomeric SMILES:C[C@@H](C1=CC=C(C=C1)CC(C)C)C(=O)O
- Recent ClinicalTrials:Phase I Study to Evaluate the Safety of Dexibuprofen 200mg Under Fasting and Fed Conditions
- Recent EU Clinical Trials:Efficacy of Non-Steroidal Anti-Inflammatory (Ibuprofen) Chronotherapy in Healing After Mandibular Third Molar Surgical Extraction – A Randomized Clinical Trial
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Description
Dexibuprofen, the S-(+)-isomer of the widely used NSAID agent ibuprofen, was
launched in Austria for the treatment of rheumatoid arthritis. While the racemic
compound is commonly used clinically, the antiinflammatory activity is mediated via
the S-isomer by inhibition of prostaglandin synthesis. It has also been
demonstrated that the R-isomer is converted to the Santipode in vivo via a CoA
thioester intermediate. Since CoA plays a pivotal role in intermediary metabolism
and maintenance of the [acyl-CoA], generation of R-ibuprofen-CoA competitively
inhibits many CoA-dependent reactions, which consequently produces
perturbations of hepatocyte Intermediary metabolism and mitocondrial function.
Pure S-ibuprofen usage, therefore, is preferred allowing a reduction in dosage level
and an improved side effect profile. Ibuprofen is a non-steroidal anti-inflammatory drug with diverse biochemical actions, most notably inhibiting COX-1 and COX-2 (IC50s = 2.6 and 1.53, μM, respectively). It is commonly synthesized as a racemic mixture of (S)- and (R)-isomers. (S)-Ibuprofen is an enantiomer that more potently inhibits COX activity, thromboxane formation, and platelet aggregation than the (R)-form. (S)-Ibuprofen also inhibits activation of NF-κB more effectively than (R)-ibuprofen (IC50s = 62 and 122 μM, respectively). However, the enantiomers are equipotent in blocking superoxide formation, β-glucuronidase release, and LTB4 generation by stimulated neutrophils (IC50 values range from 0.14 to 0.58 μM). A majority of (R)-ibuprofen can be inverted to (S)-ibuprofen in humans after oral administration.
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Uses
A nonsteroidal anti-inflammatory drug (NSAID); activity resides primarily in the (S)-isomer Ibuprofen is a non-steroidal anti-inflammatory drug with diverse biochemical actions, most notably inhibiting COX-1 and COX-2 (IC50s = 2.6 and 1.53, μM, respectively). It is commonly synthesized as a racemic mixture of (S)- and (R)-isomers. (S)-Ibuprofen is an enantiomer that more potently inhibits COX activity, thromboxane formation, and platelet aggregation than the (R)-form. (S)-Ibuprofen also inhibits activation of NF-κB more effectively than (R)-ibuprofen (IC50s = 62 and 122 μM, respectively). However, the enantiomers are equipotent in blocking superoxide formation, β-glucuronidase release, and LTB4 generation by stimulated neutrophils (IC50 values range from 0.14 to 0.58 μM). A majority of (R)-ibuprofen can be inverted to (S)-ibuprofen in humans after oral administration.
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Clinical Use
NSAID and analgesic
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Drug interactions
Potentially hazardous interactions with other drugsACE inhibitors and angiotensin-II antagonists:
antagonism of hypotensive effect, increased risk of
nephrotoxicity and hyperkalaemia.Analgesics: avoid concomitant use of 2 or more
NSAIDs, including aspirin (increased side effects);
avoid with ketorolac (increased risk of side effects
and haemorrhage).Antibacterials: possibly increased risk of convulsions
with quinolones.Anticoagulants: effects of coumarins and
phenindione enhanced; possibly increased risk of
bleeding with heparins, dabigatran and edoxaban -
avoid long term use with edoxaban.Antidepressants: increased risk of bleeding with
SSRIs and venlaflaxine.Antidiabetic agents: effects of sulphonylureas
enhanced.Antiepileptics: possibly increased phenytoin
concentration.Antivirals: increased risk of haematological toxicity
with zidovudine; concentration possibly increased by
ritonavirCiclosporin: may potentiate nephrotoxicityCytotoxics: reduced excretion of methotrexate;
increased risk of bleeding with erlotinibDiuretics: increased risk of nephrotoxicity;
antagonism of diuretic effect; hyperkalaemia with
potassium-sparing diuretics.Lithium: excretion decreased.Pentoxifylline: increased risk of bleeding.Tacrolimus: increased risk of nephrotoxicity
