Pyrithiamine (hydrobromide) |
Katalog-Nr.GC44790 |
Pyrithiamine (hydrobromide) is a thiamine analogue that inhibits the metabolism of thiamine (vitamin B1).
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Cas No.: 534-64-5
Sample solution is provided at 25 µL, 10mM.
Pyrithiamine (hydrobromide) is a thiamine analogue that inhibits the metabolism of thiamine (vitamin B1)[1]. Pyrithiamine (hydrobromide) has high affinity to thiamine transporters in neurons, with a Kd of approximately 60 nM[2]. Pyrithiamine (hydrobromide) is also a substrate of thiamine pyrophosphate kinase (TPK) and can be converted into pyrithiamine pyrophosphate (PPP)[3]. Pyrithiamine (hydrobromide) can be used in microbial culture to inhibit the growth of microorganisms that require thiamine[4].
In vitro, Pyrithiamine (hydrobromide) (10μM) treated the HeLa cell line for 4 days, significantly reducing cellular nucleotide levels, and intracellular dATP, dCTP, dGTP and dTTP were all reduced[5]. Pyrithiamine (hydrobromide) (0.25mM) treated Neuro 2a cells, resulting in a strong reduction in intracellular ThDP levels, and the cells began to die after 48 hours [6].
In vivo, Pyrithiamine (hydrobromide) (250 or 500 μg/kg/day) treated mice by intraperitoneal injection for 4 weeks, causing thiamine deficiency, leading to cognitive dysfunction and neuropathological changes in wild-type mice, but it had no effect on existing mice. There is no corresponding effect on AD model mice with obvious cognitive impairment [7]. Pyrithiamine (hydrobromide) (0.5g/kg) was administered intraperitoneally to rats for 11 days, causing thiamine deficiency, leading to enlargement of the lateral ventricles and reduced levels of choline-containing compounds in the body [8].
References:
[1] Chauhan A, Srivastva N, Bubber P. Thiamine deficiency induced dietary disparity promotes oxidative stress and neurodegeneration[J]. Indian Journal of Clinical Biochemistry, 2018, 33: 422-428.
[2] Mulholland P J, Self R L, Stepanyan T D, et al. Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro[J]. Neuroscience, 2005, 135(4): 1129-1139.
[3] Liu J Y, Timm D E, Hurley T D. Pyrithiamine as a substrate for thiamine pyrophosphokinase[J]. Journal of biological chemistry, 2006, 281(10): 6601-6607.
[4]Brandenburger E, Gressler M, Leonhardt R, et al. A highly conserved basidiomycete peptide synthetase produces a trimeric hydroxamate siderophore[J]. Applied and Environmental Microbiology, 2017, 83(21): e01478-17.
[5]Tiwana G S, Prevo R, Buffa F M, et al. Identification of vitamin B1 metabolism as a tumor-specific radiosensitizing pathway using a high-throughput colony formation screen[J]. Oncotarget, 2015, 6(8): 5978.
[6]Sambon M, Napp A, Demelenne A, et al. Thiamine and benfotiamine protect neuroblastoma cells against paraquat and β-amyloid toxicity by a coenzyme-independent mechanism[J]. Heliyon, 2019, 5(5).
[7]Zhao J, Sun X, Yu Z, et al. Exposure to pyrithiamine increases β-amyloid accumulation, Tau hyperphosphorylation, and glycogen synthase kinase-3 activity in the brain[J]. Neurotoxicity research, 2011, 19: 575-583.
[8]Zahr N M, Sullivan E V, Rohlfing T, et al. Concomitants of alcoholism: differential effects of thiamine deficiency, liver damage, and food deprivation on the rat brain in vivo[J]. Psychopharmacology, 2016, 233: 2675-2686.
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