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Repurposing of flibanserin, a recently approved treatment for hypoactive sexual desire disorder, may benefit patients with inherited retinal degenerations.

Research conducted at the Casey Eye Institute, Oregon Health & Science University, located in Portland, Oregon, has indicated that a recently approved treatment for hypoactive sexual desire disorder (HSDD) may additionally provide a neuro-protective effect on retinal tissues and function. Research on the FDA approved compound, flibanserin, a dual serotonin agonist and antagonist, showed a dose-dependent response in animal models following light-induced apoptosis. While the number of animals was small and the degeneration examined was artificially induced, the findings nevertheless support further investigation of the potential protection in retinal tissues.


Researchers injected normal rodents intraperitoneally with either increasing doses of flibanserin, ranging from 0.75 to 15 mg/kg, or with a sham control. Additionally, some animals received an antagonist prior to flibanserin administration in order to elucidate the pathways involved in the neuro-protective effect of the novel drug. Injections were given either immediately prior to light exposure or over the course of five days and then retinal structure and function were assessed using SD-OCT and ERG, respectively. Analysis of the results showed that with the five-day treatment regimen flibanserin significantly preserved outer retinal structure and function in a dose-dependent manner while even a one-day pre-treatment appeared to provide significant protection. Animals that received an inhibitor of the drug, or gene knock-out models that did not have the flibnaserin receptor, showed no protective effect. In addition, a genetic analysis highlighted the altered transcriptome of treated animals indicating how the drug may be having its effect.


The neurotransmitter targeted by the drug is the serotonin receptor (5-hydroxytryptamine or 5-HT), modulation of which has previously been shown to alter retinal processing. In humans, flibnaserin, marketed as Addyi (Sprout Pharmaceuticals), has undergone at least seven phase III clinical trials showing that a daily 100 mg dose was safe and resulted in an improvement of HSDD-related symptoms in pre-menopausal women. In HSDD, flibnaserin is thought to mediate its effect through modulation of serotonin, dopamine and norepinephrine levels in brain regions involved in “activating dopaminergic reward and sexual cue integration”. However, insufficient data on animal tissues will need to be performed to confirm similar effects in animal models. Based on the results achieved so far in their animal studies, the Oregon research team hypothesise that if the number of injections prior to light damage were increased, then the concentration of flibanserin would also increase, perhaps further enhancing the neuro-protective effects. In concluding their study the researchers commented that, “[t]he potential to repurpose flibanserin for retinal neuroprotection is exciting. However, much work remains to transition it into a viable treatment for inherited retinal dystrophies, such as evaluation of its neuroprotective effects in an animal model of inherited retinal degeneration. Other avenues of delivery, such as intraocular injection, could also be explored to reduce possible systemic side effects.”