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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
Certificates of Analysis (COA)
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Dithiobiuret-induced muscle weakness in rats: evidence for a prejunctional effect.
Neurotoxicology, 3(1), 44-54 (1982-07-01)
Toxicology and applied pharmacology, 91(2), 212-221 (1987-11-01)
To evaluate the hypothesis that depressed neuromuscular transmission causes dithiobiuret (DTB)-induced muscle weakness in rats, the temporal development of impaired treadmill performance and deficits in the nerve-elicited muscle contractions were compared during daily treatment with the toxicant (DTB, 1 mg/kg/day
Fundamental and applied toxicology : official journal of the Society of Toxicology, 16(3), 469-481 (1991-04-01)
2,4-Dithiobiuret (DTB) exposure causes a delayed onset muscle weakness in rats that has been attributed to depressed neuromuscular transmission. The present study compares the effects of DTB on both sensory and motor function in rats. Adult male Long-Evans hooded rats
Experimental neurology, 85(1), 63-68 (1984-07-01)
Urinary excretion of porphyrin precursors delta-aminolevulinic acid (ALA) and porphobilinogen (PBG) and total porphyrins was measured during intoxication of rats with 2,4-dithiobiuret (DTB), a chemical which produces delayed-onset neuromuscular weakness, in an attempt to ascertain whether or not DTB poisoning
Acta neuropathologica, 81(2), 141-147 (1990-01-01)
It has been well established that 2,4-dithiobiuret (DTB) intoxication in rats produces a rapidly progressive hindlimb paralysis within days. The cause of this has, until recently, been explained on the basis of a physiological abnormality that involves a prejunctional impairment
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