product name Pimecrolimus
Description: Pimecrolimus (also known as ASM 981), like all ascomycins, is an immunophilin ligand, which binds specifically to the cytosolic receptor, immunophilin macrophilin-12. Pimecrolimus is a cell-selective inflammatory cytokines secretion inhibitor. Pimecrolimus inhibited the secretion of inflammatory cytokines in mast cells and T cells and also inhibited the release of preformed inflammatory mediators from mast cells. Pimecrolimus exhibited a low potential to impair systemic immune reactions in the skin. In peripheral blood leukocytes contained basophil or mast cells, pimecrolimus inhibited histamine release induced by anti-IgE from basophils and mast cells by 82% and 73%, respectively.
References: J Am Acad Dermatol. 2002 Feb;46(2):228-41; J Eur Acad Dermatol Venereol. 2003 Sep;17(5):493-503.
810.45
Formula
C43H68ClNO11
CAS No.
137071-32-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (123.4 mM)
Water: <1 mg/mL
Ethanol: 100 mg/mL (123.4 mM)
Solubility (In vivo)
Synonyms
ASM 981
other peoduct :
| In Vitro |
In vitro activity: Pimecrolimus blocks T-lymphocyte activation pathway by inhibiting calcineurin function. Pimecrolimus prevents the release of cytokines and pro-inflammatory mediators from mast cells. Pimecrolimus binds to macrophilin-12, the pimecrolimusmacrophilin complex then binds to the cytosolic enzyme calcineurin phosphatase. The pimecrolimus-macrophilin complex prevents the dephosphorylation of the cytoplasmic component of the nuclear factor of activated T cells by inhibiting the action of calcineurin. Pimecrolimus inhibits not only the transcription and synthesis of cytokines from mast cells, but also the release of preformed mediators serotonin and β-hexosaminidase by the inhibition of Fc∈-RI-mediated degranulation and secretion. Pimecrolimus treatment causes a strong down-regulation of the expression of mRNA for genes associated with the macrolactam target pathway and inflammation. Kinase Assay: Cell Assay: |
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| In Vivo | Pimecrolimus is found to be as effective as cyclosporine A following oral ingestion and slightly superior after subcutaneous administration in mice. Pimecrolimus contrasts cyclosporine A and tacrolimus by inhibiting ongoing secondary inflammatory response, but not impairing the primary immune response in allergic contact dermatitis in mice. Pimecrolimus is as effective as the high-potency corticosteroid clobetasol-17-propionate in a pig model of allergic contact dermatitis (ACD). Pimecrolimus also effectively reduces skin inflammation and pruritus in hypomagnesemic hairless rats, a model that mimics acute signs of atopic dermatitis. Pimecrolimus shows only a low potential to impair systemic immune responses when compared with tacrolimus as shown in rats in (1) the localized graft-versus-host reaction, (2) the antibody formation to sheep red blood cells, and (3) kidney transplantation. |
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| Formulation & Dosage | |
| References | J Am Acad Dermatol. 2002 Feb;46(2):228-41; J Eur Acad Dermatol Venereol. 2003 Sep;17(5):493-503; Semin Cutan Med Surg. 2001 Dec;20(4):233-41. |
