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1. Anethol Dithiolthione
2. Anetholetrithione
3. Anetholtrithion
4. Anetholtrithione
5. Anisyldithiolthionine
6. Dithiolthione, Anethol
7. Felviten
8. Heporal
9. Mucinol
10. Sialor
11. Sl 25
12. Sl-25
13. Sonicur
14. Sulfarlem
15. Sulfralem
16. Tiotrifar
17. Trithio
18. Trithioanethol
19. Trithione, Anethole
20. Trithioparamethoxyphenylpropene
1. 532-11-6
2. Anetholtrithion
3. 5-(4-methoxyphenyl)-3h-1,2-dithiole-3-thione
4. Sulfarlem
5. Tiopropen
6. Trithioanethole
7. Felviten
8. Heporal
9. Mucinol
10. Sulfogal
11. Tiotrifar
12. 3h-1,2-dithiole-3-thione, 5-(4-methoxyphenyl)-
13. 5-(4-methoxyphenyl)dithiole-3-thione
14. Anetholtrithion [jan]
15. Skf 1717
16. 3-(p-methoxyphenyl)trithione
17. Trithio-(p-methoxyphenyl)propene
18. 3h-1,2-dithiole-3-thione, 5-(p-methoxyphenyl)-
19. 5-(p-methoxyphenyl)-3h-1,2-dithiole-3-thione
20. Halpen
21. 5-(p-methoxyphenyl)-1,2-dithiocyclopenten-3-thione
22. Quy32964dj
23. Mfcd00129751
24. Op2113
25. Op-2113
26. Anetholtrithion (jan)
27. Ncgc00167471-01
28. Bilitherap
29. Sulfralem
30. 5-(4-methoxyphenyl)-1,2-dithiole-3-thione
31. Dsstox_cid_26651
32. Dsstox_rid_81795
33. Dsstox_gsid_46651
34. Trithio
35. Anetholetrithione
36. Cas-532-11-6
37. Ccris 6289
38. 3-(p-anisyl)trithione
39. Sr-05000001483
40. Einecs 208-528-5
41. Brn 0158393
42. Unii-quy32964dj
43. Sufralem
44. Anethol Trithion
45. Athenentol (tn)
46. Anetholdithiolthione
47. Anethole (trithione)
48. Anethol Trithione,(s)
49. Zinc949
50. 5-19-05-00546 (beilstein Handbook Reference)
51. Mls004774038
52. Schembl225654
53. Chembl178862
54. Anethole Trithione [mi]
55. Dtxsid9046651
56. Chebi:31221
57. Hms2089n08
58. Hms3715d09
59. Anethole Trithione [mart.]
60. Anethole Trithione [who-dd]
61. Bcp13800
62. Hy-b1223
63. Tox21_112475
64. S4744
65. Akos015920023
66. Tox21_112475_1
67. Ccg-207967
68. Cs-4781
69. Db13853
70. Gs-3613
71. Ncgc00167471-02
72. Smr001550561
73. Sy046610
74. Cis-9,10-methylenehexadecanoicacid
75. 5-(p-methoxyphenyl)-1,2-dithiole-3-thione
76. Ft-0602845
77. D01584
78. 5-(p-methoxyphenyl)-1,2-dithiol-3(3h)-thione
79. Ab01275477-01
80. 532a116
81. A829446
82. Q4761739
83. Sr-05000001483-1
84. Sr-05000001483-2
85. W-105762
86. Anetholtrithion, Anethole-trithione (anetholtrithion)
| Molecular Weight | 240.4 g/mol |
|---|---|
| Molecular Formula | C10H8OS3 |
| XLogP3 | 2.8 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 4 |
| Rotatable Bond Count | 2 |
| Exact Mass | 239.97372840 g/mol |
| Monoisotopic Mass | 239.97372840 g/mol |
| Topological Polar Surface Area | 91.9 Ų |
| Heavy Atom Count | 14 |
| Formal Charge | 0 |
| Complexity | 254 |
| 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 |
The most typical uses for which anethol trithione is currently indicated for includes increasing salivary secretion in patients experiencing dry mouth or being used as an adjunctive therapy for cholecystitis, gallstone, indigestion, and acute/chronic hepatitis. In addition, although some studies have suggested that anethol trithione also possesses a certain capacity to inhibit tumorigenesis as a potential cancer therapy medication, the specific mechanism of action for this effect remains to be elucidated with certain national cancer institutes listing the agent as 'a substance that is being studied in the treatment of cancer'.
Anethol trithione (ATT) possesses a high lipophilicity (log P = 3.8) but an extremely low water solubility (0.38 ug/mL), which limits its dissolution and absorption. Furthermore, ATT is quickly metabolized into 4-hydroxy-anethole trithione (ATX, which demonstrates a similar pharmacological activity to ATT) by way of O-demethylation. As a consequence, the plasma concentration of ATT is usually fairly low, resulting in a limited oral bioavailability as well. Given this pharmacodynamic profile, there is continued interest and study in developing vehicles with which ATT can be administered in larger availabilities into the body.
A16AX02
S76 | LUXPHARMA | Pharmaceuticals Marketed in Luxembourg | Pharmaceuticals marketed in Luxembourg, as published by d'Gesondheetskeess (CNS, la caisse nationale de sante, www.cns.lu), mapped by name to structures using CompTox by R. Singh et al. (in prep.). List downloaded from https://cns.public.lu/en/legislations/textes-coordonnes/liste-med-comm.html. Dataset DOI:10.5281/zenodo.4587355
A - Alimentary tract and metabolism
A16 - Other alimentary tract and metabolism products
A16A - Other alimentary tract and metabolism products
A16AX - Various alimentary tract and metabolism products
A16AX02 - Anethole trithione
Absorption
Although anethole trithione (ATT) has a high lipophilicity (log P = 3.8) and a high intestinal permeability, it has an extremely low water solubility (0.38 ug/ml). This low solubility limits ATT dissolution and bioavailability. Regardless, after ATT was administered to twenty-two healthy Chinese volunteers, the Cmax observed was about 0.98 +/- 0.49 ng/mL and the recorded Tmax was 2.2 +/- 1.9 h.
Route of Elimination
Despite the medication being studied and discussed as early as the 1980s, detailed pharmacokinetic information about it is not readily accessible and limited new pharmacokinetic data has only been determined for the drug for the first time only very recently (as recently as 2007).
Volume of Distribution
Despite the medication being studied and discussed as early as the 1980s, detailed pharmacokinetic information about it is not readily accessible and limited new pharmacokinetic data has only been determined for the drug for the first time only very recently (as recently as 2007). Nevertheless, the poor absorption and bioavailability of anethole trithione suggests any kind of volume of distribution measurement may not be entirely accurate.
Clearance
Despite the medication being studied and discussed as early as the 1980s, detailed pharmacokinetic information about it is not readily accessible and limited new pharmacokinetic data has only been determined for the drug for the first time only very recently (as recently as 2007). Regardless, data about the estimated clearance of anethole trithione in the rat model after administration of anethole trithione oral aqueous suspension was observed to be approximately 113.20 +/- 52.37 L/h/kg.
Anethole trithione (ATT) is metabolized rapidly into 4-hydroxy-anethole trithione via O-demethylation. This metabolite demonstrates similar pharmacological activities to its parent, ATT. It is proposed that such metabolism occurs in liver microsomes, although neither this proposal or by what specific hepatic cytochrome P450 isoform(s) are involved in such metabolism has been formally elucidated.
Despite the medication being studied and discussed as early as the 1980s, detailed pharmacokinetic information about it is not readily accessible and limited new pharmacokinetic data has only been determined for the drug for the first time only very recently (as recently as 2007). Consequently, after anethole trithione was administered to twenty-two healthy Chinese volunteers, the half-life observed was about 3.78 +/- 2.12 hours.
Epidemiological studies demonstrate that the prevalence of xerostomia and salivary gland hypofunction (SGH) rises with age, and is largely associated with medications and health. In particular, anethole trithione (ATT) is believed to cause an increase in salivary secretion by upregulating the number of muscarinic receptor (whose stimulation is known to increase salivary secretion) sites on the salivary acinar cells. Moreover, the combination use of ATT and pilocarpine is also thought to be effective in a synergistic manner - as ATT increases the number of cell surface receptors on salivary acinar cells, the pilocarpine, which is a parasympathetic agent, stimulates the newly formed receptors. In addition, studies have also shown that the administration of ATT can also enhance the upregulation and release of substance P and alpha-calcitonin gene-related peptide. As receptors for peptides like alpha-calcitonin gene-related peptide are found throughout the body, the increase in these such proteins may modulate a variety of physiological functions in various body systems, even in the gastrointestinal or salivary actions. Regardless, it has been shown that the use of ATT in patients can cause an increase in salivary flow rate in patients with xerostomia caused by senile hypofunction, medication side effects, and oral cancer therapy and has been indicated for use in treating xerostomia associated with conditions like Sjogren's syndrome. Nevertheless, there exist also studies that suggest ATT is generally only effective in managing the symptoms of mild salivary gland hypofunction but is not particularly useful for treating severe salivary gland hypofunction or severe cases of Sjogren's syndrome. ATT is also used as an adjunctive therapy for cholecystitis, gallstone, indigestion, and acute/chronic hepatitis in certain countries like France, Germany, and China. With regards to this particular indication, it is believed that ATT can facilitate raises in the level of glutathione in the liver, and raises in the activity of glutamylcysteine synthetase, glutathione reductase, and glutathione S transferase. All of these effects are consequently intimately involved in the cellular antioxidant activity of glutathione where glutamylcysteine synthetase is the first enzyme involved in the cellular glutathione biosynthesis pathway; where glutathione reductase is necessary for catalyzing the reduction of pathway intermediates to glutathione; and glutathione S transferase catalyze the conjugation of the reduced form of glutathione to xenobiotic substrates for the purpose of detoxification. Finally, glutathione itself is an important antioxidant found in plants, animals, fungi, and some bacteria where it assists in preventing damage to cellular components caused by reactive oxygen species, free radicals, etc. Taken altogether, these various actions are suitable for treating cholecystitis, gall stones, indigestion, and may be used in the assisting treatment of acute and chronic hepatosis. Although the specific mechanism of action for which ATT is seemingly capable of inhibiting tumorigenesis to a certain degree remains to be elucidated, some potential plausible mechanisms have been discussed. One such potential mechanism suggests that ATT has the capability to alter the metabolism of carcinogens by increasing the rate of detoxification of carcinogens in target organs like the liver and colon, thereby decreasing the generation of carcinogen metabolites and reducing parent-carcinogen induced carcinogenesis by way of those agents. And finally, a second potential mechanism proposes that ATT can strikingly increase the antioxidant activities of colonic and liver GST, NAD(P)H:QR, and UDP-GT, therefore eliciting a chemoprotective action.
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