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Quality Level
Assay
97%
form
solid
SMILES string
NC(=S)NC(N)=S
InChI
1S/C2H5N3S2/c3-1(6)5-2(4)7/h(H5,3,4,5,6,7)
InChI key
JIRRNZWTWJGJCT-UHFFFAOYSA-N
General description
Paralytic agent.
Signal Word
Danger
Hazard Statements
Precautionary Statements
Hazard Classifications
Acute Tox. 1 Inhalation - Acute Tox. 2 Dermal - Acute Tox. 2 Oral
Storage Class Code
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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Neurotoxicology, 4(4), 57-68 (1983-01-01)
[14C] Dithiobiuret (DTB)-derived radioactivity is eliminated by adult male rats with an approximate plasma half-life of 8-10 hr. About 65-75% of an i.p. dose appears in the urine within 24 hr after treatment and about 2-4% appears in the feces
The Journal of pharmacology and experimental therapeutics, 275(3), 1453-1462 (1995-12-01)
Chronic administration of 2,4-dithiobiuret (DTB), causes delayed-onset neuromuscular weakness in rats. This effect results from inhibition of quantal release of acetylcholine (ACh) from motor nerve terminals. The effects of noncholinergic neurotransmission are unknown. The purpose of the present study was
Toxicology and applied pharmacology, 84(2), 220-231 (1986-06-30)
Effects of 2,4-dithiobiuret (DTB) treatment in rats on neuromuscular transmission and the disposition of cholinergic substances, acetylcholine (ACh) and choline (Ch), were examined in a combined electrophysiological/biochemical study using an in vitro extensor digitorum longus (EDL) muscle-peroneal nerve preparation. EDL
Acta neuropathologica, 78(1), 72-85 (1989-01-01)
2,4-Dithiobiuret was given i.p. to rats for 4 days at a daily dosage of 1 mg/kg and the development of the lesion associated with neuromuscular dysfunction studied in hindlimb lumbrical muscles. The first morphological indication of neurointoxication was the appearance
Neurotoxicology, 5(2), 25-35 (1984-01-01)
Chronic treatment of rats with dithiobiuret (DTB) produces a delayed onset muscle weakness and, as suggested by a preliminary study, a distal axonopathy. An inhibition of glycolysis resulting in an energy deficit has been suggested as a possible mechanism of
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