Hepatic to 2-amino-3-acetylamino-6-(para-fluorobenzylamino) pyridine (which has 20-30% the analgesic potential of its parent compound), para-fluorohippuric acid[3] and a mercapturic acid metabolite, presumably formed from a glutathione adduct[4]
Flupirtine is an aminopyridine that functions as a centrally acting non-opioidanalgesic that was originally used as an analgesic for acute and chronic pain[5] but in 2013 due to issues with liver toxicity, the European Medicines Agency restricted its use to acute pain, for no more than two weeks, and only for people who cannot use other painkillers.[6] In March 2018, marketing authorisations for flupirtine were withdrawn following a European Medicines Agency recommendation based on the finding that the restrictions introduced in 2013 had not been sufficiently followed in clinical practice, and cases of serious liver injury still occurred including liver failure.[7]
It first became available in Europe in 1984 under the brand name Katadolon and after it went off patent many generic brands were introduced.[9]
Uses
Flupirtine is used as an analgesic for acute pain, in moderate-to-severe cases.[5][10] Its muscle relaxant properties make it popular for back pain and other orthopaedic uses, but it is also used for migraines, in oncology, postoperative care, and gynaecology.
In 2013 due to issues with liver toxicity, the European Medicines Agency restricted its use to acute pain, for no more than two weeks, and only for people who cannot use other painkillers.[6]
Side effects
The most serious side effect is frequent hepatotoxicity which prompted regulatory agencies to issue several warnings and restrictions.[11][12]
Although some studies have reported flupirtine has no addictive properties,[15][16] there was suggestion that it may possess some abuse potential and liability.[17] There were at least two registered cases of flupirtine abuse.[18]Drug tolerance does not develop in most cases, but has individually occurred.[18]
Flupirtine was discovered and developed between the 1970s and the 1990s by Chemiewerk Homburg in Frankfurt am Main, Germany, which became Degussa Pharma Group and then through mergers, ASTA Pharma and Asta Medica.[8]Retigabine, in which the pyridine group in flupirtine is replaced with a phenyl group, was discovered as part of the same program and has a similar mechanism of action.[8]
It was approved for the treatment of pain in 1984 in Europe[19] under the brand name Katadolon.[20]
As of 2013 it was used in 11 member countries: Bulgaria, Estonia, Germany, Hungary, Italy, Latvia, Lithuania, Poland, Portugal, Romania and Slovak Republic.[19] Many generics entered the European market around 2011.[21]
It was never introduced to the United States market for any indication but in 2008, Adeona Pharmaceuticals, Inc. (now called Synthetic Biologics, Inc.) obtained an option to license issued and patent pending applications relating to flupirtine's use in the treatment of ophthalmic indications, particularly retinitis pigmentosa.[22]
In 2010 retigabine was approved by the FDA as an anticonvulsant for the treatment of refractory partial-onset seizures in treatment-experienced patients.[23]
As of 2016 it is marketed under many brand names, including Efiret, Flupigil, Flupirtin, Flupirtina, Flupirtine, Flupizen, Fluproxy, Katadolon, Metanor, Trancolong, and Zentiva.[9]
Flupirtine underwent a clinical trial as a treatment for multiple sclerosis[27] and fibromyalgia.[28] Flupirtine showed promise for fibromyalgia due to its different action than the three approved by U.S. FDA drugs: pregabalin, milnacipran, and duloxetine.[29] Additionally, there are case reports regarding flupirtine as a treatment for fibromyalgia.[30] Adeona Pharmaceuticals (now called Synthetic Biologics) sub-licensed its patents for using flupirtine for fibromyalgia to Meda AB in May 2010.[29]
^Narang PK, Tourville JF, Chatterji DC, Gallelli JF (January 1984). "Quantitation of flupirtine and its active acetylated metabolite by reversed-phase high-performance liquid chromatography using fluorometric detection". Journal of Chromatography. 305 (1): 135–143. doi:10.1016/S0378-4347(00)83321-6. PMID6707137.
^Methling K, Reszka P, Lalk M, Vrana O, Scheuch E, Siegmund W, et al. (March 2009). "Investigation of the in vitro metabolism of the analgesic flupirtine". Drug Metabolism and Disposition. 37 (3): 479–493. doi:10.1124/dmd.108.024364. PMID19074524. S2CID5661841.
^Preston KL, Funderburk FR, Liebson IA, Bigelow GE (March 1991). "Evaluation of the abuse potential of the novel analgesic flupirtine maleate". Drug and Alcohol Dependence. 27 (2): 101–113. doi:10.1016/0376-8716(91)90027-v. PMID2055157.
^Sofia RD, Diamantis W, Gordon R (1987). "Abuse potential and physical dependence liability studies with flupirtine maleate in laboratory animals". Postgraduate Medical Journal. 63 (Suppl 3): 35–40. PMID3447127.
^Gahr M, Freudenmann RW, Connemann BJ, Hiemke C, Schönfeldt-Lecuona C (December 2013). "Abuse liability of flupirtine revisited: implications of spontaneous reports of adverse drug reactions". Journal of Clinical Pharmacology. 53 (12): 1328–1333. doi:10.1002/jcph.164. PMID24037995. S2CID35299692.
^ abStoessel C, Heberlein A, Hillemacher T, Bleich S, Kornhuber J (August 2010). "Positive reinforcing effects of flupirtine--two case reports". Progress in Neuro-Psychopharmacology & Biological Psychiatry. 34 (6): 1120–1121. doi:10.1016/j.pnpbp.2010.03.031. PMID20362025. S2CID19710997.
^Klawe C, Maschke M (June 2009). "Flupirtine: pharmacology and clinical applications of a nonopioid analgesic and potentially neuroprotective compound". Expert Opinion on Pharmacotherapy. 10 (9): 1495–1500. doi:10.1517/14656560902988528. PMID19505216. S2CID11597721.
^Dhar S, Bitting RL, Rylova SN, Jansen PJ, Lockhart E, Koeberl DD, et al. (April 2002). "Flupirtine blocks apoptosis in batten patient lymphoblasts and in human postmitotic CLN3- and CLN2-deficient neurons". Annals of Neurology. 51 (4): 448–466. doi:10.1002/ana.10143. PMID11921051. S2CID23653281.