C-Statin 120 Capsules
C-StatinTM is a naturally occurring plant extract, contains a patented proteoglycan molecule (PGM) from field bindweed that is a potent angiogenesis inhibitor. Studies have demonstrated PGM to be 100 times stronger than shark cartilage. Used and recommended by healthcare professionals around the world.
- Product Literature
C-Statin capsules are an all-natural nutritional supplement proven to support normal angiogenesis.† Angiogenesis is the process which promotes the formation of new blood vessels. The recruitment of new blood vessels plays a crucial role in abnormal cell growth and survival.
C-Statin contains a proprietary extract of bindweed, comprised of proteoglycan molecules (PGMs) and has no recorded adverse side effects. PGMs have been demonstrated to have significant anti-angiogenic and immunostimulatory effects.† C-Statin has been shown to inhibit new blood vessel growth up to 73% and abnormal cell growth up to 96.8%.1 This product is commonly used with Imm-Kine.
Caution: If you are pregnant or lactating, if you are recovering from a recent surgery, or have a heart or circulatory condition consult a licensed medical professional before using this product.
†The above statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure, or prevent any disease and results may vary.
ANTI-ANGIOGENIC, ANTI-TUMOR AND IMMUNOSTIMULATORY EFFECTS OF A NON-TOXIC PLANT EXTRACT (PGM)
Authors: Riordan NH, Meng X, Riordan HD.
ABSTRACT: Recruitment of new blood vessels plays a crucial role in tumor survival and growth. Several agents that act as angiogenesis inhibitors are currently being investigated as anti-tumor agents. Proteoglycan extract (PGM) was tested for anti-angiogenic, immunostimulatory, and anti-neoplastic activity. PGM is a non-toxic extract of the ubiquitous plant, Convolvulus arvensis. In the chicken egg chorioallantoic membrane assay PGM inhibited new blood vessel growth in a dose-dependent manner. Results were 18, 55, and 73% inhibition at concentrations of 50, 100, and 200 mcg, respectively. PGM significantly inhibited tumor growth in the mouse fibrosarcoma (S-180 Kun Ming 3-4 wk old mixed male/female, 10 animals per group, 250-1000 mcg daily doses for 14 days), and mouse Lewis lung carcinoma (C57, 6 wk old mixed male/female, 10 animals per group, 250-1000 mcg daily doses for 14 days) models. Inhibition (54-77% inhibition by weight compared to controls, up to 96.8% by cellular composition) occurred regardless of route of administration: intravenous; intraperitoneal; subcutaneous; and oral. PGM induced lymphocyte growth in a dose dependent manner. The ability of PGM-treated phagocytes to phagocytose yeast cells was 85% greater than controls. We conclude that PGM is a potent angiogenesis inhibitor that has immunostimulatory activity in vitro and anti-tumor activity in vivo and that PGM should be studied further as an anti-neoplastic agent.