Potassium cyanide is a compound with the formula KCN. It is a colorless salt, similar in appearance to sugar, that is highly soluble in water. Most KCN is used in gold mining, organic synthesis, and electroplating. Smaller applications include jewellery for chemical gilding and buffing. Potassium cyanide is highly toxic, and a dose of 200 to 300 milligrams will kill nearly any human.
The moist solid emits small amounts of hydrogen cyanide due to hydrolysis (reaction with water). Hydrogen cyanide is often described as having an odor resembling that of bitter almonds.
The taste of potassium cyanide has been described as acrid and bitter, with a burning sensation similar to lye. |
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InChI=1S/CN.K/c1-2;/q-1;+1 |
NNFCIKHAZHQZJG-UHFFFAOYSA-N |
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EC 1.9.3.1 (cytochrome c oxidase) inhibitor
An EC 1.9.3.* (oxidoreductase acting on donor heme group, oxygen as acceptor) inhibitor that interferes with the action of cytochrome c oxidase (EC 1.9.3.1).
EC 1.15.1.1 (superoxide dismutase) inhibitor
An EC 1.15.* (oxidoreductase acting on superoxide as acceptor) inhibitor that interferes with the action of superoxide dismutase (EC 1.15.1.1).
neurotoxin
A poison that interferes with the functions of the nervous system.
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View more via ChEBI Ontology
cyanide of potassium
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NIST Chemistry WebBook
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Kaliumcyanid
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ChEBI
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Kaliumzyanid
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ChEBI
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KCN
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IUPAC
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Zyankali
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ChEBI
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151-50-8
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CAS Registry Number
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ChemIDplus
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151-50-8
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CAS Registry Number
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NIST Chemistry WebBook
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3593645
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Beilstein Registry Number
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Beilstein
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4652394
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Beilstein Registry Number
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ChemIDplus
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647425
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Gmelin Registry Number
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Gmelin
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Batista LA, Haibara AS, Schenberg LC, Moreira FA (2017) Effects of alprazolam and cannabinoid-related compounds in an animal model of panic attack. Behavioural brain research 317, 508-514 [PubMed:27737792] [show Abstract] Selective stimulation of carotid chemoreceptors by intravenous infusion of low doses of potassium cyanide (KCN) produces short-lasting escape responses that have been proposed as a model of panic attack. In turn, preclinical studies suggest that facilitation of the endocannabinoid system attenuate panic-like responses. Here, we compared the effects of cannabinoid-related compounds to those of alprazolam, a clinically effective panicolytic, on the duration of the escape reaction induced by intravenous infusion of KCN (80μg) in rats. Alprazolam (1, 2, 4mg/kg) decreased escape duration at doses that did not alter basal locomotor activity. URB597 (0.1, 0.3, 1mg/kg; inhibitor of anandamide hydrolysis), WIN55,212-2 (0.1, 0.3, 1mg/kg; synthetic cannabinoid), arachidonoyl-serotonin (1, 2.5, 5mg/kg; dual TRPV1 and anandamide hydrolysis inhibitor), and cannabidiol (5, 10, 20, 40mg/kg; a phytocannabinoid) did not decrease escape duration. Alprazolam also prevented the increase in arterial pressure evoked by KCN, while bradycardia was unchanged. This study reinforces the validity of the KCN-evoked escape as a model of panic attack. However, it does not support a role for the endocannabinoid system in this behavioral response. These results might have implications for the screening of novel treatments for panic disorder. | Hawk MA, Ritchie GD, Henderson KA, Knostman KA, Roche BM, Ma ZJ, Matthews CM, Sabourin CL, Wakayama EJ, Sabourin PJ (2016) Neurobehavioral and Cardiovascular Effects of Potassium Cyanide Administered Orally to Mice. International journal of toxicology 35, 604-615 [PubMed:27170681] [show Abstract] The Food and Drug Administration Animal Rule requires evaluation of cardiovascular and central nervous system (CNS) effects of new therapeutics. To characterize an adult and juvenile mouse model, neurobehavioral and cardiovascular effects and pathology of a single sublethal but toxic, 8 mg/kg, oral dose of potassium cyanide (KCN) for up to 41 days postdosing were investigated. This study describes the short- and long-term sensory, motor, cognitive, and behavioral changes associated with oral dosing of a sublethal but toxic dose of KCN utilizing functional observation battery and Tier II CNS testing in adult and juvenile mice of both sexes. Selected tissues (histopathology) were evaluated for changes associated with KCN exposure with special attention to brain regions. Telemetry (adult mice only) was used to evaluate cardiovascular and temperature changes. Neurobehavioral capacity, sensorimotor responsivity or spontaneous locomotor activity, and rectal temperature were significantly reduced in adult and juvenile mice at 30 minutes post-8 mg/kg KCN dose. Immediate effects of cyanide included bradycardia, adverse electrocardiogram arrhythmic events, hypotension, and hypothermia with recovery by approximately 1 hour for blood pressure and heart rate effects and by 2 hours for body temperature. Lesions consistent with hypoxia, such as mild acute tubular necrosis in the kidneys corticomedullary junction, were the only histopathological findings and occurred at a very low incidence. The mouse KCN intoxication model indicates rapid and completely reversible effects in adult and juvenile mice following a single oral 8 mg/kg dose. Neurobehavioral and cardiovascular measurements can be used in this animal model as a trigger for treatment. | Sabourin PJ, Kobs CL, Gibbs ST, Hong P, Matthews CM, Patton KM, Sabourin CL, Wakayama EJ (2016) Characterization of a Mouse Model of Oral Potassium Cyanide Intoxication. International journal of toxicology 35, 584-603 [PubMed:27170682] [show Abstract] Potassium cyanide (KCN) is an inhibitor of cytochrome C oxidase causing rapid death due to hypoxia. A well-characterized model of oral KCN intoxication is needed to test new therapeutics under the Food and Drug Administration Animal Rule. Clinical signs, plasma pH and lactate concentrations, biomarkers, histopathology, and cyanide and thiocyanate toxicokinetics were used to characterize the pathology of KCN intoxication in adult and juvenile mice. The acute oral LD50s were determined to be 11.8, 11.0, 10.9, and 9.9 mg/kg in water for adult male, adult female, juvenile male, and juvenile female mice, respectively. The time to death was rapid and dose dependent; juvenile mice had a shorter mean time to death. Juvenile mice displayed a more rapid onset and higher incidence of seizures. The time to observance of respiratory signs and prostration was rapid, but mice surviving beyond 2 hours generally recovered fully within 8 hours. At doses up to the LD50, there were no gross necropsy or microscopic findings clearly attributed to administration of KCN in juvenile or adult CD-1 mice from 24 hours to 28 days post-KCN challenge. Toxicokinetic analysis indicated rapid uptake, metabolism, and clearance of plasma cyanide. Potassium cyanide caused a rapid, dose-related decrease in blood pH and increase in serum lactate concentration. An increase in fatty acid-binding protein 3 was observed at 11.5 mg/kg KCN in adult but not in juvenile mice. These studies provide a characterization of KCN intoxication in adult and juvenile mice that can be used to screen or conduct preclinical efficacy studies of potential countermeasures. | Fang D, Qing Y, Yan S, Chen D, Yan SS (2016) Development and Dynamic Regulation of Mitochondrial Network in Human Midbrain Dopaminergic Neurons Differentiated from iPSCs. Stem cell reports 7, 678-692 [PubMed:27666790] [show Abstract] Mitochondria are critical to neurogenesis, but the mechanisms of mitochondria in neurogenesis have not been well explored. We fully characterized mitochondrial alterations and function in relation to the development of human induced pluripotent stem cell (hiPSC)-derived dopaminergic (DA) neurons. Following directed differentiation of hiPSCs to DA neurons, mitochondria in these neurons exhibit pronounced changes during differentiation, including mature neurophysiology characterization and functional synaptic network formation. Inhibition of mitochondrial respiratory chains via application of complex IV inhibitor KCN (potassium cyanide) or complex I inhibitor rotenone restricted neurogenesis of DA neurons. These results demonstrated the direct importance of mitochondrial development and bioenergetics in DA neuronal differentiation. Our study also provides a neurophysiologic model of mitochondrial involvement in neurogenesis, which will enhance our understanding of the role of mitochondrial dysfunctions in neurodegenerative diseases. | Kumano T, Takizawa Y, Shimizu S, Kobayashi M (2016) Nitrile-synthesizing enzyme: Gene cloning, overexpression and application for the production of useful compounds. The Journal of general and applied microbiology 62, 174-180 [PubMed:27250664] [show Abstract] One of the nitrile-synthesizing enzymes, β-cyano-L-alanine synthase, catalyzes β-cyano-L-alanine (β-CNAla) from potassium cyanide and O-acetyl-L-serine or L-cysteine. We have identified this enzyme from Pseudomonas ovalis No. 111. In this study, we cloned the β-CNAla synthase gene and expressed it in Escherichia coli and Rhodococcus rhodochrous. Furthermore, we carried out co-expression of β-CNAla synthase with nitrilase or nitrile hydratases in order to synthesize aspartic acid and asparagine from KCN and O-acetyl-L-serine. This strategy can be used for the synthesis of labeled amino acids by using a carbon-labeled KCN as a substrate, resulting in an application for positron emission tomography. | Lee JH, Jang JH, Velusamy N, Jung HS, Bhuniya S, Kim JS (2015) An intramolecular crossed-benzoin reaction based KCN fluorescent probe in aqueous and biological environments. Chemical communications (Cambridge, England) 51, 7709-7712 [PubMed:25850896] [show Abstract] A turn-on fluorescent probe was designed for selective cyanide anion sensing in aqueous and biological environments. The probe underwent an intramolecular crossed-benzoin reaction in the presence of KCN to expel the fluorophore resorufin. This probe was sensitive to KCN concentrations as low as 4 nM in aqueous media. | Yamagiwa T, Inokuchi S, Saito T, Inoue S, Morita S, Kawaguchi AT (2013) A stable in vitro method for assessing the toxicity of potassium cyanide and its antidote. The Tokai journal of experimental and clinical medicine 38, 114-122 [PubMed:24318282] [show Abstract]
BackgroundHydrogen cyanide possesses a high acid-dissociation constant of 9.14, favoring its vaporization and depletion from the culture media at physiological pH, which may cause the cyanide toxicity unstable in vitro.ObjectiveWe investigated whether adjustment of culture medium pH stabilizes cyanide concentration and decreases the effective concentration of potassium cyanide (KCN).MethodsMurine fibroblast cells were exposed to different concentrations of KCN in media maintained at pH 7.4 or 9.2, in the presence or absence of hydroxocobalamin. After incubation for 1 h, we evaluated medium pH, cyanide concentration, cytochrome activity, and cell viability.ResultsCyanide concentration decreased to 18.8% in pH 7.4 medium compared to 83.2% in pH 9.2 medium. A significant decrease in cytochrome activity was observed at 40 mM and 1.25 mM KCN in pH 7.4 and pH 9.2 media, respectively. In pH 9.2 medium, dose-dependent cytotoxicity of KCN and antidotal effects of hydroxocobalamin were observed.ConclusionAdjustment of culture medium pH to 9.2 could stabilize cyanide concentration and decrease the effective concentration of KCN, allowing stable evaluation of KCN toxicity and antidotal efficacy. | Dairam A, Chetty P, Daya S (2006) Non-steroidal anti-inflammatory agents, tolmetin and sulindac, attenuate oxidative stress in rat brain homogenate and reduce quinolinic acid-induced neurodegeneration in rat hippocampal neurons. Metabolic brain disease 21, 221-233 [PubMed:16850258] [show Abstract] Alzheimer's disease (AD) is the most common form of neurodegenerative disease in the elderly. Anti-inflammatory agents have been shown to be beneficial in preventing neurodegenerative disorders such as AD. In this study we investigated the possible antioxidant and neuroprotective properties of two non-steroidal anti-inflammatory drugs (NSAIDS), tolmetin and sulindac, using quinolinic acid (QA)-induced neurotoxicity as a model. We used the thiobarbituric acid assay to measure the extent of lipid peroxidation and the nitroblue tetrazolium assay to measure the superoxide anion generated in rat brain homogenate. QA (1 mM) induced lipid peroxidation in rat brain homogenate was significantly curtailed by co-treatment of the homogenate with tolmetin and/or sulindac. Tolmetin and sulindac both reduced the generation of superoxide anions by the known neurotoxin, potassium cyanide (KCN). Intrahippocampal injections of QA induced neurotoxicity in rat hippocampus. N-Methyl-D-Aspartate (NMDA) receptor counts were conducted do give an indication of the amount protection offered by the NSAIDS. QA drastically reduced the number of NMDA binding sites by approximately 37%. This sharp decrease was considerably attenuated by the pre-treatment of the rats with tolmetin and sulindac (5 mg/kg/bd for five days). This study shows the antioxidant and neuroprotective properties of tolmetin and sulindac and hereby postulates that these drugs have important implications in the prevention or treatment of neurodegenerative diseases such as AD. |
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