At 7 weeks, homozygous KO and KI mice on a standard diet had lower blood thiamine levels than WT mice (0.796±0.259 μM), at 0.058±0.051 and 0.126±0.092 μM, respectively. Days 5 and 14 saw a significant decrease in blood thiamine concentrations to 0.010 in WT and homozygous KO and KI mice fed a thiamine-restricted diet (thiamine: 0.60 mg/100 g of chow). 0.010±0.006 and ±0.009 μM. mice of WT (0.609±0.288 μM). In WT mice given a typical diet, the brain homogenates had a thiamine concentration of 3.81±2.18 nmol/g wet weight, while KO and KI brain homogenates had thiamine values of 1.33±0.96 and 2.16±1.55 nmol/g wet weight, respectively. Notably, following 5 days (0.95±0.72 nmol/g wet weight) and 14 days (1.11±0.24) of eating a thiamine-restricted diet (thiamine: 0.60 mg/100 g food), the KO and KI were reduced. In comparison to WT (3.65 ± 1.02 nmol/g wet weight), thiamine concentrations in mouse brain homogenates gradually drop before the mice exhibit illness symptoms [2].

On a typical diet containing 1.71 mg/100 g of thiamine, WT, homozygous and heterozygous KO, and KI mice survived for over six months without exhibiting any signs of disease. After being fed a diet restricted in thiamine (thiamine: 0.60 mg/100 g chow), homozygous KO and KI mice showed signs of paralysis, weight loss, and immobility, respectively. These mice died after 12 and 30 days, respectively. Likewise, within 14 and 18 days, respectively, homozygous KO and KI mice that were fed a diet restricted in thiamine and had a reduced thiamine percentage (thiamine: 0.27 mg/100 g of food) perished. Nevertheless, mice administered a thiamine-restricted diet (thiamine: 0.60 mg or 0.27 mg/100g of chow) in both WT and heterozygous KO and KI groups survived for over 6 months without exhibiting any signs of sickness [2].

Absorption, Distribution and Excretion
Thiamine is primarily absorbed in the jejunum. At low concentrations, it is absorbed via an active transport system involving phosphorylation; at high concentrations, it is absorbed via passive diffusion. Only a small amount of high-dose thiamine is absorbed, and elevated serum concentrations lead to active excretion of the vitamin in the urine. Thiamine is transported in the blood by red blood cells and plasma and excreted in the urine. Thiamine is absorbed in the small intestine and phosphorylated in the intestinal mucosa. Except in cases of malabsorption syndrome, B vitamins are readily absorbed from the gastrointestinal tract. Thiamine is primarily absorbed in the duodenum. For more complete data on the absorption, distribution, and excretion of vitamins B1 (8 in total), please visit the HSDB record page. Metabolism/Metabolites In vivo, it is converted to thiamine diphosphate, a coenzyme for the decarboxylation of α-keto acids.
The compounds 3-(2'-methyl-4'-amino-5'-pyrimidinylmethyl)-4-methylthiazole-5-acetic acid (i.e., thiamine acetic acid), 2-methyl-4-amino-5-carboxymethylpyrimidine, and 5-(2-hydroxyethyl)-4-methylthiazole have been identified as important metabolites of thiamine (vitamin B1).
The biotransformation of thiamine in mammals is generally thought to produce thiochrome, thiamine disulfide, 5-(2-hydroxyethyl)-4-methylthiazole, and several forms corresponding to thiamine pyrimidine residues.
Thiamine is metabolized in the liver of animals. Several urinary metabolites of thiamine have been identified in humans. After administration of physiological doses, little or no unchanged thiamine is excreted in the urine; however, after administration of larger doses, both unchanged thiamine and metabolites are excreted when tissue storage is saturated.
Biological half-life
The biological half-life of this vitamin is 9–18 days.
At higher pharmacological doses, such as repeated oral administration of 250 mg or intramuscular injection of 500 mg, it takes nearly one week to reach steady-state plasma concentrations; the average elimination half-life is estimated to be 1.8 days.
The total amount of thiamine in an adult is estimated to be approximately 30 mg, and the biological half-life of this vitamin is likely between 9 and 18 days.

Interactions
…High dietary levels of thiamine hydrochloride have been reported to inhibit the metabolism of zoxazosamide and aminopyrine in rats, but have not significantly altered the oxidative metabolism of hexobarbital. /Thiamine Hydrochloride/
In rats treated with PCBs, vitamin B1 levels in the blood, liver, and sciatic nerve were decreased, transketolase activity was reduced, and the pyrophosphate effect was enhanced. In rats treated with DDT, vitamin B1 levels in the blood, brain, and liver, as well as transketolase activity, were decreased, while the pyrophosphate effect was enhanced.
Although its clinical significance is unclear, thiamine has been reported to potentially enhance the effects of neuromuscular blocking agents.
…Alcohol inhibits the absorption of thiamine.
For more (complete) data on interactions of vitamin B1 (9 in total), please visit the HSDB records page.

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Non-human toxicity values
Rat subcutaneous injection LD50: 560 mg/kg
Rat intravenous injection LD50: 188 mg/kg
Mouse subcutaneous injection LD50: 301 mg/kg
Mouse intravenous injection LD50: 83 mg/kg

[1]. Thiamine Deficiency and Delirium. Innov Clin Neurosci. 2013 Apr; 10(4): 26-32.

[2]. High-dose thiamine prevents brain lesions and prolongs survival ofSlc19a3-deficient mice. PLoS One. 2017; 12(6): e0180279.

Thiamine (1+) chloride is a vitamin B1 and an organochlorine salt. It contains thiamine (1+). 3-((4-amino-2-methyl-5-pyrimidinyl)methyl)-5-(2-hydroxyethyl)-4-methylthiazole chloride. See also: Thiamine (note moved to). Mechanism of Action: Metabolic control analysis predicts that stimulators of transketolase synthesis, such as thiamine (vitamin B1), promote high levels of nucleoribose synthesis, which is crucial for tumor cell survival, chemotherapy resistance, and proliferation. Metabolic control analysis also predicts that transketolase inhibitors have the opposite effect on tumor cells. This could have important implications for nutrition and future treatment in cancer patients. Therapeutic Uses: Thiamine is used for the prevention and treatment of thiamine deficiency, including beriberi, Wernicke's encephalopathy syndrome, delirium, and peripheral neuritis associated with pellagra or pregnancy neuritis (with severe vomiting).
Although rigorous controlled trials have not yet confirmed any therapeutic value of thiamine, the drug has been used to treat anorexia, ulcerative colitis, chronic diarrhea, other gastrointestinal disorders, and cerebellar syndrome. Thiamine has also been used orally as an anthelmintic, but there is insufficient evidence to confirm its effectiveness for this purpose.
Low plasma thiamine concentrations have been found in patients with type 1 and type 2 diabetes. In a small placebo-controlled study, oral administration of 100 mg fenofibrate (a vitamin B1-related substance) four times daily significantly improved neuropathic pain in patients with diabetic polyneuropathy. This study evaluated the effects of thiamine supplementation on thiamine levels, functional capacity, and left ventricular ejection fraction (LVEF) in patients with moderate to severe congestive heart failure (CHF). These patients had previously received furosemide treatment for at least 3 months at a dose of 80 mg/day or higher. Patients and Methods: Thirty patients were randomly assigned to receive a 1-week double-blind inpatient treatment, receiving either intravenous thiamine 200 mg/day or placebo (n=15 per group). All prior medications were continued. After discharge, all 30 patients received outpatient oral thiamine 200 mg/day for 6 weeks. Thiamine status was measured by erythrocyte thiamine pyrophosphate effect (TPPE). Left ventricular ejection fraction (LVEF) was measured by echocardiography. Results: After intravenous placebo administration, there were no changes in TPPE, urine output, or LVEF. After intravenous thiamine administration, TPPE decreased (from 11.7% ± 6.5% to 5.4% ± 3.2%; P < 0.01). Left ventricular ejection fraction (LVEF) increased (from 0.28 ± 0.11 to 0.32 ± 0.09; P < 0.05), urine output also increased (from 1731 ± 800 mL/d to 2389 ± 752 mL/d; P < 0.02), and sodium excretion also increased (from 84 ± 52 mEq/d to 116 ± 83 mEq/d; P < 0.05). In the 27 patients who completed the full 7-week intervention, left ventricular ejection fraction (LVEF) increased by 22% (from 0.27 ± 0.10 to 0.33 ± 0.11, P < 0.01). Conclusion: Thiamine supplementation can improve left ventricular function and biochemical markers of thiamine deficiency in patients with moderate to severe congestive heart failure (CHF) receiving long-term furosemide therapy.
For more complete data on the therapeutic uses of vitamin B1 (11 types), please visit the HSDB record page.
Drug Warnings
Serious hypersensitivity/anaphylactic reactions may occur, especially after repeated administration.Intravenous or intramuscular administration of thiamine can be fatal.
Since 1938, there have been reports in the literature of systemic adverse reactions—anaphylactic shock—caused by thiamine (vitamin B1). Although the exact mechanism is not clear, the reaction appears to be an immediate hypersensitivity reaction and is only associated with parenteral administration…
Anaphylactic shock. Severe and even fatal reactions have been reported occasionally following parenteral administration of thiamine. The clinical features strongly suggest anaphylactic shock. Symptoms of thiamine-induced anaphylactic shock include anxiety, itching, dyspnea, nausea, abdominal pain, and shock, sometimes leading to death.
Although adverse reactions to thiamine are rare, hypersensitivity reactions still occur, primarily after parenteral administration. These reactions varied in severity, from very mild to fatal anaphylactic shock in rare cases… The UK Medicines and Healthcare products Safety Board (MHSB) received 90 reports of adverse reactions related to the use of high-dose vitamin B and C injections between 1970 and July 1988. The most common reactions were anaphylactic shock (41 cases, 2 of which resulted in death), dyspnea or bronchospasm (13 cases), and rash or flushing (22 cases); 78 of these reactions occurred during or shortly after intravenous administration, and the remaining 12 occurred after intramuscular administration. The MHSB recommended that parenteral administration be used only when necessary, and that facilities for treating anaphylactic shock be available if parenteral administration is used. The MHSB also recommended that if intravenous administration is used, it should be administered slowly (over 10 minutes). Several authors noted that parenteral administration is crucial for the prevention and treatment of Wernicke's encephalopathy. However, subsequent reports have indicated that injectable thiamine can cause anaphylactic reactions, one of which resulted in death. For more complete data on drug warnings for vitamin B1 (15 in total), please visit the HSDB records page.

C12H17CLN4OS

300.8076

300.081

59-43-8

Thiamine nitrate;532-43-4;Thiamine hydrochloride;67-03-8

6042

White to off-white solid powder

6 g/cm3

125 °C

1.99

2

6

4

19

269

0

MYVIATVLJGTBFV-UHFFFAOYSA-M

InChI=1S/C12H17N4OS.ClH/c1-8-11(3-4-17)18-7-16(8)6-10-5-14-9(2)15-12(10)13;/h5,7,17H,3-4,6H2,1-2H3,(H2,13,14,15);1H/q+1;/p-1

2-[3-[(4-amino-2-methylpyrimidin-5-yl)methyl]-4-methyl-1,3-thiazol-3-ium-5-yl]ethanol;chloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ≥ 100 mg/mL (~332.44 mM)
DMSO : ~1 mg/mL (~3.32 mM)

Solubility in Formulation 1: ≥ 100 mg/mL (332.44 mM) (saturation unknown) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)