high purity API Pimecrolimus 137071-32-0 exporter CAS NO.137071-32-0

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Pimecrolimus is a topical immunomodulator. It is a semi-synthetic product of ascomycin produced by Streptomyces. It is more lipophilic than tacrolimus, has a stronger affinity with the skin, and can effectively and safely control facial fat 
The symptoms and signs of dermatitis can quickly alleviate the itching symptoms of patients with dermatitis and eczema, reduce the area of ??skin lesions, and clear the signs of atopic dermatitis (eczema). It is an effective treatment for early relief and long-term control of atopic dermatitis (eczema). 
Seborrheic dermatitis is an inflammatory immune response of the body to lipophilic Malassezia. Both humoral and cellular immunity are involved in the pathogenesis. Pimecrolimus can inhibit the calcium-dependent nerves required to activate T cells. 
Transcribe proteins to selectively inhibit the activation of T cells, prevent the release of cytokines and pro-inflammatory mediators, and exhibit strong anti-inflammatory activity. 
Therefore, it is speculated that the mechanism of pimecrolimus in the treatment of seborrheic dermatitis is anti-inflammatory and immune regulation. There is no report that can directly participate in the antifungal effect, but in recent years, there have been reports in Chemicalbook that tacrolimus (a kind of 
Immunomodulators with similar chemical structure and mechanism of action) have activity against certain Malassezia species. 
Similar to tacrolimus, pimecrolimus is a cell-selective inhibitor of proinflammatory cytokine production and release. It can bind to macrophilin12 (FKBP-12) to inhibit calcium-dependent calcineurin. 
Blocking early cytokine transcription of T cells and inhibiting T cell activation, especially at the nanogram level can inhibit the synthesis of IL-2 and IFN-γ (Th1 cells) of T cells, and inhibit IL-4 and IL- 
10 (Th2 cell source) synthesis. 
In addition, in in vitro experiments, pimecrolimus can also inhibit the release of inflammatory cytokines and inflammatory mediators from antigen or IgE-stimulated mast cells [4,5]. 
Clinical data show that the blood drug concentration after topical application is very low, generally below the detected value (<0.5ng/mL). 
No accumulation of drugs.