LGM Pharma is an API distributor. LGM Pharma can supply CGMP and/or DMF products, subject to availability and manufacturer requirements. LGM Pharma does not sell or supply APIs or finished dosage products to individual patients, doctors, pharmacies, or any pharmaceutical companies.
Questions? Call our customer API support number 1-(800)-881-8210
Fingolimod is metabolized by sphingosine kinase to the active metabolite, fingolimod-phosphate. Fingolimod-phosphate is a sphingosine 1-phosphate receptor modulator, and binds with high affinity to sphingosine 1-phosphate receptors 1, 3, 4, and 5. Fingolimod-phosphate blocks the capacity of lymphocytes to egress from lymph nodes, reducing the number of lymphocytes in peripheral blood. The mechanism by which fingolimod exerts therapeutic effects in multiple sclerosis is unknown, but may involve reduction of lymphocyte migration into the central nervous system.
Fingolimod causes a transient reduction in heart rate and AV conduction at treatment initiation. Potential to prolong the QT interval. Effects on immune cell numbers in the blood- decreased lymphocyte counts. Mild decrease in the neutrophil count- about 80% of original pre-therapy count. Compared to placebo, antigen-specific IgM titers were decreased by 91% and 25% in response to KLH and PPV, respectively. IgG titers were decreased by 45% and 50%, in response to KLH and PPV. The capacity to mount a skin delayed-type hypersensitivity reaction to Candida and tetanus toxoid was decreased by approximately 30% in subjects on fingolimod 0.5 mg daily, compared to placebo. Immunologic responses were further decreased with fingolimod 1.25 mg (a dose higher than recommended for MS). Single fingolimod doses ≥5 mg (10-fold the recommended dose) are associated with a dose-dependent increase in airway resistance.
3 main pathways: -reversible stereoselective phosphorylation to the pharmacologically active (S)-enantiomer of fingolimod-phosphate. -oxidative biotransformation mainly via the cytochrome P450 4F2 isoenzyme and subsequent fatty acid-like degradation to inactive metabolites. -by formation of pharmacologically inactive non-polar ceramide analogs of fingolimod.
Bradyarrhythmia and Atrioventricular Blocks Risk of infections Macular Edema Respiratory Effects Hepatic Effects
Fetal Risk Blood Pressure Effects Immune System Effects Following Fingolimod Discontinuation
1. An X, Kezuka T, Usui Y, Matsunaga Y, Matsuda R, Yamakawa N, Goto H: Suppression of experimental autoimmune optic neuritis by the novel agent fingolimod. J Neuroophthalmol. 2013 Jun;33(2):143-8. doi: 10.1097/WNO.0b013e31828ea2fc. [PubMed:23609767]
2. Ali R, Nicholas RS, Muraro PA: Drugs in development for relapsing multiple sclerosis. Drugs. 2013 May;73(7):625-50. doi: 10.1007/s40265-013-0030-6. [PubMed:23609782]
Products currently covered by valid US Patents are offered for R&D use in accordance with 35 USC 271(e)+A13(1). Any patent infringement and resulting liability is solely at buyer risk.
LGM currently offers Monoclonal Antibodies (mAbs) for non-GMP/R&D use. Please inquire about Monoclonal Antibodies produced under GMP conditions.
Questions? Call our customer API support number 1-(800)-881-8210.
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