1. 2-amino-2-(2-(4-octylphenyl)ethyl)-1,3-propanediol Hydrochloride
2. Fingolimod Hydrochloride
3. Fty 720
4. Fty-720
5. Fty720
6. Gilenia
7. Gilenya
1. 162359-55-9
2. 2-amino-2-[2-(4-octylphenyl)ethyl]propane-1,3-diol
3. 2-amino-2-(4-octylphenethyl)propane-1,3-diol
4. Fty-720
5. Fingolimod [inn]
6. 2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol
7. 2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propandiol
8. 1,3-propanediol, 2-amino-2-[2-(4-octylphenyl)ethyl]-
9. Gilenya (tn)
10. 3qn8byn5qf
11. 1,3-propanediol, 2-amino-2-(2-(4-octylphenyl)ethyl)-
12. Chembl314854
13. Chebi:63115
14. Fingolimod (inn)
15. 2-amino-2-(2-(4-octylphenyl)ethyl)propane-1,3-diol
16. Fty-720a
17. Unii-3qn8byn5qf
18. 2-amino-2-(2-(4-octylphenyl)ethyl)-1,3-propanediol
19. Fingolimodum
20. Fingolimod Base
21. Fingolimod- Bio-x
22. Fingolimod [mi]
23. Fingolimod [vandf]
24. Fingolimod [mart.]
25. Schembl7445
26. Fingolimod [who-dd]
27. 2-(4-octylphenylethyl)-2-aminopropane-1,3-diol
28. Gtpl2407
29. Fingolimod [orange Book]
30. Dtxsid40167363
31. Hms3743o13
32. Amy22173
33. Bcp05969
34. Zinc1542002
35. Bdbm50158336
36. Nsc755643
37. S5950
38. Stl445699
39. Akos015999594
40. Db05286
41. Db08868
42. Nsc-755643
43. Ncgc00188399-01
44. Ncgc00188399-03
45. Ncgc00188399-04
46. Ncgc00188399-06
47. Ncgc00188399-16
48. Ac-25899
49. As-68987
50. Bf164460
51. Hy-11063
52. Db-064455
53. Ft-0660847
54. 2-(4-octylphenethyl)-2-aminopropane-1,3-diol
55. D70458
56. 2-amino-2-(4-octylphenyl)ethylpropane-1,3-diol
57. Q425137
58. 2-amino-2-hydroxymethyl-4-(4-(octyl)phenyl)butanol
59. Brd-k88025533-003-01-7
60. 2-amino-2-[2-(4-octyl-phenyl)-ethyl]-propane-1,3-diol
| Molecular Weight | 307.5 g/mol |
|---|---|
| Molecular Formula | C19H33NO2 |
| XLogP3 | 4.2 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 12 |
| Exact Mass | 307.251129295 g/mol |
| Monoisotopic Mass | 307.251129295 g/mol |
| Topological Polar Surface Area | 66.5 Ų |
| Heavy Atom Count | 22 |
| Formal Charge | 0 |
| Complexity | 258 |
| 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 |
Fingolimod is indicated for the treatment of patients aged 10 and above with relapsing forms of multiple sclerosis, which may include clinically isolated syndrome, relapsing-remitting disease, as well as active secondary progressive disease. This drug is being studied for administration in patients infected with COVID-19 with a high risk for acute respiratory distress syndrome, or ARDS. As of April 3 2020, this is currently not an approved indication and clinical trials are underway.
Gilenya is indicated as single disease modifying therapy in highly active relapsing remitting multiple sclerosis for the following groups of adult patients and paediatric patients aged 10 years and older:
- Patients with highly active disease despite a full and adequate course of treatment with at least one disease modifying therapy (for exceptions and information about washout periods see sections 4. 4 and 5. 1).
or
- Patients with rapidly evolving severe relapsing remitting multiple sclerosis defined by 2 or more disabling relapses in one year, and with 1 or more Gadolinium enhancing lesions on brain MRI or a significant increase in T2 lesion load as compared to a previous recent MRI.
Indicated as single disease modifying therapy in highly active relapsing remitting multiple sclerosis for the following groups of adult patients and paediatric patients aged 10 years and older:
Patients with highly active disease despite a full and adequate course of treatment with at least one disease modifying therapy
or
Patients with rapidly evolving severe relapsing remitting multiple sclerosis defined by 2 or more disabling relapses in one year, and with 1 or more Gadolinium enhancing lesions on brain MRI or a significant increase in T2 lesion load as compared to a previous recent MRI.
Indicated as single disease modifying therapy in highly active relapsing remitting multiple sclerosis for the following groups of adult and paediatric patients aged 10 years and older:
Patients with highly active disease despite a full and adequate course of treatment with at least one disease modifying therapy (for exceptions and information about washout periods see sections 4. 4 and 5. 1)
or
Patients with rapidly evolving severe relapsing remitting multiple sclerosis defined by 2 or more disabling relapses in one year, and with 1 or more Gadolinium enhancing lesions on brain MRI or a significant increase in T2 lesion load as compared to a previous recent MRI.
In multiple sclerosis, fingolimod binds to sphingosine receptors, reducing its associated neuroinflammation.In COVID-19, it may reduce lung inflammation and improve the clinical outcomes of patients with this disease. Cardiovascular effects Fingolimod causes a transient reduction in heart rate and AV conduction during treatment initiation. It has the potential to prolong the QT interval.
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.)
Sphingosine 1 Phosphate Receptor Modulators
Agents that affect the function of G-protein coupled SPHINGOSINE 1-PHOSPHATE RECEPTORS. Their binding to the receptors blocks lymphocyte migration and are often used as IMMUNOSUPPRESSANTS. (See all compounds classified as Sphingosine 1 Phosphate Receptor Modulators.)
L04AA27
L04AA27
L04AA27
L04AA27
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
L - Antineoplastic and immunomodulating agents
L04 - Immunosuppressants
L04A - Immunosuppressants
L04AA - Selective immunosuppressants
L04AA27 - Fingolimod
Absorption
Fingolimod is slowly but efficiently absorbed in the gastrointestinal tract. AUC varies greatly, depending on the patient, and pharmacokinetic studies demonstrate a range of AUC values for fingolimod. The Tmax of fingolimod ranges between 12-16 hours and its bioavailability is 90-93%. Steady-state concentrations of fingolimod are achieved within 1-2 months after initiation when it is administered in a single daily dose.
Route of Elimination
About 81% of an oral dose of fingolimod is excreted in the urine in the form of inactive metabolites. Intact fingolimod and its active metabolite account for less than 2.5% of the dose, and can be found excreted in the feces.
Volume of Distribution
The volume of distribution of fingolimod is about 1200260 L. It is approximately 86% distributed in the red blood cells (RBC).
Clearance
Fingolimod blood clearance is 6.32.3 L/h, according to prescribing information. Another resource mentions it ranges from 6-8 L/h.
Sphingosine kinase metabolizes fingolimod to an active metabolite, fingolimod phosphate. Fingolimod metabolism occurs via 3 major metabolic pathways: firstly, phosphorylation of the (S)-enantiomer of fingolimod-phosphate (pharmacologically active), secondly, oxidation by cytochrome P450 4F2 (CYP4F2), and thirdly, fatty acid-like metabolism to various inactive metabolites. The formation of inactive non-polar ceramide analogs of fingolimod also occurs during its metabolism.
The half-life of fingolimod and its active metabolite ranges from 6-9 days.
Sphingosine1phosphate (S1P) is an important phospholipid that binds to various Gproteincoupled receptor subtypes, which can be identified as S1P15R. S1P and the receptors it binds to perform regular functions in the immune, cardiovascular, pulmonary, and nervous system. S1P can be expressed ubiquitously, playing an important role in regulating inflammation. S1P1R, S1P2R, and S1P3R receptors can be found in the cardiovascular, immune, and central nervous systems. S1P4R is found on lymphocytic and hematopoietic cells, while S1P5R expression is found only on the spleen (on natural killer cells) or in the central nervous system. The active form of the drug, fingolimod phosphate, is a sphingosine 1-phosphate receptor modulator that exerts its mechanism of action in MS by binding to various sphingosine 1-phosphate receptors (1, 3, 4, and 5). It suppresses the exit of lymphocytes from lymph nodes, leading to a lower level of lymphocytes circulating in peripheral circulation. This reduces the inflammation that is associated with MS. The mechanism of action of fingolimod is not fully understood, but may be related to reduced lymphocyte circulation into the central nervous system. Immune modulating treatment such as fingolimod is not typically employed for SARS-CoV-2 pneumonia. Despite this, with the tissue findings of pulmonary edema and hyaline membrane formation, the timely use of immune modulators such as fingolimod can be considered to prevent acute respiratory distress syndrome (ARDS) associated with COVID-19.
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