(R)-(-)-Ibuprofen

Research use only, not for human use.

An enantiomer of Ibuprofen that is generally not considered a COX inhibitor and is instead thought to be involved in pathways of lipid metabolism as it is incorporated into triglycerides along with fatty acids.

An enantiomer of Ibuprofen that is generally not considered a COX inhibitor and is instead thought to be involved in pathways of lipid metabolism as it is incorporated into triglycerides along with fatty acids; inhibits NF-κB activation (IC50=121.8 uM) in response to T-cell stimulation as well as block superoxide formation, β-glucuronidase release, and LTB4 generation by stimulated neutrophils (IC50 =40-100 uM).Pain Approved.

(R)-(-)-Ibuprofen is the R enantiomer of Ibuprofen, with no inhibitory effect on COX, but is involved in pathways of lipid metabolism and is incorporated into triglycerides along with endogenous fatty acids. (R)-(-)-Ibuprofen (1 μM) significantly reduces NF-κB activation and completely prevents NF-κB induction at 10 μM. (R)-(-)-Ibuprofen inhibits NF-κB luciferase activity with an IC50 of 121.8 μM, weaker than that of S(+)-ibuprofen (IC50, 61.7 μM). Furthermore, (R)-(-)-Ibuprofen (10 mM) has no effect on HSF.

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R)-Ibuprofen

Apoptosis

NF-κB

NF-κB

Neurological Disease

Pain

51146-57-7

206.2808

C13H18O2

>98% (HPLC)

10 mM in DMSO

O=C(O)[C@H](C)C1=CC=C(CC(C)C)C=C1

Benzeneacetic acid, α-methyl-4-(2-methylpropyl)-,(αR)-

(-20℃)

With Ice Pack

≥ 2 years