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雷帕鸣在国内上市没?

Author: Medicalhalo
Release time: 2025-10-19 11:44:20

A drug manufactured by Pfizer of the United States, Rapamin-Sirolimus Oral Solution is a new generation of immunosuppressant following the advent of cyclosporine A, mycophenolate mofetil and tacrolimus. It was launched in the United States and Europe in 1999 and in China at the end of 2003. Because it has low nephrotoxicity, it can maintain long-term stability of renal function, and it can also reduce the incidence of tumors in transplant patients while suppressing immunity.  

Rapamin oral liquid is suitable for patients undergoing kidney transplantation to prevent organ rejection. Clinical recommendations include the combined use of rapamycin with cyclosporine and corticosteroids. This medicine should be started as soon as possible after transplantation. For new transplant recipients, the loading dose of this drug should be taken, which is 3 times the maintenance dose. The recommended loading dose for kidney transplant patients is 6 mg and the maintenance dose is 2 mg/day. Although the loading dose of 15 mg and the maintenance dose of 5 mg/day used in clinical trials are satisfactory, the therapeutic benefit of doses above 2 mg is unclear for kidney transplant patients. Patients who take 2 mg of this drug daily have better overall safety than those who take 5 mg of this drug every day. To minimize differences in the absorption of this drug, this drug should be taken regularly with or without food. 

Through a completely different mechanism of action from other immunosuppressants, it inhibits the activation and proliferation of T lymphocytes stimulated by antigens and cytokines (interleukins IL-2, IL-4 and IL-15). Sirolimus also inhibits antibody production. In cells, sirolimus binds to the immunophilin FK-binding protein-12 (FKBP-12) to generate an immunosuppressive complex. This sirolimus FKBP-12 complex has no effect on calcineurin activity. This complex binds to the mammalian sirolimus target molecule (mTOR, a key regulatory kinase) and inhibits its activity. This inhibition blocks cytokine-driven T cell proliferation, that is, inhibits the progression from the G1 phase to the S phase of the cell cycle.

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