P60205
2-Pyridinealdoxime methiodide
99%
Synonym(s):
2-PAM, 2-PAM iodide, Pralidoxime iodide
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About This Item
Empirical Formula (Hill Notation):
C7H11IN2O
CAS Number:
Molecular Weight:
266.08
NACRES:
NA.22
PubChem Substance ID:
UNSPSC Code:
12352100
EC Number:
202-349-6
MDL number:
Related Categories
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
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Lorise C Gahring et al.
American journal of physiology. Lung cellular and molecular physiology, 319(4), L683-L692 (2020-07-30)
Nicotine of unprecedented concentrations and purity is being inhaled by those using commercially available electronic nicotine delivery systems (ENDS). The consequences of this route of self-administration on the immunological response to inhaled allergens are not known. In mice, sensitization and
Kevin G McGarry et al.
Toxicological sciences : an official journal of the Society of Toxicology, 174(1), 124-132 (2019-12-28)
Organophosphorus (OP) compounds, which include insecticides and chemical warfare nerve agents (CWNAs) such as sarin (GB) and VX, continue to be a global threat to both civilian and military populations. It is widely accepted that cholinesterase inhibition is the primary
Kazuhito Nomura et al.
Scientific reports, 10(1), 15834-15834 (2020-09-29)
Whether central apnoea or hypopnoea can be induced by organophosphorus poisoning remains unknown to date. By using the acute brainstem slice method and multi-electrode array system, we established a paraoxon (a typical acetylcholinesterase inhibitor) poisoning model to investigate the time-dependent
Jay Spampanato et al.
Epilepsia, 60(7), 1387-1398 (2019-05-28)
Exposure to organophosphates (OPs) and OP nerve agents (NAs) causes status epilepticus (SE) and irreversible brain damage. Rapid control of seizure activity is important to minimize neuronal injury and the resulting neurological and behavioral disorders; however, early treatment will not
Kimberly D Spradling et al.
Journal of neuroinflammation, 8, 84-84 (2011-07-23)
Although the acute toxicity of organophosphorus nerve agents is known to result from acetylcholinesterase inhibition, the molecular mechanisms involved in the development of neuropathology following nerve agent-induced seizure are not well understood. To help determine these pathways, we previously used
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