Last Updated: September 28, 2022

Sulbutiamine is a synthetic molecule which consists of two Thiamine (Vitamin B1) molecules bound together by a sulfur group, and appears to be somewhat useful in alleviating fatigue; especially that associated with infection.

Sulbutiamine is most often used for.

Don't miss out on the latest research


Sources and Composition

Sulbutiamine is a molecule which is two Thiamine (B1) molecules bound together, similar to how Pyritinol is two Pyridoxine (B6) molecules bound together. Sulbutiamine is known as isobutyryl thiamine disulfide and sometimes referred to by its Brand Names of Ereon or Arcalion; it is most commonly used for Asthenia, or weakness (part neurological and part myopathic) as well as treatment of somatic and psychic inhibition.[1] It is said to not possess psychostimulant properties, although it is designed to act centrally (in the brain).[1]



Sulbutiamine is synthesized from Thiamine, where after opening of the thiazole ring of Thiamine and dimerisation to a disulfide compound it is then esterified.[2]


Neurology and the Brain


Kinetics and Distribution

Due to the lipophilicity (fat-solubility) of Sulbutiamine, transport into the brain from systemic circulation is greater relative to Thiamine. After an injection of Sulbutiamine (16mg/kg) and Thiamine (15.4mg/kg) were both able to acutely increase plasma thiamine levels without influencing serum Thiamine Diphosphate (demonstrating the efficacy of Sulbutiamine as a vitamin delivery form, able to biotransform into Thiamine in vivo).[3] A chronic study of injecting sulbutiamine (52mg/kg) and thiamine (50mg/kg) daily for 2 weeks in rats noted that despite these similar doses that sulbutiamine was able to increase total circulating thiamine, Thiamine diphosphate, and Thiamine Monophosphate levels 2.41 times higher than that of Thiamin itself.[3] In other measured organs (hippocampus, medulla, cerebellum, cortex, and kidney) levels of Thiamine Triphophate were only increased with sulbutiamine, and sulbutiamine increased total thiamine compounds higher than Thiamine in all organs except the hippocampus.[3]



Sulbutiamine may protect neuronal cells (in the hippocampus) from oxygen/glucose deprivation according to one study.[4] This study used a staining protocol to identify dead cells from glucose/oxygen deprivation, and the 6.1-fold increase seen in control was attenuated to a 4.1-fold increase when Sulbutiamine was incubated at 50uM. The disruption of synaptic transmission that occurs under these conditions of nutrient deprivation[5] was preserved with sulbutiamine to a degree, measuring preservation at 25.1+/-2.21%, 47.3+/-3.11% and 66.3+/-11.0% for the concentrations of 1, 10, and 50uM when control was standardized to 100% and the group without Sulbutiamine recorded 12.8+/-9.8%.[4]



A 6 week trial in humans with type II diabetes and diabetic neuropathy using Sulbutiamine at 400mg daily noted that on the signs and symptoms scores (constricting sensation, paraesthesia, pain and weakness for symptoms; etc.) there was an improvement when compared against baseline but no improvement against placebo (and thus it was deemed no overall improvement).[6] Improvement was noted in electrophysical measures, including nerve conduction velocity and compound motor action potential.[6]


Glutaminergic Signalling

Positive glutaminergic and dopaminergic transmission has been noted in anterior corticol regions, specifically the prefrontal and cingular cortices which organize decisions and strategies.[1] Daily injections of 12.5mg/kg sulbutiamine for 2 weeks prior to sacrifice noted decreases in kainate receptors in tested areas as well as decreased dopamine levels, despite no changes in dopamine receptor content.[1]

No variations in dopaminergic or glutaminergic receptors were noted in the nuclear accumbens,[1] and in a model of glucose/oxygen deprivation, Sulbutiamine at 1, 5, and 50uM failed to modify excitability of neurons in the hippocampus.[4]


Cholinergic Signalling

In an animal model where Sulbutiamine was fed at 300mg/kg for 10 days, the rate of sodium-dependent choline uptake into the hippocampus appeared to be increased approximately 10.1% when compared to gum acacia control.[7]



In a model of BALB/c mice 14-16 weeks of age, 10 days of 300mg/kg sulbutiamine by oral gavage with 5% gum acacia appeared to improve memory (assessed by operant task); this study noted that there were no differences between groups in acquisition but there were significant differences in retention which resulted in increased performance.[7]

Injections of 12.5 and 25mg/kg Sulbutiamine daily for 9 weeks failed to modify performance in a DNMTS task (operant conditioning maze) and at times 12.5mg sulbutiamine was associated with a greater amount of encoding errors.[8] When dizocilpine (NMDA antagonist that induces amnesia) was administered during the DNMTS task, sulbutiamine was able to negate the amnesiac effects of it on the mice and preserve performance.[8]

Sulbutiamine has been implicated in increasing object-recognition memory in mice at both 12.5 and 25mg/kg injections over 9 weeks.[8]



One study has been conducted on chronic postinfectious fatigue (CPIF) with sulbutiamine at either 400 or 600mg daily for 28 days noted that both groups had significantly less fatigue than placebo, but that for the most part there was no significant difference between groups with the 600mg group inconsistently performing better at times.[9] A similar study using a large (uncontrolled, unblinded) sample of persons seeing their doctors about infection who reported at least one symptom of fatigue given 400mg Sulbutiamine at breakfast daily for 15 days alongside their anti-infective treatment noted complete resolution of self-reported asthenic symptoms in 51.7% of the study population.[10]

Improvement has also been noted regarding fatigue in 91.37% of persons tested (n=60) with Multiple Sclerosis, with 74.13% of the sample reporting the improvement as 'substantial' (analysis was done via subjective improvement) with no reported exacerbation in fatigue state.[11]


Addiction and Withdrawal

A case study currently exists where a patient with bipolar disorder became addicted to sulbutiamine.[12] The subject was using high dose antipsychotics (olanzapine and haloperidol at 20mg, the benzodiazepines diazepam and temazepam at 40mg and 10mg, 10mg biperiden, unspecified doses of lithium and carbamazepine) and reported that his large doses (above 600mg but otherwise unspecified) made him feel stronger and warmer.[12]

One study in primate using a large dose of sulbutiamine (300mg/kg daily for 10 days) noted that Sulbutiamine was able to influence the circadian rhythm (increasing wakefulness and reducing phase 2 sleep while increasing phase 1 and not affecting REM). These effects persisted after 2-5 days of cessasion of sulbutiamine treatment.[13]


Interactions with Glucose Metabolism

An intervention over 6 weeks in type II diabetics using 400mg sulbutiamine failed to find a decrease in blood glucose or HbA1c associated with treatment.[6]


Interactions with Organ Systems



Due to the interactions of prooxidation and excitotoxicity in glaucoma as well as Thaimine being lower in glaucoma patients[14] with a case study showing Thiamine injections increase visual acuity,[15] Sulbutiamine has been investigated for its interactions with retinal cells.[16] An in vitro study using RGC-5 (Ganglion-like) cells noted that Sulbutiamine was able to attenuate cell death when cells were deprived of serum, and 10uM Sulbutiamine was as effective as 10uM Trolox (anti-oxidant standard) while attenuation was seen significantly at 1uM; these protective effects were associated with a sequestering the increase in superoxide and peroxide radicals, with no influence on hydroxyl radicals, and a relative increase in glutathione.[16]


Interactions with Sexuality

At least one study has noted benefits to psychogenic erectile dysfunction that can be treated with Sulbutiamine, increasing performance as assessed by the International Index of Erectile Function (IIEF) from 17.5 to 24.8 on average.[17]

1.^Trovero F, Gobbi M, Weil-Fuggaza J, Besson MJ, Brochet D, Pirot SEvidence for a modulatory effect of sulbutiamine on glutamatergic and dopaminergic cortical transmissions in the rat brainNeurosci Lett.(2000 Sep 29)
3.^Bettendorff L, Weekers L, Wins P, Schoffeniels EInjection of sulbutiamine induces an increase in thiamine triphosphate in rat tissuesBiochem Pharmacol.(1990 Dec 1)
6.^Kiew KK, Wan Mohamad WB, Ridzuan A, Mafauzy MEffects of sulbutiamine on diabetic polyneuropathy: an open randomised controlled study in type 2 diabeticsMalays J Med Sci.(2002 Jan)
7.^Micheau J, Durkin TP, Destrade C, Rolland Y, Jaffard RChronic administration of sulbutiamine improves long term memory formation in mice: possible cholinergic mediationPharmacol Biochem Behav.(1985 Aug)
13.^Balzamo E, Vuillon-Cacciuttolo GFacilitation of a state of wakefulness by semi-chronic treatment with sulbutiamin (Arcalion) in Macaca mulattaRev Electroencephalogr Neurophysiol Clin.(1982 Dec)
15.^Sedel F, Challe G, Mayer JM, Boutron A, Fontaine B, Saudubray JM, Brivet MThiamine responsive pyruvate dehydrogenase deficiency in an adult with peripheral neuropathy and optic neuropathyJ Neurol Neurosurg Psychiatry.(2008 Jul)
16.^Kang KD, Majid AS, Kim KA, Kang K, Ahn HR, Nho CW, Jung SHSulbutiamine counteracts trophic factor deprivation induced apoptotic cell death in transformed retinal ganglion cellsNeurochem Res.(2010 Nov)