(R)-Flurbiprofen

(R)-Flurbiprofen is a COX-inactive enantiomer of the racemic non-selective COX inhibitor flurbiprofen (Item No. 70250) that has diverse biological activities.^1,2,3,4 It inhibits γ-secretase activity in vitro and, in vivo, it reduces formation of amyloid-β peptide 1-42 (Aβ42) and improves axonal transport in young Aβ-plaque free mice but not old mice with existing Aβ plaques in the Tg2576 transgenic model of Alzheimer's disease.^1,4 (R)-Flurbiprofen inhibits NF-kB activation and DNA binding as well as AP-1 DNA binding in RAW 264.7 macrophages and reduces paw edema in a rat model of zymosan-induced inflammation via COX-independent inhibition of NF-κB and AP-1 activation when administered at doses of 1, 3, and 9 mg/kg.² It also suppresses prostate tumor cell growth in vitro by inducing p75^NTR protein expression and reduces tumor growth and metastasis in multiple mouse models of intestinal neoplasia.^3,2

WARNING This product is not for human or veterinary use.

1. Kukar, T.L., Ladd, T.B., Bann, M.A., et al. Substrate-targeting g -secretase modulators. Nature 453, 925-929 (2008).

2. Tegeder, I., Niederberger, E., Israr, E., et al. Inhibition of NF-kB and AP-1 activation by R- and S-flurbiprofen1,2. The FASEB Journal 15, 595-597 (2001).

3. Quann, E.J., Khwaja, F., Zavitz, K.H., et al. The aryl propionic acid R-flurbiprofen selectively induces p75NTR-dependent decreased survival of prostate tumor cells. Cancer Res. 67(7), 3254-3262 (2007).

4. Smith, K.D., Paylor, R., and Pautler, R.G. R-flurbiprofen improves axonal transport in the Tg2576 mouse model of Alzheimer’s disease as determined by MEMRI. Magn. Reson. Med. 65(5), 1423-1429 (2011).