Product Name:Fingolimod hydrochloride CAS:162359-56-0 MF:C19H34ClNO2 MW:343.93 EINECS:680-631-1 Mol File:162359-56-0.mol Melting point:102-107°C storage temp. -20°C Freezer solubility water: soluble10mg/mL, clear form powder color white to beige Merck 14,4083
Description Fingolimod hydrochloride is the first oral drug for the treatment of multiple sclerosis. It is successfully developed by the pharmaceutical company Novartis, and it has been approved for marketing by the US Food and Drug Administration (FDA). The recommended dose is 0.5mg once a day for oral administration. Multiple sclerosis is a debilitating neurological disease that can cause the patient to lose a sense of balance, appear muscle spasms and other movement disorders. The disease has been treated with injectable drugs. This kind of medication brought great inconvenience to patients. Fingolimod is a sphingosine-l-phosphate (S1PR) receptor modulator. After phosphorylation, It is bound to s1P receptor that is on the surface of lymphocyte, which will change lymphocyte migration, and promote cells into the lymphatic tissue, and prevent lymphocytes from leaving the lymphoid tissue and get into the graft. Thereby, it will prevent these cells from infiltrating the central nervous system (CNS), which achieves the effect of immunosuppression. According to the drug's introduction, drugmaker Novartis said that this process of pharmacological effects is reversible. If medication is stopped, the level of lymphocytes in circulating system will return to normal. The above information is edited by the chemicalbook of Kui Ming.
PHARMACOLOGIC INHIBITION OF ALDOSTERONE Cyclosporin, heparin sodium, and calcium channel blockers specifically inhibit aldosterone production from the zona glomerulosa. Cyclosporin blocks angiotensin II-induced aldosterone production and inhibits "growth" and steroidogenic capacity of adrenocortical cells.63 The latter effect may be caused by an impairment of protein synthesis. Additionally, cyclosporin and tacrolimus (FK506) inhibit MR transcription activity without affecting aldosterone binding.64 Polysulfated glycosaminoglycans, such as heparin sodium, impair aldosterone biosynthesis. With prolonged administration, heparin sodium can produce significant hypoaldosteronism with severe hyperkalemia65 .
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