X
API Suppliers
US DMFs Filed
0
CEP/COS Certifications
0
JDMFs Filed
0
Other Certificates
0
Other Suppliers
0
USA (Orange Book)
0
Europe
0
Canada
0
Australia
0
South Africa
0
Uploaded Dossiers
0
U.S. Medicaid
0
Annual Reports
0
0
1. Chloride, Methyl
2. Methyl Chloride
1. Methyl Chloride
2. 74-87-3
3. Methane, Chloro-
4. Monochloromethane
5. Methylchloride
6. Artic
7. Methylchlorid
8. Ch3cl
9. Clorometano
10. Chloor-methaan
11. Metylu Chlorek
12. Chlor-methan
13. Cloruro Di Metile
14. Chlorure De Methyle
15. Rcra Waste Number U045
16. Chlorocarbon
17. R 40
18. Mecl
19. Refrigerant R40
20. Chebi:36014
21. A6r43525yo
22. R-40
23. Freon 40
24. Caswell No. 557
25. Clorometano [italian]
26. Chlor-methan [german]
27. Methylchlorid [german]
28. Methyl Chloride (ca. 5.7% In Tetrahydrofuran, Ca. 1mol/l)
29. Chloor-methaan [dutch]
30. Metylu Chlorek [polish]
31. Mfcd00000872
32. Cloruro Di Metile [italian]
33. 2108-20-5
34. Chlorure De Methyle [french]
35. Merrifield's Peptide Resin, 50-100 Mesh
36. Ccris 1124
37. Hsdb 883
38. Einecs 200-817-4
39. Un1063
40. Rcra Waste No. U045
41. Epa Pesticide Chemical Code 053202
42. Carbon-chlorine
43. Chloro-methane
44. Methyl-chloride
45. Unii-a6r43525yo
46. Ai3-01707
47. Chloro Methyl Group
48. Cl-me
49. A Rt I C
50. Chloromethyne Radical
51. Chloromethane 99.9%
52. Ec 200-817-4
53. Chloromethane, >=99.5%
54. Methyl Chloride [ii]
55. Methyl Chloride [mi]
56. Methyl Chloride [hsdb]
57. Methyl Chloride [iarc]
58. Chembl117545
59. Dtxsid0021541
60. Methyl Chloride [mart.]
61. Chloromethane 1.0 M In Diethyl Ether
62. Un 1063
63. Methylene, Chloro-(6ci,7ci,8ci,9ci)
64. Methyl Chloride, Or Refrigerant Gas R 40
65. Merrifield's Peptide Resin, 200-400 Mesh
66. Chloromethane On Rasta Resin, 50-100 Mesh
67. Ft-0628715
68. M2813
69. C19446
70. Chloromethane Solution, 1.0 M In Diethyl Ether
71. Q422709
72. Chloromethane 1m, In Tert-butyl Methyl Ether, Anhydrous
73. Chloromethane Solution, 1.0 M In Tert-butyl Methyl Ether, Anhydrous
74. Chloromethane Solution, 200 Mug/ml In Methanol, Analytical Standard
75. (chloromethyl)polystyrene, Extent Of Labeling: ~1.1 Mmol/g Cl Loading
76. (chloromethyl)polystyrene, Extent Of Labeling: ~1.7 Mmol/g Cl Loading
77. Methyl Chloride, Or Refrigerant Gas R 40 [un1063] [flammable Gas]
78. (chloromethyl)polystyrene, Porous, Extent Of Labeling: ~5.5 Mmol/g Cl Loading
79. Chloromethane 100 Microg/ml In Methanol. Short Expiry Date Due To Chemical Nature Of Component(s)
80. Jandajel(tm)-cl, 100-200 Mesh, Extent Of Labeling: 0.8-1.2 Mmol/g Cl Loading, 2 % Cross-linked
81. Jandajel(tm)-cl, 200-400 Mesh, Extent Of Labeling: 0.45-0.70 Mmol/g Cl Loading, 2 % Cross-linked
82. Jandajel(tm)-cl, 50-100 Mesh, Extent Of Labeling: 0.45-0.70 Mmol/g Cl Loading, 2 % Cross-linked
83. Merrifield's Peptide Resin, 100-200 Mesh, Extent Of Labeling: 3.5-4.5 Mmol/g Cl- Loading, 1 % Cross-linked
84. Merrifield's Peptide Resin, 200-400 Mesh, Extent Of Labeling: 1.0-1.5 Mmol/g Cl- Loading, 2 % Cross-linked
85. Merrifield's Peptide Resin, 200-400 Mesh, Extent Of Labeling: 1.5-2.0 Mmol/g Cl- Loading, 1 % Cross-linked
86. Merrifield's Peptide Resin, 200-400 Mesh, Extent Of Labeling: 2.0-2.5 Mmol/g Cl- Loading, 2 % Cross-linked
87. Merrifield's Peptide Resin, 200-400 Mesh, Extent Of Labeling: 3.0-3.5 Mmol/g Cl- Loading, 1 % Cross-linked
88. Merrifield's Peptide Resin, 200-400 Mesh, Extent Of Labeling: 3.5-4.5 Mmol/g Cl- Loading, 1 % Cross-linked
89. Merrifield's Peptide Resin, 50-100 Mesh, Extent Of Labeling: 2.5-4.0 Mmol/g Cl- Loading, 1 % Cross-linked With Divinylbenzene
90. Merrifield's Peptide Resin, 70-90 Mesh, Extent Of Labeling: 1.0-1.5 Mmol/g Cl- Loading, 1 % Cross-linked
91. Merrifield's Peptide Resin, 70-90 Mesh, Extent Of Labeling: 1.5-2.0 Mmol/g Cl- Loading, 1 % Cross-linked
92. Stratospheres(tm) Pl-cms Resin, 100-200 Mesh, Extent Of Labeling: 1.0 Mmol/g Loading, 1 % Cross-linked
93. Stratospheres(tm) Pl-cms Resin, 100-200 Mesh, Extent Of Labeling: 2.0 Mmol/g Loading, 1 % Cross-linked
94. Stratospheres(tm) Pl-cms Resin, 200-400 Mesh, Extent Of Labeling: 1.0 Mmol/g Loading, 1 % Cross-linked
95. Stratospheres(tm) Pl-cms Resin, 30-40 Mesh, Extent Of Labeling: 1.0 Mmol/g Loading, 1 % Cross-linked
96. Stratospheres(tm) Pl-cms Resin, 30-40 Mesh, Extent Of Labeling: 2.0 Mmol/g Loading, 1 % Cross-linked
97. Stratospheres(tm) Pl-cms Resin, 50-100 Mesh, Extent Of Labeling: 2.0 Mmol/g Loading, 1 % Cross-linked
98. Stratospheres(tm) Pl-cms Resin, 50-100 Mesh, Extent Of Labeling: 4.0 Mmol/g Loading, 1 % Cross-linked
| Molecular Weight | 50.49 g/mol |
|---|---|
| Molecular Formula | CH3Cl |
| XLogP3 | 0.8 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 0 |
| Rotatable Bond Count | 0 |
| Exact Mass | 49.9923278 g/mol |
| Monoisotopic Mass | 49.9923278 g/mol |
| Topological Polar Surface Area | 0 Ų |
| Heavy Atom Count | 2 |
| Formal Charge | 0 |
| Complexity | 2 |
| 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 |
Physiologically based pharmacokinetic (PBPK) models are often optimized by adjusting metabolic parameters so as to fit experimental toxicokinetic data. The estimates of the metabolic parameters are then conditional on the assumed values for all other parameters. Meanwhile, the reliability of other parameters, or the structural model, is usually not questioned. Inhalation exposures with human volunteers in our laboratory show that non-conjugators lack metabolic capacity for methyl chloride entirely, and that elimination in these subjects takes place via exhalation only. Therefore, data from these methyl chloride exposures provide an excellent opportunity to assess the general reliability of standard inhalation PBPK models for humans. A hierarchical population PBPK model for methyl chloride was developed. The model was fit to the experimental data in a Bayesian framework using Markov chain Monte Carlo (MCMC) simulation. In a Bayesian analysis, it is possible to merge a priori knowledge of the physiological, anatomical and physicochemical parameters with the information embedded in the experimental toxicokinetic data obtained in vivo. The resulting estimates are both statistically and physiologically plausible. Model deviations suggest that a pulmonary sub-compartment may be needed in order to describe the inhalation and exhalation of volatile methyl chloride adequately. The results also indicate that there may be significant intra-individual variability in the model parameters. ...
PMID:11482516 Jonsson F et al; Arch Toxicol 75 (4): 189-99 (2001)
After exposure to 50 ppm, chloromethane breath levels range from 50-80 ug/L; while chloromethane blood levels range from 35-100 ug/L.
Lelkin, J.B., Paloucek, F.P., Poisoning & Toxicology Compendium. LEXI-COMP Inc. & American Pharmaceutical Association, Hudson, OH 1998., p. 664
... Methyl chloride is rapidly absorbed from the lungs and rapidly reaches equilibrium with levels in blood and expired air approximately proportional to the exposure concentrations. At high concentrations, kinetic processes such as metabolism or excretion may become saturated limiting the rate of uptake. Animals studies show that methyl chloride is absorbed from the lungs and extensively distributed throughout 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. V5 6
During inhalation exposure to methyl chloride, blood:gas equilibrium is rapidly attained. Respiration and hepatic perfusion appear to be rate-limiting factors of gas uptake at low toxicant concentrations, while capacity of liver to conduct metabolism is rate-limiting at high concentrations.
PMID:7394779 Andersen ME et al; Toxicol Appl Pharmacol 54 (1): 100-16 (1980)
For more Absorption, Distribution and Excretion (Complete) data for METHYL CHLORIDE (15 total), please visit the HSDB record page.
The aim of the present study was to investigate how the genetic polymorphism in glutathione transferase T1 (GSTT1) affects the metabolism and disposition of methyl chloride in humans in vivo. The 24 volunteers (13 males and 11 females) who participated in the study were recruited from a group of 208 individuals previously phenotyped for GSTT1 by measuring the glutathione transferase activity with methyl chloride in lysed erythrocytes ex vivo. Eight individuals with high (+/+), eight with medium (+/0) and eight with no (0/0) GSTT1 activity were exposed to methyl chloride gas (10 ppm) in an exposure chamber for 2 hr. Uptake and disposition was studied by measuring the concentration of methyl chloride in inhaled air, exhaled air and blood. A two-compartment model with two elimination pathways corresponding to exhalation and metabolism was fitted to experimental data. The average net respiratory uptake of methyl chloride was 243, 158, and 44 umol in individuals with high, intermediate and no GSTT1 activity, respectively. Metabolic clearance was high (4.6 L/min) in the +/+ group, intermediate (2.4 L/min) in the +/0 group, and close to zero in 0/0 individuals, while the exhalation clearance was similar in the three groups. No exposure related increase in urinary S-methyl cysteine was detected. However, gender and the GSTTl phenotype seemed to affect the background levels. In conclusion, GSTT1 appears to be the sole determinant of methyl chloride metabolism in humans. Thus, individuals with nonfunctional GSTT1 entirely lack the capacity to metabolize methyl chloride.
PMID:11037805 Lof A et al; Pharmacogenetics 10 (7): 645-53 (2000)
Hepatic to formaldehyde and carbon dioxide. Elimination: Renal (N-acetyl-S-methylcysteine).
Lelkin, J.B., Paloucek, F.P., Poisoning & Toxicology Compendium. LEXI-COMP Inc. & American Pharmaceutical Association, Hudson, OH 1998., p. 664
Methyl chloride is metabolized by conjugation with glutathione to yield S-methylglutathione, S-methylcysteine, and other sulfur-containing compounds that are excreted in the urine or further metabolized to methanethiol. Cytochrome P450-dependent metabolism of methanethiol may yield formaldehyde and formic acid, whose carbon atoms are then available to the one-carbon pool for incorporation into macromolecules or for formation of CO2. Alternatively, formaldehyde may be directly produced from chloromethane via a P450 oxidative dechlorination.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V5 6
The conjugation of chloromethane with glutathione is primarily enzyme-catalyzed. In contrast to all other animal species investigated (rats, mice, bovine, pigs, sheep, and rhesus monkeys), human erythrocytes contain a glutathione transferase isoenzyme that catalyzes the conjugation of glutathione with methyl chloride. There are two distinct human subpopulations based on the amount or forms of this transferase.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V5 6
For more Metabolism/Metabolites (Complete) data for METHYL CHLORIDE (13 total), please visit the HSDB record page.
50-90 minutes
Lelkin, J.B., Paloucek, F.P., Poisoning & Toxicology Compendium. LEXI-COMP Inc. & American Pharmaceutical Association, Hudson, OH 1998., p. 664
... Apparent steady-state blood methyl chloride (MeCl) concentrations were proportionate to exposure concentration in rats and dogs exposed to 50 and 1000 ppm. Furthermore, blood MeCl concentrations were similar in both species when they were exposed to the same concentration. A linear two-compartment open model described the blood MeCl data: alpha and beta phase elimination half-times corresponded to approximately 4 and 15 min, respectively, in rats, and 8 and 40 min in dogs.
PMID:6857680 Landry TD et al; Toxicol Appl Pharmacol 68 (3): 473-86 (1983)
/Chloromethane ... /causes/ central nervous system depression.
Lelkin, J.B., Paloucek, F.P., Poisoning & Toxicology Compendium. LEXI-COMP Inc. & American Pharmaceutical Association, Hudson, OH 1998., p. 664
Cytotoxicity, the primary effect of methyl chloride, resulted in the disruption of the cell metab. and altered the electron transport processes of the respiratory chain. Thus, following 2-30 day inhalation exposure in rats (4 hr daily), the response was max by 8th day. Initially the activities of succinate dehydrogenase, alpha-glycerophosphate dehydrogenase, nonspecific esterase, decreased somewhat, whereas NAD-diaphorase and cytochrome oxidase increased. The activity of the diaphorase in the lymphoid tissue was high during the progress of the primary response. The secondary response was noted by 30th day when cytochrome oxidase activities are informative of the progress of toxic processes.
PMID:3710226 Mamedov AM, Aliev VA; Gig Sanit 4: 84-5 (1986)
Previous data have demonstrated that methyl chloride is toxic to B6C3F1 mice under both acute and chronic exposure conditions, and that conjugation of methyl chloride with glutathione is a key step in the metabolism of methyl chloride. This study examined the role of glutathione in mediating the acute toxicity of methyl chloride to liver, kidney, and brain of male B6C3F1 mice. The lethal effects of a single 6 hr inhalation exposure of B6C3F1 males to 2500 ppm methyl chloride were completely prevented by pretreatment with the glutathione synthesis inhibitor, L-buthionine-S,R-sulfoximine (4 mmol L-BSO/kg, ip 1.5 hr prior to methyl chloride exposure). ... These results indicate that glutathione is an important component in the toxicity of methyl chloride to multiple organ systems in B6C3F1 mice. Reaction of methyl chloride with glutathione appears to constitute a mechanism of toxication, contrary to the role usually proposed for glutathione in detoxifying xenobiotics.
PMID:3764938 Chellman GJ et al; Toxicol Appl Pharmacol 86 (1): 93-104 (1986)
Inhalation of methyl chloride by male B6C3F1 mice resulted in a concentration-dependent depletion of glutathione in liver, kidney, and brain. Exposure for 6 hr to 100 ppm methyl chloride decreased the concentration of glutathione in mouse liver by 45%, while exposure to 2500 ppm for 6 hr lowered liver glutathione to approximately 2% of control levels. For those exposures which decreased liver glutathione to less than 20% of control levels, the extent of liver glutathione depletion was closely correlated with the capacity of a 9000 g supernatant fraction from the liver to undergo lipid peroxidation in vitro. Glutathione was depleted to a lesser extent in mouse brain and kidney, compared to liver, and no relationship to peroxidation was observed for single exposures to methyl chloride. ... Exposure of rats to 2000 ppm methyl chloride reduced liver glutathione to 20% of control levels, compared to 4.5% in mice similarly exposed, and under these exposure conditions the amount of lipid peroxidation measured in vitro was 40 fold greater in mouse liver than in rat liver. During exposure of mice to 2500 ppm methyl chloride, ethane expiration increased to an extent comparable to that produced by administration of 2 ml/kg of carbon tetrachloride. These findings suggest that glutathione depletion in liver may be an important component of methyl chloride induced hepatotoxicity.
PMID:6710490 Kornbrust DJ, Bus JS; Toxicol Appl Pharmacol 72 (3): 388-99 (1984)
The effect of acute methyl chloride inhalation on F-344 rat tissue nonprotein SH (NPSH), largely reduced glutathione was studied. Rats were exposed to methyl chloride concentrations of 1500, 500 or 100 ppm. A 6 hr exposure to 1500 ppm methyl chloride decreased the nonprotein SH content of liver, kidney and lungs to 17, 27 and 30% of control values, respectively, while 500 ppm methyl chloride lowered the liver, kidney and lung nonprotein SH to 41, 59 and 55% of control values, respectively, demonstrating a concentration-related effect. Blood nonprotein SH did not differ from controls in either group. No statistically significant changes from controls in tissue or blood nonprotein SH were observed following a 100-ppm methyl chloride exposure. The extent of tissue nonprotein SH loss depended on exposure duration. Liver and kidney nonprotein SH returned to control nonprotein SH concentrations within 8 hr following exposure of 1500 ppm methyl chloride. Pretreatment of rats with Aroclor 1254 or SKF-525A (proadifen hydrochloride) did not alter the methyl chloride-induced decrease in tissue nonprotein SH. Methyl chloride reacted extensively with tissue nonprotein SH in vivo in a concentration-related fashion following acute inhaltion exposure. The most likely nonprotein SH constituent with which methyl chloride reacted was reduced glutathione. The finding that blood nonprotein SH was not affected, in contrast to liver, kidney or lung nonprotein SH, indicated a tissue-specific reaction between methyl chloride and SH groups, a reaction in which the tissue enzyme glutathione-S-alkyltransferase may play a role.
PMID:7058527 Dodd DE et al; Toxicol Appl Pharmacol 62 (6): 228-36 (1982)
Market Place
