[9] Various animals, plants, insects, and bacteria have been found to convert myo-inositol to scyllo-inositol,[5] including Streptomyces griseus, where that conversion is part of the synthesis of streptomycin.

[13] In 2011 a genetically engineered strain of this organism was developed which interrupted that pathway and converted part of the myo-inositol in the medium to scyllo-inositol in 48 hours.

[16] Several derivatives of scyllo-inositol have been synthesized and studied in the laboratory, such as phosphates (variants of phytic acid)[9] and orthoformates with an adamantane structure.

[17] Scyllitol is widely distributed in nature in fish, insects, mammalian tissues and urine, certain bacteria, and plants[5][14] such as Calycanthus occidentalis.

[19][20] The concentration of scyllo-inositol in coconut milk (the fluid inside the fruit of Cocos nucifera) is 0.5 g/L, five times that of myo-inositol.

[22] However a concentration of scyllo-inositol 300% higher than normal was measured in a healthy volunteer, without a corresponding increase in myo-inositol; suggesting that metabolism of the two isomers are independently regulated.

[25] Scyllitol was found to inhibit in vitro the aggregation of α-synuclein into fibrils, a phenomenon implicated in Parkinson's disease.

[26] Previous intravenous administration of either myo- or scyllo-inositol was found to reduce the duration and intensity of chemically-induced seizures in rats.

[6] In the early 2000s it was reported that scyllo–inositol crossed blood-brain barrier and, when given to mice (TgCRND8) that were genetically engineered to exhibit Alzheimers-like symptoms, it inhibited cognitive deficits and significantly improved the disease pathology.

[29][30] More recently, it has also been found to inhibit the binding of Aβ oligomers to plasma membranes and interfering with synaptic function.

[31] Motivated by these and other results, in about 2008 Transition Therapeutics set to investigate scyllo-inositol as a disease-modifying therapy for Alzheimer's disease, under the designation AZD-103.

[32] A clinical investigation of ELND005 with approximately 353 patients, planned to take 18 months, was started in 2008 and received fast track designation from the U.S. Food and Drug Administration.

[7] The study initially used daily doses of 500, 2000, and 4000 mg; however, the last two were discontinued by December 2009, due to suspected adverse effects, including 9 deaths.

[33][34] A new 12-week fast-track trial with 296 moderate to advanced Alzheimer's was started in November 2012, to investigate the effect of a single dose of ELND005 on the NPI-C agitation and aggression scores.