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Sulbutiamine

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$14.99

SKU: TN-N-0011

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Sulbutiamine is a molecule made up of two B1 (Thiamin) molecules joined together by 2 sulfur atoms. It is also referred to as an isobutyryl thiamine disulfide, and its brand names are Youvitan, Bisbuthiamine, Arcalion or Ereon. Sulbutiamine is a semi-synthetic compound that is synthesized from Thiamine. Sulbutiamine is simply a nootropic vitamin that mimics Vitamin B1 since it is just an advanced modification of thiamine. In its development, the thiazole ring in Thiamine is opened and attached to a disulfide compound to form the sulbutiamine molecule. Sulbutiamine is lipophilic and therefore, it easily crosses blood brain barrier and dissolves across fatty tissues and cell membranes more rapidly compared to thiamine. It was specifically designed to act within the brain, although it has been noted not to have psychostimulant effects. In most cases, it is used as therapy for asthenia (neurological and myopathic weaknesses) and treatment of somatic and psychic inhibition.

The chemical formula is C32H46N8O6S2, and its estimated half-life is about 5 hours. Sulbutiamine has a high efficacy and, therefore, can be used alone or stacked with other nootropic agents. It is glutamatergic, cholinergic and dopaminergic. Sulbutiamine is thought to boost memory through potentiation of glutamatergic activity within the Prefrontal Cortex. Sulbutiamine is a dietary supplement that boosts the levels of Thiamine and Thiamine esters in the brain and, therefore, leads to better energy metabolism and nerve transmissions. Within the hippocampus, Sulbutiamine increases cholinergic activities and, therefore, boost both short and long term memory.

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HISTORY

Sulbutiamine was first synthesized in Japan to aid in treating Asthenia, Vitamin B1 deficiency (Beriberi) and to assist boost the lipophilicity of Vitamin B1 (Thiamine) and Thiamine Esters within the brain leading to higher efficiency in treatment compared to other forms of Vitamin B1. Records on Sulbutiamine can be traced back to 1973 although this date is not certain. The history of Sulbutiamine is closely associated with the study of thiamine in Japan. Due to the prevalence of beriberi in Japan until the twentieth century, researchers tried to synthesize thiamine whose deficiency resulted in beriberi. The synthesis of thiamine was done in 1936 following its initial isolation in 1926. The first lipophilic thiamine derivative was isolated from garlic in 1951.

Sulbutiamine was developed by reducing its compound polarity to assist it to move easily across the blood-brain barrier. When thiamine is converted into sulbutiamine, its passage into the brain is easier. Sulbutiamine is mostly used in clinical treatment of asthenia and other conditions linked to chronic fatigue. However, its popularity is mostly attributed to its use as a nootropic agent that acts as an energy supplement and cognitive enhancer. You can obtain Sulbutiamine as a dietary supplement within the U.S.. However, the FDA has indicated that it might be classified as a drug in the future.


CLINICAL STUDIES

A clinical trial was performed in patients with type II diabetes and diabetic neuropathy in which Sulbutiamine was administered at doses of 400mg every day for six weeks. When the scores on symptoms and signs (paraesthesia, constricting sensation, etc.) were evaluated, there was significant enhancement when contrasted with the baseline, on the other hand, no improvement was noted when compared to the placebo, therefore, no overall improvement. This study observed improvements in electro-physical measures like compound motor action potential and nerve conduction velocity.

A clinical trial aimed at evaluating the ability of Sulbutiamine to protect neuronal cells within the hippocampus from deprivation of both oxygen and glucose gave positive results. The study employed a staining protocol to spot cells that had died from oxygen or glucose deprivation. When Sulbutiamine was incubated at around 50uM, the 6.1 fold increase observed in the control group dropped to 4.1 fold increase. The interference of synaptic transmission observed in these conditions (nutrient deprivation) was conserved with the use of sulbutiamine to some extent.

In another model that used BALB/c mice aged between 14 to 16 weeks, Sulbutiamine was administered orally for 10 days at a dose of 300mg/kg with 5% gum acacia indicated improvements in memory when evaluated using the operant task. The results showed no disparities in the groups in acquisition although significant variations were observed in retention that leads to increased performance. In another case, a 9 week study showed that injections of 12.5mg/kg and 25mg/kg sulbutiamine on a daily basis did not affect performance in a DNMTS task using the operant conditioning maze and in some instances the 12.5mg/kg dosage was linked to increased levels of encoding errors. Administration of dizocilpine during the DNMTS task, Sulbutiamine was observed to reduce its amnesiac effects in the mice and preserve performance. Dizocilpine is an NMDA antagonist that stimulates amnesia. Sulbutiamine was noted to improve mice's object recognition memory when administered at doses of 12.5mg/kg and 25mg/kg for 9 weeks.

A human study was performed on chronic post-infectious fatigue in which sulbutiamine was administered at doses of 400mg or 600mg once every day for 28 days. The two doses showed significant drops in fatigue compared to the placebo. The two groups did not exhibit any significant variations between them although in some erratic instances the 600mg group performed better. Another quite similar study used a larger sample and was uncontrolled and unblended involving patients who had reported symptoms of fatigue. The patients were administered with 400mg of Sulbutiamine after breakfast on a daily basis for 15 days in combination with their anti-infective therapy. The researchers noted that 51.7% of the study subjects had complete resolution of self-report asthenic symptoms. In another study involving 60 patients who had been diagnosed with Multiple Sclerosis also noted a 91.37% improvement in fatigue, and 74.13% of the patients reporting substantial improvements. The study used subjective improvement to analyze the results and no exacerbation in fatigue were reported.

In a clinical study carried out in patients with diabetic polyneuropathy, the patients were allocated to Sulbutiamine or no treatment (control group) with each cluster being randomly assigned 15 patients. The Glycaemic control after Sulbutiamine therapy was evaluated by HbA1 and blood glucose. Symptoms and sign scores, and electrophysiological parameters like compound muscle action potential were used to assess the severity of neuropathy before the commencement of the study and after the 6 weeks of the study. The treatment group showed enhancements in electrophysiological parameters when contrasted with the control group with substantial improvements in peroneal compound muscle action potential, compound muscle action potential, median nerve conduction velocity, and peroneal nerve conduction velocity. The two groups did not exhibit any significant variance in symptom and sign scores although when contrasted with the baseline the sulbutiamine treated group had significant improvements. For glycaemic control, both groups registered insignificant differences at baseline and showed stability throughout the study. There was a substantial enhancement in peripheral nerve function in diabetic polyneuropathy, but the symptoms score showed no improvements (may be as a result of the short period of the study).

Another study was carried out in which the effects of sulbutiamine on hippocampal neurons were evaluated in an in vitro model of ischemia, OGD (oxygen glucose deprivation). The researchers observed that in the presence of sulbutiamine, exposure to OGD had significant increases in neuronal viability and boosted electrophysiological properties like intrinsic neuronal membrane input resistance and excitatory synaptic transmissions in a concentration-dependant manner. This study presented the neuroprotective evidence on the effects of Sulbutiamine on hippocampal CA1 pyramidal neurons under OGD, as such; there is a possibility of Sulbutiamine functioning as a therapeutic substance in the treatment of ischemic insult.

A study focusing on the effects of Sulbutiamine on psychogenic erectile dysfunction showed positive effects whereby it was observed to increase performance (assessments were carried out by International Index of Erectile Function and recorded improvement from 17.5 to 24.8 on average. Another study also showed that Sulbutiamine helped to correct erectile dysfunction in 16 patients out of the 20 who were enrolled in the 30-day long study. The study showed that sulbutiamine was an effective therapy for erectile dysfunction. Sulbutiamine has been observed to assist in treating different psycho-behavioral inhibitions like depression and shyness, and when combined with other nootropic substances like Aniracetam may be helpful in assisting those with conditions like depression and social anxiety. Despite being helpful in the treatment and rehabilitation of depression patients, it is not an antidepressant. A double-blind clinical trial showed that Sulbutiamine was a potential therapy in the early stages of Alzheimer's disease by potentiating both cholinergic and glutamatergic transmissions of the Hippocampus and Prefrontal Cortex when compared to donepezil and a placebo in a 3-month long study.

A rat modeled study was used to evaluate the effects of chronic treatments with sulbutiamine on memory using a spatial delayed-non-match-to-sample task in a radial maze and an additional two trial object recognition task. The rats were trained in the DNMTS task and then administered with Sulbutiamine or saline by injections of 12.5mg/kg or 25mg/kg every day for 9 weeks. The results showed that sulbutiamine had no effects on memory in the DNMTS task, but it improved memory in the object recognition task. Dizocilpine was observed to impair acquisition and retention in the DNMTS task in the group treated with saline. In the sulbutiamine treated group, Dizocilpine did not have effects indicating that Sulbutiamine can counter the amnesia stimulated by a blockade of the N-methyl-D-aspartate glutamate receptors. These results show that sulbutiamine has positive effects on working and episodic memory.

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