X
Please Wait
Applying Filters...
1. Methylformamide
2. Monomethylformamide
3. Nsc 3051
1. 123-39-7
2. Methylformamide
3. Formamide, N-methyl-
4. Monomethylformamide
5. N-formylmethylamine
6. N-methyl-formamide
7. Nsc 3051
8. N-monomethylformamide
9. Ek 7011
10. Hconhch3
11. X 188
12. Formamide, Methyl-
13. Methylimidoformic Acid
14. N-methyl-formimidic Acid
15. Nmf
16. (e)-methylimidoformic Acid
17. (z)-methylimidoformic Acid
18. Chebi:7438
19. Xpe4g7y986
20. Nsc3051
21. N-methyl-formic Acid-amide
22. Nsc-3051
23. N-methylformamide, 99%
24. Methanimidic Acid, Methyl-
25. N-methyl Formamide
26. Formic Acid Amide, N-methyl-
27. Hsdb 100
28. Einecs 204-624-6
29. Brn 1098352
30. Unii-xpe4g7y986
31. Ai3-26076
32. N-methylcarboxamide
33. N-methylmethanamide
34. Methyl-methanimidic Acid
35. N-methylformamide-[18o]
36. N-methyl Formic Acid Amide
37. Wln: Vhm1
38. Ec 204-624-6
39. Chembl9240
40. Formamide, N-methyl- ( )
41. 4-04-00-00170 (beilstein Handbook Reference)
42. N-methylformamide [mi]
43. Dtxsid0025608
44. N-methylformamide [hsdb]
45. Zinc8214610
46. Bbl027430
47. Mfcd00003280
48. Stl146549
49. Akos000118787
50. Sb85388
51. Nci60_002574
52. Db-046834
53. F0059
54. Ft-0638572
55. Ft-0652807
56. A805066
57. Q138742
58. J-004934
59. F0001-0365
| Molecular Weight | 59.07 g/mol |
|---|---|
| Molecular Formula | C2H5NO |
| XLogP3 | -1 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Exact Mass | 59.037113783 g/mol |
| Monoisotopic Mass | 59.037113783 g/mol |
| Topological Polar Surface Area | 29.1 Ų |
| Heavy Atom Count | 4 |
| Formal Charge | 0 |
| Complexity | 20 |
| 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 |
NMF is an investigational anticancer drug... .
Snyder, R. (ed.). Ethel Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 175
Antineoplastic Agents
Substances that inhibit or prevent the proliferation of NEOPLASMS. (See all compounds classified as Antineoplastic Agents.)
Radiation-Sensitizing Agents
Drugs used to potentiate the effectiveness of radiation therapy in destroying unwanted cells. (See all compounds classified as Radiation-Sensitizing Agents.)
8 healthy male subjects were exposed to dimethylformamide vapor at a concn of 8.79 + or - 0.33 ppm for 6 hr/day for 5 consecutive days. All urine voided by the subjects was collected from the beginning of the first exposure to 24 hr past the end of the last exposure & each sample was analyzed for monomethylformamide. Monomethylformamide was rapidly eliminated from the body with urine values peaking within a few hr following the end of each exposure period. The mean for the 7 hr (end of exposure) sample was 4.74 ug/ml urine or 736.8 ug.
PMID:627935 Krivanek ND et al; J Occup Med 20 (3): 179-182 (1978)
Dimethylformamide reached an average level of 2.8 mg/l in the blood of subjects exposed to 21 ppm of the vapor for 4 hr, & was undetectable at 4 hr after the exposure; the metabolite, methylformamide, averaged between 1 & 2 mg/l in the blood & this level was maintained for at least 4 hr after exposure. Maximal blood levels of about 14 & 8 mg/l were observed for dimethylformamide & methylformamide, respectively, at 0 & 3 hrs, after a 4 hr exposure to 87 ppm of the vapor. Repeated daily exposures to 21 ppm of dimethylformamide did not result in accumulation of the chemical or its metabolite in blood. /Dimethylformamide and methylformamide/
Baselt, R.C. Biological Monitoring Methods for Industrial Chemicals. 2nd ed. Littleton, MA: PSG Publishing Co., Inc. 1988., p. 128
It is known that dimethylformamide is metabolized in man by sequential N-demethylation to methylformamide & formamide, which are largely eliminated in the urine.
Baselt, R.C. Biological Monitoring Methods for Industrial Chemicals. 2nd ed. Littleton, MA: PSG Publishing Co., Inc. 1988., p. 128
In mice, NMF is metabolized mainly to carbon dioxide, which is exhaled with the breath, & to methylamine, which is excreted with the urine. Of the radioactivity injected with [C14]formyl-NMF (400 mg/kg), 39% was exhaled as carbon dioxide. The amount of the drug excreted unchanged in the urine in mice was only 26% & 15% of the dose was metabolized to methylamine. A mercapturate, N-acetyl-S-(N-methylcarbamoyl)cysteine was identified as a major metabolite of NMF in the urine of mice, rats, & patients. Formation of the novel metabolite involves oxidation of the formyl moiety & subsequent conjugation with glutathione. On GLC analysis of the urine of mice which had received NMF, small amounts of formamide were also detected. Some evidence suggests that this metabolite was actually N-hydroxy-methylformamide, the immediate product of N-methyl-C-hydroxylation of NMF, & not formamide. N-Hydroxymethylformamide, like N-hydroxymethyl-N-methylformamide, the principal metabolite of dimethylformamide, is thermally labile & breaks down to give formamide & formaldehyde; but it is stable in aqueous soln. In alkaline soln N-hydroxymethylformamide undergoes facile hydrolysis. Only 14% of the radioactivity injected with [C14]methyl-NMF was exhaled as labeled carbon dioxide. Formate was not a urinary metabolite of NMF in mice.
Snyder, R. (ed.). Ethel Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 170
N-methylformamide has known human metabolites that include Methyl Isocyanate.
S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560
The mechanism by which NMF causes hepatotoxicity is currently under investigation. Evidence is accumulating which suggests that a reactive metabolite of NMF is involved. In vitro NMF was cytotoxic only at concns in the 0.1 M range whereas the maximum NMF concn in the plasma of animals which showed evidence of hepatotoxicity was below 0.01 M. The hypothesis that a reactive metabolite is formed which might be responsible for NMF-induced hepatotoxicity is supported by the following findings: 1) NMF caused the depletion of hepatic glutathione levels in vivo, & in hepatocytes in vitro; 2) an NMF metabolite (or metabolites) was covalently bound to liver microsomal protein; & 3) pretreatment of mice with cysteine or N-acetylcysteine protected against NMF-induced hepatotoxicity. Liver mitochondria may be a target for the reactive metab, as NMF has been shown to inhibit the ability of mouse liver mitochondria to sequester calcium ions when a hepatotoxic dose was admin ip.
Snyder, R. (ed.). Ethel Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 174
Market Place
