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Also known as: Methanamine, Aminomethane, 74-89-5, Monomethylamine, Carbinamine, Mercurialin
Molecular Formula
CH5N
Molecular Weight
31.057  g/mol
InChI Key
BAVYZALUXZFZLV-UHFFFAOYSA-N
FDA UNII
BSF23SJ79E

CAS 74-89-5
Methylamine is a uremic toxin. Uremic toxins can be subdivided into three major groups based upon their chemical and physical characteristics: 1) small, water-soluble, non-protein-bound compounds, such as urea; 2) small, lipid-soluble and/or protein-bound compounds, such as the phenols and 3) larger so-called middle-molecules, such as beta2-microglobulin. Chronic exposure of uremic toxins can lead to a number of conditions including renal damage, chronic kidney disease and cardiovascular disease. Methylamine occurs endogenously from amine catabolism and its tissue levels increase in some pathological conditions, including diabetes. Interestingly, methylamine and ammonia levels are reciprocally controlled by a semicarbazide-sensitive amine oxidase activity that deaminates methylamine to formaldehyde with the production of ammonia and hydrogen peroxide. Methylamine also targets the voltage-operated neuronal potassium channels, probably inducing release of neurotransmitter(s). Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the deamination of primary amines. Such deamination has been shown capable of regulating glucose transport in adipose cells. It has been independently discovered that the primary structure of vascular adhesion protein-1 (VAP-1) is identical to SSAO. Increased serum SSAO activities have been found in patients with diabetic mellitus, vascular disorders and Alzheimer's disease. The SSAO-catalyzed deamination of endogenous substrates like methylamine led to production of toxic formaldehyde. Chronic elevated methylamine increases the excretion of malondialdehyde and microalbuminuria. Amine oxidase substrates such as methylamine have been shown to stimulate glucose uptake by increasing the recruitment of the glucose transporter GLUT4 from vesicles within the cell to the cell surface. Inhibition of this effect by the presence of semicarbazide and catalase led to the suggestion that the process is mediated by the H2O2 produced in the oxidation of these amines. (A3265, A3266, A3267).
1 2D Structure

CAS 74-89-5

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
methanamine
2.1.2 InChI
InChI=1S/CH5N/c1-2/h2H2,1H3
2.1.3 InChI Key
BAVYZALUXZFZLV-UHFFFAOYSA-N
2.1.4 Canonical SMILES
CN
2.2 Other Identifiers
2.2.1 UNII
BSF23SJ79E
2.3 Synonyms
2.3.1 MeSH Synonyms

1. Aminomethane

2. Methylamine Bisulfite

3. Methylamine Hydride

4. Methylamine Hydrobromide

5. Methylamine Hydrochloride

6. Methylamine Hydrochloride, 14c-labeled

7. Methylamine Hydrofluoride

8. Methylamine Hydrogen Cyanide

9. Methylamine Hydroiodide

10. Methylamine Ion (1-)

11. Methylamine Nitrate

12. Methylamine Perchlorate

13. Methylamine Sulfate (1:1)

14. Methylamine Sulfate (2:1)

15. Methylamine, 13c-labeled

16. Methylamine, 14c-labeled

17. Methylamine, 15n-labeled

18. Methylamine, Cesium Salt

19. Methylamine, Monopotassium Salt

20. Methylamine, Monosodium Salt

21. Methylammonium

22. Methylammonium Ion

23. Monomethylamine

24. Monomethylammonium Ion

2.3.2 Depositor-Supplied Synonyms

1. Methanamine

2. Aminomethane

3. 74-89-5

4. Monomethylamine

5. Carbinamine

6. Mercurialin

7. N-methylamine

8. Methylaminen

9. Metilamine

10. Metyloamina

11. Methylamine Aq

12. Anhydrous Methylamine

13. Monomethyl Amine

14. Methylamine Solutions

15. Methyl-amine

16. Menh2

17. Ch3nh2

18. Bsf23sj79e

19. Chebi:16830

20. Mfcd00008104

21. Nme

22. Methylaminen [dutch]

23. Metilamine [italian]

24. Metyloamina [polish]

25. Methylamin

26. Methyl Amine

27. Ccris 2508

28. Hsdb 810

29. Methylamine, Anhydrous

30. Einecs 200-820-0

31. Un1061

32. Un1235

33. Unii-bsf23sj79e

34. Ai3-15637-x

35. Methaneamine

36. Methlamine

37. Methlyamine

38. Methyamine

39. Methylammonia

40. Methylarnine

41. Metylamine

42. Methyl Group

43. Methylamine-

44. Mono-methylamine

45. N-methyl Amine

46. Methylamine, In Aqueous Solution

47. Mono Methyl Amine

48. Mono-methyl Amine

49. Methylamine Solution

50. Methylamine Anhydrous

51. Methylamine Solution (42% Or Less)

52. Aminomethylidyneradical

53. H2nme

54. Nh2me

55. Methylamine [mi]

56. Dea Code 8520

57. Methylamine [hsdb]

58. H2nch3

59. Nh2ch3

60. Ec 200-820-0

61. Methylamine Aqueous Solution

62. Methylamine, >=99.0%

63. Methylamine, 2m In Methanol

64. Ch3-nh2

65. Methylamine, Aqueous Solution

66. Integrase Inhibitor, R3{3}

67. Un 1235 (salt/mix)

68. Chembl43280

69. Methylamine, 33% In Ethanol

70. Methylamine, Purum, >99.5%

71. Dtxsid7025683

72. Methylamine, Solution In Ethanol

73. Methylamine, Anhydrous, >=98%

74. Methylamine, Purum, >=99.0%

75. Methanamine-d2;methyl(2h2)amine

76. Methylamine, Ca. 2 M In Ethanol

77. Methyl Of Gamma-n-methylasparagine

78. Methylamine, 2m In Tetrahydrofuran

79. Bcp31897

80. Str00032

81. Bdbm50416492

82. Bp-11399b

83. Stl281863

84. Methylamine Solution, 2.0 M In Thf

85. Akos009031510

86. Db01828

87. Methylamine (ca. 9% In Acetonitrile)

88. Un 1061

89. Methylamine Solution, 2.0 M In Methanol

90. Methylamine Solution, 40 Wt. % In H2o

91. Ft-0628859

92. M0137

93. M1016

94. M2108

95. M2323

96. M2324

97. M3340

98. M3341

99. C00218

100. Q409304

101. Gadodiamide Hydrate Impurity C [ep Impurity]

102. Methylamine Solution, 33 Wt. % In Absolute Ethanol

103. Methylamine, Anhydrous [un1061] [flammable Gas]

104. Methylamine (ca. 7% In N,n-dimethylformamide, Ca. 2.0mol/l)

105. Methylamine, Aqueous Solution [un1235] [flammable Liquid]

106. Polystyrene Am-nh2, Macrobeads, Extent Of Labeling: 0.8-1.4 Mmol/g N Loading

107. 3p8

108. Jandajel(tm)-nh2, 100-200 Mesh, Extent Of Labeling: 1.0 Mmol/g N Loading, 2 % Cross-linked

109. Jandajel(tm)-nh2, 200-400 Mesh, Extent Of Labeling: 1.0 Mmol/g N Loading, 2 % Cross-linked

110. Jandajel(tm)-nh2, 50-100 Mesh, Extent Of Labeling: 1.0 Mmol/g N Loading, 2 % Cross-linked

2.4 Create Date
2004-09-16
3 Chemical and Physical Properties
Molecular Weight 31.057 g/mol
Molecular Formula CH5N
XLogP3-0.7
Hydrogen Bond Donor Count1
Hydrogen Bond Acceptor Count1
Rotatable Bond Count0
Exact Mass g/mol
Monoisotopic Mass g/mol
Topological Polar Surface Area26
Heavy Atom Count2
Formal Charge0
Complexity2
Isotope Atom Count0
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Pharmacology and Biochemistry
4.1 Absorption, Distribution and Excretion

Methylamine can be converted by semicarbazide-sensitive amine oxidase (SSAO) to formaldehyde and hydrogen peroxide, which have been proven to be toxic towards cultured endothelial cells. /The authors/ investigated whether or not these deaminated products from methylamine can exert potentially hazardous toxic effects in vivo. Long lasting residual radioactivity in different tissues was detected following administration of [14C]-methylamine in the mouse. Approximately 10% of the total administered radioactivity could even be detected 5 days after injection of [14C]-methylamine. Eighty percent of the formation of irreversible adducts can be blocked by a highly selective SSAO inhibitor, (E)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride (MDL-72974A). The residual radioactivity was primarily associated with the insoluble tissue components and the soluble macromolecules. Radioactively labelled macromolecules were fragmented following enzymatic proteolysis. Results suggest that the formaldehyde derived from methylamine interacts with proteins in vivo. In the streptozotocin-induced diabetic mice, both SSAO activity and the formation of residual radioactivity were found to be significantly increased in the kidney. Chronic administration of methylamine enhances blood prorenin level, which strongly suggests that uncontrolled deamination of methylamine may be a risk factor for initiation of endothelial injury, and subsequent genesis of atherosclerosis.

PMID:8645360 Yu PH, Zuo DM; Atherosclerosis 120 (1-2): 189-97 (1996)


/MILK/ ...The presence of volatile aliphatic amines ... in human breast milk and amniotic fluid /was measured/ to assess their role in neonatal hypergastrinemia. These volatile nitrogenous amino acid metabolites have been previously demonstrated to stimulate gastrin release in in vivo and in vitro laboratory preparations. ... The present study ... demonstrated that these gastrin-stimulatory volatile amines were present in significant concentrations in breast milk during the first several weeks after parturition and in amniotic fluid. The individual amines that were identified in both human milk and amniotic fluid samples were methylamine, dimethylamine, ethylamine, trimethylamine, propylamine, isobutylamine, and butylamine. This study provides indirect evidence to support the possibility that the hypergastrinemia measured in the fetus/neonate during the period immediately before and after birth may be attributable, in part, to the ingestion of fluid containing high concentrations of gastrin-stimulating amines.

PMID:1779307 Lichtenberger LM et al; J Pediatr Gastroenterol Nutr 13 (4): 342-6 (1991)


BACKGROUND: Dialysis adequacy is currently judged by measures of urea clearance. However, urea is relatively non-toxic and has properties distinct from large classes of other retained solutes. In particular, intracellularly sequestered solutes are likely to behave differently than urea. METHODS: We studied an example of this class, the aliphatic amine monomethylamine (MMA), in stable hemodialysis outpatients (n = 10) using an HPLC-based assay. RESULTS: Mean MMA levels pre-dialysis in end-stage renal disease subjects were 76 +/- 15 ug/L compared to 32 +/- 4 ug/L in normal subjects (n = 10) (P < 0.001). Mean urea reduction was 62% while the reduction ratio for MMA was 43% (P < 0.01). MMA levels rebounded in the 1 hour post-dialytic period to 85% of baseline, whereas urea levels rebounded only to 47% of baseline. MMA had a much larger calculated volume of distribution compared to urea, consistent with intracellular sequestration. Measures of intra-red blood cell (RBC) MMA concentrations confirmed greater levels in RBCs than in plasma with a ratio of 4.9:1. Because of the intracellular sequestration of MMA, we calculated its clearance using that amount removed from whole blood. Clearances for urea averaged 222 +/- 41 mL/min and for MMA 121 +/- 14 mL/min, while plasma clearance for creatinine was 162 +/- 20 mL/min (P < 0.01, for all differences). Using in vitro dialysis, in the absence of RBCs, solute clearance rates were similar: 333 +/- 6, 313 +/- 8 and 326 +/- 4 mL/min for urea, creatinine and MMA, respectively. These findings suggest that the lower MMA clearance relative to creatinine in vivo is a result of MMA movement into RBCs within the dialyzer blood path diminishing its removal by dialysis. CONCLUSION: In conclusion, we find that, in conventional hemodialysis, MMA is not cleared as efficiently as urea or creatinine and raise the possibility that RBCs may limit its dialysis not merely by failing to discharge it, but by further sequestering it as blood passes through the dialyzer.

PMID:20019016 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910329 Ponda MP et al; Nephrol Dial Transplant 25 (5): 1608-13 (2010)


In this study, we examined the effect of two creatine monohydrate supplementation regimes on 24-hr urinary creatine and methylamine excretion. Nine male participants completed two trials, separated by 6 weeks. Participants ingested 4 x 5 g x day(-1) creatine monohydrate for 5 days in one trial and 20 x 1 g x day(-1) for 5 days in the other. We collected 24-hr urine samples on 2 baseline days (days 1-2), during 5 days of supplementation (days 3-7), and for 2 days post-supplementation (days 8-9). Urine was assayed for creatine using high-performance liquid chromatography and methylamine using gas chromatography. Less creatine was excreted following the 20 x 1 g x day(-1) regime (49.25 +/- 10.53 g) than the 4 x 5 g x day(-1) regime (62.32 +/- 9.36 g) (mean +/- s; P < 0.05). Mean total excretion of methylamine (n = 6) over days 3-7 was 8.61 +/- 7.58 mg and 24.81 +/- 25.76 mg on the 20 x 1 g x day(-1) and 4 x 5 g x day(-1) regimes, respectively (P < 0.05). The lower excretion of creatine using 20 x 1 g x day(-1) doses suggests a greater retention in the body and most probably in the muscle. Lower and more frequent doses of creatine monohydrate appear to further attenuate formation of methylamine.

PMID:19437189 Sale C et al; J Sports Sci 27 (7): 759-66 (2009)


For more Absorption, Distribution and Excretion (Complete) data for Methylamine (8 total), please visit the HSDB record page.


4.2 Metabolism/Metabolites

PURPOSE: It has been claimed that oral creatine supplementation might have potential cytotoxic effects on healthy consumers by increasing the production of methylamine and formaldehyde. Despite this allegation, there has been no scientific evidence obtained in humans to sustain or disprove such a detrimental effect of this widely used ergogenic substance. METHODS: Twenty young healthy men ingested 21 g of creatine monohydrate daily for 14 consecutive days. Venous blood samples and 24-hr urine were collected before and after the 14th day of supplementation. Creatine and creatinine were analyzed in plasma and urine, and methylamine, formaldehyde, and formate were determined in 24-hr urine samples. RESULTS: Oral creatine supplementation increased plasma creatine content 7.2-fold (P < 0.001) and urine output 141-fold (P < 0.001) with no effect on creatinine levels. Twenty-four-hour urine excretion of methylamine and formaldehyde increased, respectively, 9.2-fold (P = 0.001) and 4.5-fold (P = 0.002) after creatine feeding, with no increase in urinary albumin output (9.78 +/- 1.93 mg/24 hr before, 6.97 +/- 1.15 mg/24 hr creatine feeding). CONCLUSION: This investigation shows that short-term, high-dose oral creatine supplementation enhances the excretion of potential cytotoxic compounds, but does not have any detrimental effects on kidney permeability. This provides indirect evidence of the absence of microangiopathy in renal glomeruli.

PMID:16260971 Poortmans JR et al; Med Sci Sports Exerc 37 (10): 1717-20 (2005)


Mono- and trimethylamines are converted to dimethylamine in the body.

Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V4 708


The regulation of methylamine and formaldehyde metabolism in Arthobacter P1 was investigated in carbon-limited continuous cultures. Evidence was obtained that the synthesis of enzymes involved in the conversion of methylamine into formaldehyde and in formaldehyde fixation is induced sequentially in this organism.

Levering PR et al; Arch Microbiol 144 (3): 272-8 (1986)


The metabolism of methylamine has been investigated in the rat in order to elucidate the role of monoamine oxidase and intestinal bacteria in the metabolism of the compound. In a series of experiments in which short and long acting inhibitors of monoamine oxidase were administered either alone or in combination prior to methyl (14)C amine hydrochloride injection, the excretion of radioactivity in the expired air and the urine was examined to indirectly assess the role of monoamine oxidase in the metabolism of methylamine. The data ... provide indirect evidence to demonstrate that the effect of iproniazid, an inhibitor of methylamine oxidation, is mediated through enzyme systems separate from MAO systems which have been invoked as major contributors to metabolism of methylamine by other investigators. The bacterial oxidation of methylamine in the intestine plays a minor role in the overall metabolism of the compounds.

PMID:2867948 Dar MS et al; Gen Pharmacol 16 (6): 557-60 (1985)


For more Metabolism/Metabolites (Complete) data for Methylamine (7 total), please visit the HSDB record page.


Uremic toxins tend to accumulate in the blood either through dietary excess or through poor filtration by the kidneys. Most uremic toxins are metabolic waste products and are normally excreted in the urine or feces.


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CAS Number : 74-89-5

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