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Chemistry

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Also known as: 2682-20-4, Methylisothiazolinone, 2-methylisothiazol-3(2h)-one, 2-methyl-3(2h)-isothiazolone, 2-methyl-4-isothiazoline-3-one, 3(2h)-isothiazolone, 2-methyl-
Molecular Formula
C4H5NOS
Molecular Weight
115.16  g/mol
InChI Key
BEGLCMHJXHIJLR-UHFFFAOYSA-N
FDA UNII
229D0E1QFA

2-Methyl-4-Isothiazolin-3-One
1 2D Structure

2-Methyl-4-Isothiazolin-3-One

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
2-methyl-1,2-thiazol-3-one
2.1.2 InChI
InChI=1S/C4H5NOS/c1-5-4(6)2-3-7-5/h2-3H,1H3
2.1.3 InChI Key
BEGLCMHJXHIJLR-UHFFFAOYSA-N
2.1.4 Canonical SMILES
CN1C(=O)C=CS1
2.2 Other Identifiers
2.2.1 UNII
229D0E1QFA
2.3 Synonyms
2.3.1 MeSH Synonyms

1. 2-methyl-4-isothiazolin-3-one Hydrochloride

2. 243-k-cg

3. Methyl-isothiazolinone

4. Methylisothiazolidinone

5. Methylisothiazolinone

6. Methylisothiazolone

7. N-methylisothiazolone

2.3.2 Depositor-Supplied Synonyms

1. 2682-20-4

2. Methylisothiazolinone

3. 2-methylisothiazol-3(2h)-one

4. 2-methyl-3(2h)-isothiazolone

5. 2-methyl-4-isothiazoline-3-one

6. 3(2h)-isothiazolone, 2-methyl-

7. 2-methyl-1,2-thiazol-3-one

8. N-methyl-3-oxodihydroisothiazole

9. 2-methyl-3-isothiazolone

10. 2-methyl-1,2-thiazol-3(2h)-one

11. N-methyl-3-oxodihydro Isothiazole

12. Mit

13. 229d0e1qfa

14. Chebi:53620

15. N-methylisothiazolin-3-one

16. 2682-20-4 (free Base)

17. Neolone

18. Caswell No. 572a

19. 2-methyl-2h-isothiazol-3-one

20. Microcare Mt

21. Kordek Mlx

22. Einecs 220-239-6

23. Mit (biocide)

24. Acticide M 10

25. Acticide M 20

26. Bestcide 600

27. Kordek 50

28. Kordek 50c

29. Kordek 573f

30. Kathon Cg 243

31. Unii-229d0e1qfa

32. Hsdb 8200

33. Mit 950

34. Mt 10

35. 2-methyl-4-isothiazoline-3-ketone

36. Kb 838

37. Mfcd01742315

38. 2-methyl-4-isothiazolin-3-one (mi)

39. 2-methyl-4-isothiazolinone

40. Dsstox_cid_14259

41. Dsstox_gsid_34259

42. Schembl17863

43. Schembl113898

44. Methylisothiazolinone Free Base

45. Chembl1620780

46. Dtxsid2034259

47. 2-methyl 4-isothiazoline 3-one

48. Methylisothiazolinone [ii]

49. Methylisothiazolinone [mi]

50. 2-methyl-3(2h)-isothiazolone #

51. Methylisothiazolinone [inci]

52. Zinc1849933

53. Methylisothiazolinone [vandf]

54. Tox21_303814

55. Bbl104136

56. Methylisothiazolinone [mart.]

57. Stl557951

58. Akos007930246

59. Am84857

60. Cs-w011236

61. Hy-w010520

62. 2-methyl-4-isothiazolin-3-one, 95%

63. Ncgc00357093-01

64. Cas-2682-20-4

65. Db-005250

66. Ft-0601044

67. F21330

68. 682m204

69. Q423870

70. 2-methyl-4-isothiazolin-3-one, Analytical Standard

71. W-107150

72. 2-methyl-4-isothiazolin-3-one, 50% Aqueous Solution

73. 2-methyl-4-isothiazolin-3-one 100 Microg/ml In Methanol

74. 2-methyl-4-isothiazolin-3-one 1000 Microg/ml In Methanol

75. 2-methyl-4-isothiazolin-3-one 100 Microg/ml In Acetonitrile

2.4 Create Date
2005-03-27
3 Chemical and Physical Properties
Molecular Weight 115.16 g/mol
Molecular Formula C4H5NOS
XLogP30
Hydrogen Bond Donor Count0
Hydrogen Bond Acceptor Count2
Rotatable Bond Count0
Exact Mass115.00918496 g/mol
Monoisotopic Mass115.00918496 g/mol
Topological Polar Surface Area45.6 Ų
Heavy Atom Count7
Formal Charge0
Complexity121
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 MeSH Pharmacological Classification

Disinfectants

Substances used on inanimate objects that destroy harmful microorganisms or inhibit their activity. Disinfectants are classed as complete, destroying SPORES as well as vegetative forms of microorganisms, or incomplete, destroying only vegetative forms of the organisms. They are distinguished from ANTISEPTICS, which are local anti-infective agents used on humans and other animals. (From Hawley's Condensed Chemical Dictionary, 11th ed) (See all compounds classified as Disinfectants.)


Anti-Infective Agents

Substances that prevent infectious agents or organisms from spreading or kill infectious agents in order to prevent the spread of infection. (See all compounds classified as Anti-Infective Agents.)


4.2 Mechanism of Action

Neurodegenerative disorders in humans may be triggered or exacerbated by exposure to occupational or environmental agents. ...a brief exposure to methylisothiazolinone, a widely used industrial and household biocide, is highly toxic to cultured neurons but not to glia. /The study/ also show that the toxic actions of this biocide are zinc dependent and require the activation of p44/42 extracellular signal-regulated kinase (ERK) via a 12-lipoxygenase-mediated pathway. The cell death process also involves activation of NADPH oxidase, generation of reactive oxygen species, DNA damage, and overactivation of poly(ADP-ribose) polymerase, all occurring downstream from ERK phosphorylation. The toxic effects of methylisothiazolinone and related biocides on neurons have not been reported previously. Because of their widespread use, the neurotoxic consequences of both acute and chronic human exposure to these toxins need to be evaluated.

PMID:12196562 Du S et al; J Neurosci 22 (17): 7408-16 (2002)


Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase (PTK) which acts as an early modulator in the integrin signaling cascade. FAK phosphorylation and its consequent activation regulate several basic biological cellular functions. On the contrary, dysregulation of FAK signaling is implicated in the malignant transformation of cells, as well as in nonmalignant pathological conditions. With respect to cytotoxicity, accumulating data indicate that FAK participates in the mechanism of action of the known cytotoxic reactive oxygen species (ROS). Additionally, evidence was presented that different cytotoxic substances, such as arsenic (As), lead (Pb), acrylamide, methylisothiazolinone (MIT), dichlorovinylcysteine (DCVC) and halothane, acted, at least in part, by downregulating FAK tyrosine phosphorylation, while the bacterial toxins Pasteurella multocida toxin and Escherichia coli cytotoxic necrotizing factor, have been shown to exert cytotoxic effects by inducing FAK tyrosine phosphorylation. The observation that upregulation as well as downregulation of FAK activity both result in cytotoxic effects seems contradictory. Even though a common mode of action, with respect to the dysregulation of FAK signaling, for these cytotoxic substances has not yet been discovered, a cumulative approach could be established by focusing on FAK activation and signaling cascade. According to these data, interfering with FAK signaling might be of a potential use in blocking these cytotoxic effects.

PMID:18215454 Chatzizacharias NA et al; Toxicology 245 (1-2): 1-10 (2008)


Methylisothiazolinone (MIT) is a biocide widely used in industrial and cosmetic products with potential as a neurotoxicant. /it was/ previously reported that short acute exposures to relatively high concentrations of MIT (100 uM) lead to widespread and selective neuronal death in vitro. To evaluate the biological properties of chronic exposures to MIT, freshly dissociated rat cortical neurons were continuously exposed to low concentrations (0.1-3 uM) of the biocide in serum-containing media. Although /this study/ observed minimal effects on cell viability, MIT induced a dramatic inhibition of neurite outgrowth. Immunoblotting and immunoprecipitation experiments revealed that focal adhesion kinase (FAK) phosphorylation was primarily affected by the MIT treatment. The phosphorylation level at tyrosines 576 and 861 of FAK was significantly decreased and likely contributed to the overall reduction of tyrosine phosphorylation of this protein. MIT inhibited Src family kinases (SFKs) in cell-free assays and led to the physical dissociation of FAK from the signaling complexes that it normally forms with c-Src and Fyn in developing neurons. High-density neuronal cultures were then employed to increase cell-to-cell contact. This approach resulted in an overall enhancement of SFKs and FAK phosphorylation and could overcome the deficits induced by MIT. This study suggests that a disruption of FAK-SFK complexes due to SFK inhibition leads to FAK dysfunction, with detrimental effects to immature neurons. Prolonged exposure to low levels of MIT and related compounds may have damaging consequences to the developing nervous system.

PMID:16547166 He K et al; J Pharmacol Exp Ther 317 (3): 1320-9 (2006)


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