1. Bromide, Cyanogen
1. 506-68-3
2. Bromine Cyanide
3. Cyanobromide
4. Bromocyanide
5. Bromocyanogen
6. Bromocyan
7. Campilit
8. Carbononitridic Bromide
9. Cyanogen Monobromide
10. Bromure De Cyanogen
11. Cyanogen Bromide (brcn)
12. Bromocyane
13. Cyanic Bromide
14. Cyanogen Bromide ((cn)br)
15. Rcra Waste Number U246
16. Tl 822
17. Brcn
18. Nsc 89684
19. Os382ohj8p
20. Bromoformonitrile
21. Nsc-89684
22. Cyanogenbromide
23. Bromine Monocyanide
24. Bromure De Cyanogen [french]
25. Hsdb 708
26. Einecs 208-051-2
27. Mfcd00011597
28. Un1889
29. Rcra Waste No. U246
30. Unii-os382ohj8p
31. Brn 1697296
32. Bromcyane
33. Bromo Cyane
34. Ai3-28715
35. Cyanic Bromide #
36. Cnbr
37. Bromocyanide(brcn)
38. Bromocyanide (brcn)
39. Br-cn
40. Bromine Cyanide(brcn)
41. (cn)br
42. Bromine Cyanide (brcn)
43. Dsstox_cid_1550
44. Wln: E Cn
45. Dsstox_gsid_21550
46. 4-03-00-00092 (beilstein Handbook Reference)
47. Cyanogen Bromide [mi]
48. Cyanogen Bromide [hsdb]
49. Chembl3561885
50. Dtxsid9021550
51. Nsc89684
52. Tox21_303779
53. Tl-822
54. Cyanogen Bromide, >=98.5% (rt)
55. Akos009152676
56. Cyanogen Bromide, Reagent Grade, 97%
57. Un 1889
58. Cyanogen Bromide [un1889] [poison]
59. Ncgc00356964-01
60. Bp-10442
61. Cas-506-68-3
62. Ft-0665252
63. Cyanogen Bromide Solution, 5 M In Acetonitrile
64. Cyanogen Bromide, 99.995% Trace Metals Basis
65. Cyanogen Bromide Solution, 5.0 M In Acetonitrile
66. Q420258
67. J-520130
68. J-802176
69. Cyanogen Bromide Solution, 3.0 M In Methylene Chloride
| Molecular Weight | 105.92 g/mol |
|---|---|
| Molecular Formula | CBrN |
| XLogP3 | 1.1 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Exact Mass | 104.92141 g/mol |
| Monoisotopic Mass | 104.92141 g/mol |
| Topological Polar Surface Area | 23.8 Ų |
| Heavy Atom Count | 3 |
| Formal Charge | 0 |
| Complexity | 31.3 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
0.4 mg/L (92 ppm) in air is fatal after 10 min. /From table/
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 1399
Cyanide is distributed to all organs and tissues via the blood, where its concn in red cells is greater than that in plasma by a factor of two or three. Presumably, the accumulation of cyanide in erythrocytes is a reflection of its binding to methemoglobin. /Cyanide/
USEPA; Ambient Water Quality Criteria Doc: Cyanides p.C-9 (1980) EPA 440/5-80-037
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 to relatively nontoxic thiocyanate ion. /Cyanide/
Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 904
Once absorbed into the body, cyanide can form complexes with heavy metal ions. /Cyanide/
NIOSH; Criteria Document: Hydrogen Cyanide and Cyanide Salts p.45 (1976) DHEW Pub. NIOSH 77-108
Presumably, the accumulation of cyanide in erythrocytes is a reflection of its binding to methemoglobin. /Cyanide/
USEPA; Ambient Water Quality Criteria Doc: Cyanides p.C-9 (1980) EPA 440/5-80-037
The small quantity of cyanide always present in human tissues is metabolized at the approximate rate of 17 ug/kg x min, primarily by the hepatic enzyme rhodanese, which catalyzes the irreversible reaction of cyanide and a sulfane to produce thiocyanate, a relatively nontoxic compound excreted in the urine. ... The limiting factor under normal conditions is the availability of a sulfane as a substrate for rhodanese, and sulfur is administered therapeutically as sodium thiosulfate to accelerate this reaction. The lethal dose of cyanide is time dependent because of the ability of the body to detoxify small amounts of cyanide via the rhodanese-catalyzed reaction with sulfane. A given amount of cyanide absorbed slowly may cause no biological effects even though the same amount administered over a very short period of time may be lethal. /Hydrogen cyanide and cyanogen chloride/
U.S. Army Research Institute of Chemical Defense, Chemical Casualty Care Division; Medical Management of Chemical Casualties Handbook, 3rd Ed. Aberdeen Proving Ground, MD (July 2000) Available from, as of August 28, 2013: https://www.operationalmedicine.org/TextbookFiles/mmccthirdeditionjul2000.pdf
... 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/
Parke, D. V. The Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 96
/One of/ the major mechanism/s/ for removing cyanide from the body is its enzymatic conversion, by the mitochondrial enzyme rhodanese (transsulfurase), to thiocyanate, which is relatively ... /less toxic/. /Cyanide/
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1688
Half-life for the conversion of cyanide to thiocyanate from a non-lethal dose in man is between 20 min and 1 hr. /Cyanide/
Feldstein M, Klendshoj NC; J Lab Chin Med 44: 166-70 (1954) as cited in NIOSH; Criteria Document: Hydrogen Cyanide and Cyanide Salts p.45 (1976) DHEW Pub. NIOSH 77-108
Cyanide has a very high affinity for iron in the ferric state. When absorbed /cyanide/ ... reacts readily with trivalent iron of cytochrome oxidase in mitochondria; cellular respiration is thus inhibited & cytotoxic hypoxia results. Since utilization of oxygen is blocked, venous blood is oxygenated and is almost as bright red as arterial blood. Respiration is stimulated because chemoreceptive cells respond as they do to decreased oxygen. A transient stage of CNS stimulation with hyperpnea and headache is observed; finally there are hypoxic convulsions and death due to respiratory arrest. /Cyanide/
Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1688
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