6-Methyl-2-propyl-4-pyrimidinyl N,N-dimethylcarbamate｜Huagongshe

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HCID 17325Erstellt: 27. Oktober 2026

6-Methyl-2-propyl-4-pyrimidinyl N,N-dimethylcarbamate

Pyramat · G-23330 · ENT-19059 · Geigy G-23330 · N,N-Dimethylcarbamic acid 6-methyl-2-propylpyrimidin-4-yl ester · Carbamic acid, N,N-dimethyl-, 6-methyl-2-propyl-4-pyrimidinyl ester

https://huagongshe.com/de/chemical/17325

Molekülstruktur von 6-Methyl-2-propyl-4-pyrimidinyl N,N-dimethylcarbamate

Identifikatoren & physikalische Daten

CAS No.	2532-49-2
Summenformel	C11H17N3O2
Durchschnittliche Molmasse	223,27 g/mol
Monoisotopische Masse	223,13207678 g/mol
SMILES	CCCc1nc(C)cc(OC(=O)N(C)C)n1
InChIKey	CQRUIYKYVFQBRT-UHFFFAOYSA-N
PubChem CID	17325
DTXSID	DTXSID2041549

Chemische & physikalische Eigenschaften

XLogP	1,9
Polarare Oberfläche (TPSA)	55,3
H-Brücken-Donoren	0
H-Brücken-Akzeptoren	4
Frei drehbare Bindungen	4
Schwere Atome	16
Formalladung	0
Komplexität	233
Siedepunkt	364.56°C (rough estimate)
Dichte	1.1269 (rough estimate)
Brechungsindex	1.4930 (estimate)
pKa (Säurekonstante)	2.34±0.30(Predicted)
EPA chemische Informationen	6-Methyl-2-propyl-4-pyrimidinyl dimethylcarbamate (2532-49-2)

Sicherheit & Vorschriften

Treatment	If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.
Gesundheitliche Auswirkungen	Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).
Expositionspfade	Inhalation (L793)oral (L793)dermal (L793)
Toxizitätsübersicht	6-Methyl-2-propyl-4-pyrimidinyl dimethylcarbamate is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.

Signs and Symptoms

As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)