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1. Ethylene Glycol Monomethyl Ether
2. Methyl Cellosolve
3. Methyl Cellosolve, Calcium Salt
4. Methyl Cellosolve, Potassium Salt
5. Methyl Cellosolve, Sodium Salt
6. Methylcellosolve
1. 109-86-4
2. Ethylene Glycol Monomethyl Ether
3. Methyl Cellosolve
4. Ethanol, 2-methoxy-
5. Methyl Oxitol
6. Methoxyethanol
7. 2-methoxy-1-ethanol
8. Methylglykol
9. Methoxyhydroxyethane
10. 3-oxa-1-butanol
11. Monomethyl Glycol
12. Egme
13. Glycol Ether Em
14. Dowanol Em
15. Poly-solv Em
16. 1-hydroxy-2-methoxyethane
17. Glycol Monomethyl Ether
18. Prist
19. Mecs
20. Metil Cellosolve
21. Jeffersol Em
22. 2-metossietanolo
23. Ethylene Glycol Methyl Ether
24. Amsco-solv Ee
25. 2-methoxy-aethanol
26. Polyethylene Glycol Monomethyl Ether
27. Methylcelosolv
28. Metoksyetylowy Alkohol
29. .beta.-methoxyethanol
30. 2-methoxyethyl Alcohol
31. 2-methoxy Ethanol
32. Hoch2ch2och3
33. Beta-methoxyethanol
34. Methoxy Polyethylene Glycol
35. Monomethoxypolyethylene Glycol
36. Monomethyl Ether Of Ethylene Glycol
37. Aethylenglykol-monomethylaether
38. Ethyleneglycol Monomethyl Ether
39. Monoethylene Glycol Methyl Ether
40. Monomethyl Ethylene Glycol Ether
41. Glycolmethyl Ether
42. Nsc 1258
43. 2-hydroxyethyl Methyl Ether
44. Ether Monomethylique De L'ethylene-glycol
45. Methoxypolyethylene Glycol
46. Mfcd00002867
47. Ek1l6xwi56
48. Ethylene Glycol Monomethylether
49. Ethylene Glycol-monomethyl Ether
50. Dtxsid5024182
51. Chebi:46790
52. Nsc-1258
53. Karl Fischer Reagent
54. Mpeg
55. Methylcellosolve
56. Methyl-cellosolve
57. Dowanol 7
58. Karl Fischer Reagent Diluent
59. Caswell No. 551
60. Methylglykol [german]
61. 2-methoxyethan-1-ol
62. Methylcelosolv [czech]
63. Metil Cellosolve [italian]
64. 2-methoxy-ethanol
65. 2-metossietanolo [italian]
66. Hsdb 97
67. 2-methoxy-aethanol [german]
68. Ccris 5826
69. Metoksyetylowy Alkohol [polish]
70. Polyethylene Glycol Methyl Ether
71. Einecs 203-713-7
72. Un1188
73. Unii-ek1l6xwi56
74. Epa Pesticide Chemical Code 042202
75. Methoxypoly(ethylene Glycol)
76. Aethylenglykol-monomethylaether [german]
77. Brn 1731074
78. 2methoxyethanol
79. Methyl Ethoxol
80. Methyl Icinol
81. Ai3-18363
82. Methylcello-solve
83. Ektasolve Em
84. O-methyl Glycol
85. 2-methoxylethanol
86. 2 -methoxyethanol
87. Poly(ethylene Glycol Methyl Ether)
88. Ether Monomethylique De L'ethylene-glycol [french]
89. Moe
90. 2-(methoxy)ethanol
91. 2-(methyloxy)ethanol
92. Methyl Cellosolve(r)
93. Hisolve Mc
94. Dsstox_cid_4182
95. Ec 203-713-7
96. 2-methoxyethanol Acs Grade
97. Dsstox_rid_77319
98. Dsstox_gsid_24182
99. Ethyleneglycol Monomethylether
100. Methoxyethanol [inci]
101. 4-01-00-02375 (beilstein Handbook Reference)
102. Wln: Q2o1
103. 2-methoxyethanol [mi]
104. Chembl444144
105. Dimethyleneglycol Monomethylether
106. 2-methoxyethanol [hsdb]
107. Chebi:53449
108. Nsc1258
109. 2-methoxyethanol [mart.]
110. 2-methoxyethanol [usp-rs]
111. Polyethylene Glycol Monomethyl Ester
112. Zinc1591817
113. Tox21_301080
114. Stk399974
115. 2-methoxyethanol, Analytical Standard
116. 2-methoxyethanol, Anhydrous, 99.8%
117. Akos000119041
118. Db02806
119. Rp10062
120. Un 1188
121. Ncgc00163767-01
122. Ncgc00163767-02
123. Ncgc00163767-03
124. Ncgc00163767-04
125. Ncgc00254981-01
126. 2-methoxyethanol, For Synthesis, 99.0%
127. Alpha-hydro-omega-methoxypoly(oxyethylene)
128. Bp-13395
129. Cas-109-86-4
130. Ethylene Glycol Monomethyl Ether (egmee)
131. Nci60_000597
132. Polyethylene Glycol Monomethyl Ester (nf)
133. 2-methoxyethanol, For Hplc, >=99.9%
134. 2-methoxyethanol 500 Microg/ml In Methanol
135. Ft-0626334
136. Ft-0689213
137. Ft-0700869
138. M0111
139. 2-methoxyethanol, Saj First Grade, >=99.0%
140. Carbowax Sentry Methoxypolyethylene Glycol (tn)
141. D05554
142. 2-methoxyethanol, Jis Special Grade, >=99.0%
143. 2-methoxy-ethanol (glycolmonoethylether)
144. Q903362
145. Ethylene Glycol Monomethyl Ether Reagent Grade Acs
146. J-509861
147. F1908-0118
148. 2-methoxyethanol, For Amino Acid Analysis, >=99.5% (gc)
149. Ethyleneglycol-monomethyl Ether 100 Microg/ml In Methanol
150. Ethyleneglycol-monomethyl Ether 1000 Microg/ml In Methanol
151. 2-methoxyethanol, Suitable For Amino Acid Analysis, >=99.0%
152. Ethylene Glycol Monomethyl Ether [un1188] [flammable Liquid]
153. 2-methoxyethanol, Contains 50 Ppm Bht As Stabilizer, Acs Reagent, >=99.3%
154. 2-methoxyethanol, Pharmaceutical Secondary Standard; Certified Reference Material
155. 2-methoxyethanol, Puriss. P.a., Acs Reagent, Reag. Ph. Eur., >=99.5% (gc)
156. 2-methoxyethanol, Reagentplus(r), >=99.0%, Contains 50 Ppm Bht As Stabilizer
| Molecular Weight | 76.09 g/mol |
|---|---|
| Molecular Formula | C3H8O2 |
| XLogP3 | -0.8 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 2 |
| Exact Mass | 76.052429494 g/mol |
| Monoisotopic Mass | 76.052429494 g/mol |
| Topological Polar Surface Area | 29.5 Ų |
| Heavy Atom Count | 5 |
| Formal Charge | 0 |
| Complexity | 14.4 |
| 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 |
/EXPL THER/ Structure-activity studies with nine glycol alkyl ethers were conducted with a cellular leukemia transplant model in male Fischer rats. This in vivo assay measures the effects of chemical treatment on neoplastic progression in transplant recipients. Chemicals were given ad libitum in the drinking water simultaneously with the transplants and continued throughout the study. In all, 20 million leukemic cells were injected sc into syngeneic rats, which after 60 days resulted in a 10-fold increase in relative spleen weights, a 100-fold increase in white blood cell counts, and a 50% reduction in red blood cell (RBC) indices and platelet counts. At this interval, ethylene glycol monomethyl ether (2-ME) given at a dose of 2.5 mg/mL in the drinking water completely eliminated all clinical, morphological, and histopathological evidence of leukemia, whereas the same dose of ethylene glycol monoethyl ether (2-EE) reduced these responses by about 50%. Seven of the glycol ethers were ineffective as anti-leukemic agents, including ethylene glycol, the monopropyl, monobutyl, and monophenyl ethylene glycol ethers, diethylene glycol, and the monomethyl and monoethyl diethylene glycol ethers. 2-ME more than doubled the latency period of leukemia expression and extended survival for at least 210 days. A minimal effective dose for a 50% reduction in the leukemic responses was 0.25 mg/mL 2-ME in the drinking water (15 mg/kg body weight), whereas a 10-fold higher dose of 2-EE was required for equivalent antileukemic activity. In addition, the in vitro exposure of a leukemic spleen mononuclear cell culture to 2-ME caused a dose- and time-dependent reduction in the number of leukemia cells after a single exposure to 1-100 uM concentrations, whereas the 2-ME metabolite, 2-methoxyacetic acid, was only half as effective. The two glycol alkyl ethers with demonstrable anti-leukemic activity, 2-ME and 2-EE, also exhibited a favorable efficacy-to-toxicity ratio and should be considered for further development as chemotherapeutic agents.
PMID:2357763 Dieter MP et al; Cancer Chemother Pharmacol 26 (3): 173-80 (1990)
Teratogens
An agent that causes the production of physical defects in the developing embryo. (See all compounds classified as Teratogens.)
Immunosuppressive Agents
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging. (See all compounds classified as Immunosuppressive Agents.)
The material /2-methoxyethanol/ was detected in rat urine 30 min after an ip administration of 1.0 mg/kg and remained present for a total of 7 hr after the injection, 3 hr after it was last seen in the blood.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 92
Male Fischer 344 rats were given a single oral dose of approx 1 or 8.7 mmol/kg of (14)C-ethylene glycol monomethyl ether. Approx 50 to 60% of the admin (14)C was excreted in urine, and about 12% was eliminated as (14)CO2 within 48 hr.
PMID:6836577 MILLER RR ET AL; TOXICOL APPL PHARMACOL 67 (2): 229-37 (1983)
The uptake of /ethylene glycol monomethyl ether/ (EGME) and the urinary excretion of its major metabolite /methoxyacetic acid/ (MAA) was studied in seven male volunteers during experimental exposure to EGME at rest. The exposure concentration was set at 16 mg/cu m, the present Threshold Limit Value. A high retention (0.76) remained unchanged during the 4-hr exposure period. In combination with a constant pulmonary ventilation and a fixed exposure concentration this resulted in an uptake rate that showed no significant variation in time. The total amount of EGME inhaled corresponded to a dose of only 0.25 mg/kg. During and up to 120 hr after the start of the exposure, MAA was detected in the urine. The elimination half-life was on average 77.1 hr. The total amount of MAA excreted was calculated by extrapolation and averaged 85.5% of the inhaled EGME. ...
PMID:2722247 Groeseneken D et al; Int Arch Occup Environ Health 61 (4): 243-7 (1989)
...The current study evaluated the metabolism of (14)C-labeled 2ME and the distribution of methoxyacetic acid (MA) in maternal and fetal tissues of pregnant Sprague-Dawley rats either exposed to RF radiation at 10 mHz or sham conditions. Additionally, adduct formation for both plasma and fetal protein was tested as a possible biomarker for the observed 2ME/RF teratogenicity. Rats were administered (ethanol-1,2-(14)C)-2ME (150 mg/kg, 161 uCi/rat average) by gavage on day 13 of gestation immediately before RF radiation body temperature elevation to 42 C/30 min. Concurrent sham and RF rats were sacrificed at 3, 6, 24 or 48 hr for harvest of maternal blood, urine, fetuses and embryonic fluid. Tissues were either digested for determination of radioactivity or deproteinized with /Trichloroacetic Acid/ (TCA) and analyzed by HPLC for quantification of 2ME metabolites. Results show the presence of 2ME and seven metabolites, with the major metabolite, MA, peaking at 6 hr in the tissues tested. MA, the proximal teratogen, was detectable in maternal serum, urine, fetus and embryonic fluid 48 hr after dosing. Clearance of total body (14)C was significantly reduced for the RF animals (p>0.05) for the 24-48 hr period, but MA values for serum, fetus and embryonic fluid were similar for both sham and RF rats. Additionally, no difference was noted for 2ME metabolite profiles in urine or tissue for sham or RF rats thus eliminating an effect of RF radiation on MA production as a possible explanation for the reported RF/2ME synergism. Subsequently, serum and fetus protein-bound adducts were evaluated by analysis of covalently bound radioactivity. Serum protein binding was significantly higher for sham than RF rats at 3- and 6-hr -- highest for sham rats at 6 hr (519 +/- 95 ug as parent 2ME/g of protein) whereas RF serum values were highest at 24 hr (266 +/- 79 ug/g protein). Fetal protein binding was significantly higher for sham rats at 6 hr, but binding was highest for both groups at 24 hr (sham = 229 +/- 71 ug/g, RF = 185 +/- 48 ug/g). Formation of protein adducts after 2ME is thought to be related to levels of methoxyacetaldehyde, a reactive intermediate in the formation of MA.
Cheever KL et al; Toxicologist 51 (1): 197 (1995)
For more Absorption, Distribution and Excretion (Complete) data for 2-METHOXYETHANOL (18 total), please visit the HSDB record page.
The metabolic transformation of /2-methoxyethanol/ (2-ME) gives two primary metabolites: /methoxyacetic acid/ (MAA) and 2-methoxyacetyl glycine. Metabolism to carbon dioxide represents a secondary, minor route. The conversion in plasma of 2-ME to MAA is rapid, with a half-life of 0.6 hr in rats, but the excretion of MAA is slow, with a half-life of about 20 hr in the rat and 77 hr in man.
International Program on Chemical Safety; Environmental Health Criteria 115 for 2-Methoxyethanol, and 2-Ethoxyethanol, and their acetates. Available from, as of 05.9.2014: https://www.inchem.org/documents/ehc/ehc/ehc115.htm
The role of metabolism in 2-methoxyethanol (ME)-induced testicular toxicity has been investigated with Sprague-Dawley rats. Following administration of [(14)C]ME (250 mg/kg, ip) to a group of animals, there was evidence of testicular damage, identified as depletion of the spermatocyte population. Radioactivity detected in urine over 48 hr after treatment accounted for 55% of the dose. The major urinary metabolites were identified by HPLC and isotope dilution analysis, as methoxyacetic acid (MAA) and methoxyacetylglycine (accounting for 50 to 60% and 18 to 25%, respectively, of urinary radioactivity). Analysis of plasma revealed a rapid conversion of ME to MAA (t1/2 for disappearance of ME = 0.6 +/- 0.03 hr) and gradual clearance of radioactivity (t1/2 = 19.7 +/- 2.3 hr). Pretreatment of animals with pyrazole (400 mg/kg, ip) 1 hr prior to [(14)C]ME dosing gave complete protection against the testicular toxicity of ME. Radioactivity detected in the urine from the pyrazole-pretreated groups over 48 hr (18%) was significantly lower than in the ME-only group. The major radioactive peak co-chromatographed with ME (30 to 36% of the total urinary radioactivity). MAA and methoxyacetylglycine were not major metabolites. Analysis of plasma revealed almost complete inhibition of the conversion of ME to MAA (t1/2 for disappearance of ME = 42.6 +/- 5.6 hr, clearance of radioactivity t1/2 = 51.0 +/- 7.8 hr). The results demonstrate that metabolic activation is required for 2-methoxyethanol to exert toxicity to the male reproductive system.
PMID:4035689 Moss EJ et al; Toxicol Appl Pharmacol 79 (3): 480-9 (1985)
The secondary metabolite of dimethoxyethyl phthalate (DMEP) methoxyacetic acid (MAA), but not the diester or its primary metabolites monomethoxyethyl phthalate and methoxyethyanol (ME) interfered with normal growth and development of organogenesis phase rat embryos in culture. These in vivo observations suggested that the teratogenicity of DMEP in vivo was due to enzymic cleavage of the diester to ME, followed by oxidation of the latter to MAA in the maternal compartment. /Metabolites of dimethoxyethyl phthalate/
PMID:6719491 Yonemoto J et al; Toxicol Lett 21 (1): 97-102 (1984)
When human volunteers inhaled 5 ppm EGME for 4 hours, 76% of the inspired /ethylene glycol monomethyl ether/ (EGME) was retained and 85% of the absorbed dose appeared in the urine as 2-methoxyacetic acid. The human elimination half-time for the 2-methoxyacetic acid arising from the catabolism of EGME was 66 to 89 hours.
American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 5
For more Metabolism/Metabolites (Complete) data for 2-METHOXYETHANOL (20 total), please visit the HSDB record page.
...Ethylene glycol methyl ether was found equally distributed in brain, plasma, lung, and liver 1 hr after administration and ...the half-life in the body was approx 1 to 2 hr, unless dose levels were near the lethal level. In inhalation studies the plasma levels of ethylene glycol methyl ether increased nearly linearly from exposures of 1, 2, 4, and 6 hr to 3317 ppm. When the exposure was extended to 8 hr, the concentration in the plasma was more than double that found after the 6-hr exposure, suggesting that metabolic and/or excretory mechanisms were saturated.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V7 92
The human elimination half-time for the 2-methoxyacetic acid arising from the catabolism of EGME was 66 to 89 hours. /2-methoxyacetatic acid/
American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 5
... . The conversion in plasma of /2-methoxyethanol/ (2-ME) to /methoxyacetic acid/ (MAA) is rapid, with a half-life of 0.6 hr in rats, ...
International Program on Chemical Safety; Environmental Health Criteria 115 for 2-Methoxyethanol, and 2-Ethoxyethanol, and their acetates. Available from, as of 05.9.2014: https://www.inchem.org/documents/ehc/ehc/ehc115.htm
The role of metabolism in 2-methoxyethanol (ME)-induced testicular toxicity has been investigated with Sprague-Dawley rats. Following administration of [(14)C]ME (250 mg/kg, ip) to a group of animals, there was evidence of testicular damage, ... Radioactivity detected in urine over 48 hr after treatment accounted for 55% of the dose. ... Analysis of plasma revealed a rapid conversion of ME to MAA (t1/2 for disappearance of ME = 0.6 +/- 0.03 hr) and gradual clearance of radioactivity (t1/2 = 19.7 +/- 2.3 hr). ... Analysis of plasma revealed almost complete inhibition of the conversion of ME to MAA (t1/2 for disappearance of ME = 42.6 +/- 5.6 hr, clearance of radioactivity t1/2 = 51.0 +/- 7.8 hr). ...
PMID:4035689 Moss EJ et al; Toxicol Appl Pharmacol 79 (3): 480-9 (1985)
For more Biological Half-Life (Complete) data for 2-METHOXYETHANOL (7 total), please visit the HSDB record page.
Cell death was analyzed in neurulating mouse embryos after in vivo doses of 2-methoxyethanol (2-ME) that produce anterior neural tube defects. Characterization of 2-ME-induced cell death was performed by evaluating: (1) vital fluorochrome staining in whole embryos applying confocal laser scanning microscopy; (2) characteristics of cell debris in conventional histological sections revealed by light microscopy; and (3) Apoptag in situ immunohistochemical staining for apoptosis using light microscopy. ...Physiological cell death in control embryos primarily occurred in the neural crest region during neural fold elevation. Embryos exposed to 2-ME had expanded areas of cell death in the neural crest and also new areas of cell death in medial regions of the anterior neural tube. Both physiological and 2-ME-induced embryonic cell death had morphological, immunohistochemical, and fluorochrome staining characteristics of apoptosis. When fluorescence data from confocal microscopic analysis of vital fluorochrome-stained embryos were analyzed, a dose-dependent increase was found in embryos exposed to 2-ME. Similar results were obtained when cell death was analyzed in either conventional histological sections or sections prepared for immunohistochemical detection of apoptosis.
PMID:9894672 Ambroso JL et al; Teratology 58 (6): 231-40 (1998)
A mechanistic role for Ca2+ has been promoted. .../It was/ observed that a Ca2+ channel blocker afforded protection against 2-ME induced pachytene spermatocyte cell death. /It was/ hypothesized that 2-ME induces spermatocyte apoptosis in both the rat and guinea pig, and activates or induces an endogenous endonuclease. An increase in intracellular Ca2+ is thought by many to be the trigger for endonuclease activation/induction and subsequent apoptotic cell death.
Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 6th ed. New York, NY: McGraw-Hill, 2001., p. 899
Metabolites /of ethylene glycol monoethyl ether/ such as 2-methoxyethanol (2-ME) ...induce testicular toxicity. They may cause testicular atrophy, decreased sperm motility, and an increased incidence of abnormal sperm. Most likely, the metabolism of monoalkyl glycol ethers occurs via alcohol and aldehyde dehydrogenases, leading to the formation of methoxyacetic acid (MAA). MAA is believed to be the ultimate toxic metabolite of 2-ME. However, methoxyacetaldehyde (MALD), an intermediate metabolite of 2-ME,can also produce testicular lesions. Although the site of action was thought to be upon the late spermatocyte, it now appears that the Sertoli cells are the prime target for 2-ME. It is unclear whether the mechanism of testicular toxicity of 2-ME induces germ cell death by interfering with interregulating signal transduction pathways within either Sertoli cells or germ cells, causing a disruption of cell-to-cell communication.
Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 6th ed. New York, NY: McGraw-Hill, 2001., p. 690
Once oxidized to 2-methoxyacetic acid (2-MAA), 2-ME is teratogenic in all species tested. Upon single administration at 0800 hr, gestation day (gd) 8 (copulation plug + = gd 0) was most sensitive to induction of /exencephaly/. In this study, the effects of 2-ME/2-MAA on brain differentiation were assessed soon after gd 8 treatment. Physiological cell death (CD) in control embryos and chemically-enhanced CD were compared by Nile blue sulfate staining (4, 8, 12 hr after 2-ME; 0, 250 or 325 mg/kg). Its intensity in fore-, mid- and hindbrain was scored as scattered, moderate or intense. These CD patterns were confirmed by propidium iodide fluorescence staining. The most consistent CD staining was observed 8 hr after 325 mg 2-ME/kg. In controls, scattered CD was apparent in the pros-, mes- and rhombencephalon, while moderate to intense CD appeared uniformly in the caudal rim of the open forebrain and along its midline when closure was occurring. In 2-ME exposed embryos, CD patterns in the forebrain were comparable to those in controls. However, CD in the mid- and hindbrains was markedly increased. Moderate to intense CD in about half of the embryos was observed in the mes- and rhombencephalon. Rhombomeres 1-3 and the dorsal lateral neural tube were particularly remarkable in their staining intensity. Neural tube closure status and brain morphology (250 mg 2-ME/kg) were evaluated on gd 9.25 and gd 10.25. The mean somite number was unaffected by 2-ME treatment. However, in control embryos the neuropores were closed in all but 1 of 119 embryos, while in 23% (35 of 142; 82% of litters) of 2-ME embryos they were patent, and 8% (11 of 133; 36% of litters) still had that condition on gd 10.25. For comparison other pregnancies progressed to gd 18 when 12% of the live fetuses (in 40% of litters) had EX. There were also numerous morphological differences from developmental-age-matched controls consistent with 2-MAA-induced embryotoxicity, which caused developmental delay. Its incidence on gd 9.25 was five times higher (embryos) and affected twice as many litters as in concurrent controls. On gd 10.25 twice as many embryos as in control litters still displayed this differentiation delay phenomenon.
Welsch F et al; Teratology 49 (5): 392 (1994)
For more Mechanism of Action (Complete) data for 2-METHOXYETHANOL (16 total), please visit the HSDB record page.
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