Planta Med 2008; 74 - PC77
DOI: 10.1055/s-0028-1084595

Quantification of characteristic marker substances in various Cimicifuga racemosa products and evaluation of their effects on MCF-7 cell proliferation

MA Omer-Adam 1, H Zieg 1, RB Volk 1, C Bodinet 1, E Liske 2
  • 1Pharmaceutical Laboratories, Schaper & Brümmer GmbH Co. KG, Bahnhofstr. 35, D-38259 Salzgitter, Germany
  • 2International Medical Affairs, Schaper & Brümmer GmbH Co. KG, Bahnhofstr. 35, D-38259 Salzgitter, Germany

Cimicifuga racemosa (CR) as an alternative to hormone therapy is the most extensively studied medicinal herb used for the alleviation of menopausal symptoms. In the last two decades a considerable amount of investigations in research and clinic documented for the special isopropanolic CR rootstock extract (iCR, Remifemin®) significant efficacy and safety [1]. Up to now the active principle of CR is not fully understood, however, the two major groups of constituents, triterpene glycosides and polyphenolic compounds are under discussion, represented by actein respectively caffeic acid as well-established analytical marker substances. In this investigation iCR was compared with 5 US-marketed CR containing products regarding (i) their amounts of both marker substances per recommended daily dose and (ii) their effects on MCF-7 cell proliferation according to [2]. Using standard analytical methods for medicinal preparations, actein amounts ranging from 0 to 230µg (170µg for iCR) were determined. Polyphenolic compounds calculated as caffeic acid varied from 148 to 2198µg (148µg for iCR). In the MCF-7 assay none of the CR products stimulated the proliferation of human estrogen-receptor positive breast cancer cells.

The observed quantitative differences in the marker substances suggest product-specific variations in the spectrum of CR-constituents. Further investigations are necessary to clarify whether these are of relevance for clinical efficacy and safety, both already proven for iCR (Remifemin®). The MCF-7 results confirm that CR does not exert estrogen agonistic effects on breast tissue [2,3].

References: 1. Osmers, R. et al. (2005) Obstet. Gynocol. 105:1074–87.

2. Bodinet, C. et al. (2002) Breast Cancer Res. Treat. 76:1–10.

3. Linden-Hirschberg, A. et al. (2007) Menopause 14: 89–96.