Sodium cyanide appears as a white crystalline solid, lump solid or powder. A deadly human poison by ingestion. Toxic by skin absorption through open wounds, by ingestion, and by inhalation of dust.
颜色/状态：
White cubic crystals
气味：
Odorless when perfectly dry, emits odor of hydrogen cyanide when damp
沸点：
1496 °C
熔点：
563 °C
闪点：
Not combustible (EPA, 1998)
溶解度：
Solubility in water, g/l at 20 °C: 480-520 (freely soluble)
密度：
1.595 g/cu cm @ 20 °C
蒸汽压力：
1 mm Hg @ 817 °C; 10 mm Hg @ 983 °C
稳定性/保质期：
AQ SOLN ... RAPIDLY DECOMPOSES ON STANDING.
自燃温度：
Not flammable (USCG, 1999)
分解：
... If involved in a fire decomposes to produce hydrogen cyanide and oxides of nitrogen.
OPOSSUMS WERE DOSED WITH SODIUM CYANIDE BY ... STOMACH TUBE. ... ANALYSIS INDICATED THAT MAJOR ROUTE OF DETOXICATION ... WAS BY CONVERSION TO THIOCYANATE, WHICH WAS EXCRETED IN URINE. TRACES OF 2-IMINO-4-THIAZOLIDINE CARBOXYLIC ACID WERE OBSERVED IN CRUDE CONCENTRATED EXTRACT OF URINE.
... CYANIDE ION IS CONJUGATED WITH SULFUR TO FORM THIOCYANATE. ... CONJUGATION IS CATALYZED BY THE ENZYME RHODANESE WHICH IS WIDELY DISTRIBUTED IN MOST ANIMAL TISSUES EXCEPT BLOOD, LIVER BEING PARTICULARLY ACTIVE. ... THE RHODANESE MECHANISM IS CAPABLE OF DETOXICATING ONLY LIMITED AMT OF CYANIDE, SUCH AS ARE FORMED DURING NORMAL METAB. /ANOTHER SULFUR DONOR IS 3-MERCAPTOPYRUVATE. THE ENZYME, MERCAPTOSULFUR TRANSFERASE IS LOCALIZED IN CYTOSOL./ /CYANIDE/
Salmonella typhimurium strain (OASS positive) (OASS, O-acetylserine sulfhydrylase) synthesize a toxic but non-mutagenic metabolite from cyanide and O-acetylserine. Salmonella typhimurium mutant DW379 (OASS deficient) is neither able to carry out this reaction in vitro nor produce the toxic metabolite in vivo. L-Cysteine reverses the cyanide metabolite mediated inhibition and thus allows OASS positive strains to grow in medium containing cyanide and O-acetylserine. The results suggest that the enzyme O-acetylserine sulfhydrylase catalyzes the reaction of cyanide and O-acetylserine to form the toxic metabolite. This metabolite from ninhydrin-positive, adheres strongly to the cation-exchange column, and migrates in thin layer chromatography to an Rf value similar to that of beta-cyanoalanine.
/ONE OF/ THE MAJOR MECHANISMS FOR REMOVING CYANIDE FROM THE BODY IS ITS ENZYMATIC CONVERSION, BY THE MITOCHONDRIAL ENZYME RHODANESE (TRANSSULFURASE), TO THIOCYANATE, WHICH IS RELATIVELY ... /LESS TOXIC/. /CYANIDE/
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
IDENTIFICATION: Other cyanides, such as sodium and potassium cyanide, are solid or crystalline hygroscopic salts widely used in ore extracting processes for the recovery of gold and silver, electroplating, case-hardening of steel, base metal flotation, metal degreasing, dyeing, printing, and photography. They are also widely used in the synthesis of organic and inorganic chemicals (e.g., nitriles, carboxylic acids, amides, esters, and amines; heavy metal cyanides) and in the production of chelating agents. HUMAN EXPOSURE: Cyanides are well absorbed via the gastrointestinal tract or skin and rapidly absorbed via the respiratory tract. Once absorbed, cyanide is rapidly and ubiquitously distributed throughout the body, although the highest levels are typically found in the liver, lungs, blood, and brain. There is no accumulation of cyanide in the blood or tissues following chronic or repeated exposure. Approximately 80% of absorbed cyanide is metabolized to thiocyanate in the liver by the mitochondrial sulfur transferase enzyme rhodanese and other sulfur transferases. Thiocyanate is excreted in the urine. Minor pathways for cyanide detoxification involve reaction with cystine to produce aminothiazoline- and iminothiazolidinecarboxylic acids and combination with hydroxycobalamin (vitamin B12a) to form cyanocobalamin (vitamin B12); these end-products are also excreted in the urine. The principal features of the toxicity profile for cyanide are its high acute toxicity by all routes of administration, with a very steep and rate-dependent dose-effect curve, and chronic toxicity, probably mediated through the main metabolite and detoxification product, thiocyanate. The toxic effects of cyanide ion in humans and animals are generally similar and are believed to result from inactivation of cytochrome oxidase and inhibition of cellular respiration and consequent histotoxic anoxia. The primary targets of cyanide toxicity in humans are the cardiovascular, respiratory, and central nervous systems. The endocrine system is also a potential target for long-term toxicity, as a function of continued exposure to thiocyanate, which prevents the uptake of iodine in the thyroid and acts as a goitrogenic agent. Sequele after severe acute intoxications may include neuropsychiatric manifestations and Parkinson-type disease. Cyanide from tobacco smoke has been implicated as a contributing factor in tobacco-alcohol amblyopia. Long-term exposure to lower concentrations of cyanide in occupational settings can result in a variety of symptoms related to central nervous system effects. Cyanides are weakly irritating to the skin and eye; alkali salts have not been identified. ANIMAL/PLANT STUDIES: The principal features of the toxicity profile for cyanide are its high acute toxicity by all routes of administration, with a very steep and rate-dependent dose-effect curve, and chronic toxicity, probably mediated through the main metabolite and detoxification product, thiocyanate. The toxic effects of cyanide ion in humans and animals are generally similar and are believed to result from inactivation of cytochrome oxidase and inhibition of cellular respiration and consequent histotoxic anoxia. The primary targets of cyanide toxicity in animals are the cardiovascular, respiratory, and central nervous systems. The endocrine system is also a potential target for long-term toxicity, as a function of continued exposure to thiocyanate, which prevents the uptake of iodine in the thyroid and acts as a goitrogenic agent. In a 13-week repeated-dose toxicity study in which cyanide was administered in drinking-water, there were no clinical signs associated with central nervous system effects or histopathological effects in the brain or thyroid of rats or mice. There were slight changes in the reproductive tract in male rats, which, although they apparently would not affect fertility in rats. The examination of neurotoxicity in this study was limited to clinical observation and optical microscopy in autopsy. The few available studies specifically intended to investigate neurotoxicity, while reporting adverse effects at exposure levels of 1.2 mg cyanide/kg body weight per day in rats and 0.48 mg cyanide/kg body weight per day in goats, suffer from weaknesses that preclude their quantitative assessment. In relation to characterization of concentration-response for repeated-dose toxicity for inhalation (relevant principally to the occupational environment), in three separate studies in rats, there were no adverse systemic effects in rats exposed to acetone cyanohydrin, which is rapidly hydrolysed to hydrogen cyanide at physiological pH, at concentrations up to 211 mg/m3 (corresponding to a concentration of 67 mg hydrogen cyanide/m3). The steepness of the dose-effect curve is illustrated by the observation of 30% mortality among rats exposed part of the day to 225 mg acetone cyanohydrin/m3 (71 mg hydrogen cyanide/m3). Adverse effects of exposure to the low concentrations of cyanide that are generally present in the general environment (<1 ug/m3 in ambient air; <10 ug/litre in water) are unlikely. /Cyanide/
Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌物分类
对人类不具有致癌性（未被国际癌症研究机构IARC列名）。
No indication of carcinogenicity to humans (not listed by IARC).
Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
暴露途径
这种物质可以通过吸入、皮肤接触和摄入被身体吸收。
The substance can be absorbed into the body by inhalation, through the skin and by ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
IN 30 DAYS, 72% OF (14)C FROM AN IP DOSE OF (14)C-CYANIDE TO MICE WAS EXCRETED IN URINE AND FECES, 25% IN EXPIRED AIR AND 3% WAS RETAINED IN ANIMALS. PEAK EXCRETION OCCURRED WITHIN 10 MIN IN EXPIRED AIR AND WITHIN 6-24 HR IN URINE AND FECES. /CYANIDE/
CYANIDES ARE RAPIDLY ABSORBED FROM SKIN & ALL MUCOSAL SURFACES & ARE MOST DANGEROUS WHEN INHALED, BECAUSE TOXIC AMT ARE ABSORBED THROUGH BRONCHIAL MUCOSA & ALVEOLI. /CYANIDES/
THE CYANIDE ION IS READILY ABSORBED AFTER ORAL OR PARENTERAL ADMIN. PROLONGED LOCAL CONTACT WITH CYANIDE SOLN ... MAY RESULT IN ABSORPTION OF TOXIC AMT THROUGH SKIN. PART OF ABSORBED CYANIDE IS EXCRETED UNCHANGED BY THE LUNG. LARGER PORTION ... IS CONVERTED BY SULFURTRANSFERASE RELATIVELY NONTOXIC TO THIOCYANATE ION. /CYANIDE/
As estimated in rats given 30 mg sodium cyanide intraperitoneally over a period of 8 days, 80 percent of the total cyanide is excreted in the urine in the form of thiocyanate.
Compositions for Treatment of Cystic Fibrosis and Other Chronic Diseases
申请人：Vertex Pharmaceuticals Incorporated
公开号：US20150231142A1
公开（公告）日：2015-08-20
The present invention relates to pharmaceutical compositions comprising an inhibitor of epithelial sodium channel activity in combination with at least one ABC Transporter modulator compound of Formula A, Formula B, Formula C, or Formula D. The invention also relates to pharmaceutical formulations thereof, and to methods of using such compositions in the treatment of CFTR mediated diseases, particularly cystic fibrosis using the pharmaceutical combination compositions.
[EN] CRBN LIGANDS AND USES THEREOF<br/>[FR] LIGANDS CRBN ET LEURS UTILISATIONS
申请人：KYMERA THERAPEUTICS INC
公开号：WO2019140387A1
公开（公告）日：2019-07-18
The present invention provides compounds, compositions thereof, and methods of using the same for the inhibition of CRBN, and the treatment of CRBN-mediated disorders.
本发明提供了化合物、其组合物以及使用这些化合物抑制CRBN并治疗CRBN介导的疾病的方法。
Studies on transition-metal cyano-complexes. Part 3. Heptacyano-complexes of tungsten, molybdenum, and vanadium, and a hydrido-heptacyano-complex of tungsten
作者：Ana-Maria Soares、William P. Griffith
DOI：10.1039/dt9810001886
日期：——
The new complexes K5[W(CN)7]·H2O and K4[WH(CN)7]·2H2O are reported, and have been characterised by 1H, 13C n.m.r., and vibrational spectra. Vibrational and e.s.r. data are also presented for the new salt NaK3[Mo(CN)7]·2H2O and earlier data are extended for K4[Mo(CN)7]·2H2O and K4[V(CN)7]·2H2O.
[EN] ROR-GAMMA INHIBITORS<br/>[FR] INHIBITEURS DE ROR-GAMMA
申请人：GLAXOSMITHKLINE IP DEV LTD
公开号：WO2019063748A1
公开（公告）日：2019-04-04
The present invention relates to compounds of formula I and pharmaceutical compositions comprising compounds of formula I. Compounds of Formula I are useful in treatment of inflammatory, metabolic or autoimmune diseases which are mediated by RORy.
