Immunosuppression

(-)-Asarinin
Catalog No: CFN90144

Asarinin, a mammalian lignan precursor, has immunosuppression activity in vitro. Asarinin can decrease peripheral blood concentration of interleukin (IL)-12 and inhibit the expression of Toll-like receptor 4 (TLR4) and chemokine (C-X-C motif) receptor 3 (CXCR3), which means asarinin may have a role on TLR4 pathway and produced prolongation of allograft heart survival.

Solasodine
Catalog No: CFN90200

Solasodine has anticonvulsant, anti-oxidant, neuroprotection, and central nervous system depressant activities.Solasodine stimulates in situ neurogenesis from resident neuronal progenitors as part of neuron replacement therapy.

Cyclo(Phe-Pro)
Catalog No: CFN90271

Cyclo(Phe-Pro) inhibition of cholera toxin and toxin-coregulated pilus production correlated with reduced transcription of the virulence regulator tcpPH and was alleviated by overexpression of tcpPH.Cyclo(Phe-Pro) has been shown to inhibit cancer cell growth and induce apoptosis in HT-29 colon cancer cells.

Cimicifugoside
Catalog No: CFN90481

Cimicifugoside is a novel specific nucleoside transport inhibitor that displays synergistic potentiation of methotrexate cytotoxicity. Cimicifugoside shows immunosuppressive activity, which is preferentially directed toward B-cell function with larger doses being required for suppression of T-cell function. Cimicifugoside is also a phytoestrogen, it can selectively inhibit nicotinic acetylcholine receptor (nAChR) -mediated response in bovine chromaffin cells.

Kurarinone
Catalog No: CFN92003

Kurarinone exhibits anti-tumor, estrogenic, and anti-inflammatory activities, it also shows strong inhibitory effect on immune responses. Kurarinone may ameliorate chronic inflammatory skin diseases through the suppression of pathogenic CD4(+) T-cell differentiation and the overall immune response. Kurarinone sensitizes TNF-related apoptosis inducing ligand (TRAIL)-induced tumor cell apoptosis via suppression of NF-κB-dependent cFLIP expression; it may be by way of down-regulating Smad3 expression to interfere its induction on intercellular signal transduction and consequently ameliorate renal interstitial fibrosis.