Ipriflavone is an isoflavone which has been studied for its potential in alleviating osteoporosis. At this time, there is no conclusive evidence that ipriflavone is effective for this purpose. To keep up with the latest research on ipriflavone and isoflavones, consider a free supplement research newsletter by email. There is a trademarked ipriflavone product called Ostivone.
Chromosone damage prevention
Food Chem Toxicol. 2014. Antimutagenic activity of ipriflavone against the DNA-damage induced by cyclophosphamide in mice. In the present study we evaluated the potential of ipriflavone against the cytotoxic and mutagenic effects induced by cyclophosphamide chemotherapeutic agent in bone marrow cells of mice, using the micronucleus assay in vivo on cells of bone marrow. The study was performed following three protocols: pre-treatment, simultaneous treatment and post treatment. The results demonstrated that ipriflavone has a protective effect against mutagenicity induced by cyclophosphamide in the pre-treatment and post-treatment and against the cytotoxicity in all treatments. There was variation between the genders in some of the experimental groups. To evaluate their possible mechanisms of action, it was performed the DPPH assay, which showed no ability to donate hydrogens, suggesting that it acts through other mechanisms. Due to its ability to prevent chromosomal damage, ipriflavone is likely to open an interest field concerning its possible the use in clinical applications.
Gynecol Endocrinology. 2010. Effects of ipriﬂavone on postmenopausal syndrome and osteoporosis. To investigate the therapeutic effects of ipriflavone on postmenopausal syndrome and osteoporosis in women. A randomized and double-blind study was conducted. Sixty postmenopausal women with osteoporosis were chosen and they were randomly divided into three groups: Treatment group I was given oral compound calcium acid chelate and Vitamin AD guttate; treatment group II was given oral compound calcium acid chelate, Vitamin AD guttate and ipriflavone; Control group was given placebo and compound calcium acid chelate. The postmenopausal syndrome, bone mineral density (BMD), and bone biochemical markers were assessed 6 and 12 months after the treatment. In treatment group II, hot flush and ostalgia syndromes were dramatically relieved, BMD and serum calcium level increased markedly and alkaline phosphatase, parathyroid hormone and tartrate-resistant acid phosphatase decreased markedly, comparing with treatment group I and control group. Ipriflavone could inhibit bone resorption and promote bone formation. It is an effective drug for the prevention and treatment to menopausal syndrome and osteoporosis.
Ipriflavone modulates IGF-I but is unable to restore bone in rats.
Phytother Res. 2005. Deyhim F, Soung do Y, Juma S, Devareddy L, Arjmandi BH. Department of Human Sciences, Texas A&M University, Kingsville, 78363
Previously it has been reported that ipriflavone can prevent bone loss in ovarian hormone deficient rats. The present study evaluated whether ipriflavone was able to restore bone mass in osteopenic ovariectomized rats. Seventy-two, 90 day-old Sprague-Dawley rats were divided into six groups (sham two groups; ovariectomized four groups). Thirty-five days from the date of surgery, one sham and one ovx group were killed to verify the occurrence of bone loss. The remaining four groups were sham, ovx, ovx + ipriflavone, or ovx + 17beta-estradiol for a period of 65 days. Ipriflavone was ineffective in restoring bone density and unlike estrogen did not prevent bone resorption as evidenced by increased urinary excretion of hydroxyproline and serum tartrate-resistant acid phosphatase activity. Ipriflavone increased the expression of IGF-I in the femur. These observations suggest that higher doses of ipriflavone or longer-term studies may be necessary to restore bone mass.
Inhibition of COX isoforms by nutraceuticals.
J Herb Pharmacother. 2004. Seaver B. University of Montana, Missoula, MT
Humans have two isoforms of Prostaglandin H Synthase or cyclooxygenase: COX-1 and COX-2. COX-1 is cytoprotective. COX-2 inhibitors reduce inflammation without the risk of ulceration and kidney damage. The ideal nutraceutical would inhibit COX-2 synthesis while preserving COX-1 synthesis. The hypothesis for this research was that COX inhibitors would fall primarily into three categories: COX-2 specific inhibition, non-specific inhibition (COX-1 and COX-2), and minimal inhibition. The human Cayman COX inhibitor screening assay was used to determine the inhibitory concentration 50 of COX-1/ COX-2 activity of each nutraceutical. Positive results were seen for ipriflavone, resveratrol, MSV-60, amentoflavone, ruscus extract and notoginseng. Glucosamine, nexrutine, and berberine did not inhibit either isoform.
Effects of ipriflavone on bone loss following a
bilateral ovariectomy and menopause: a randomized placebo-controlled study.
Calcif Tissue Int. 2001.
A randomized placebo controlled study was undertaken to evaluate the effect of ipriflavone against the bone loss in premenopausal ovariectomized women and postmenopausal women. Thirty-seven Japanese women who underwent premenopausal bilateral ovariectomy within 3 months (early stage group) and 52 Japanese women who were ovariectomized or who had undergone menopause more than 3 years before the start of the study (late stage group) were enrolled. The patients were randomly allocated into two groups: those who received ipriflavone (600 mg/day) and those who received placebo. The bone mineral density (BMD) of the lumbar vertebrae was measured by dual energy X-ray absorptiometry, and the markers of bone metabolism were measured at the same time that BMD was measured. In the early stage group, the ipriflavone group showed a 6.7% decrease in BMD from baseline levels, whereas the placebo group showed a 10.7% decrease at 12 months of treatment, and 7% and 12% decrease at 24 months of treatment, respectively. In the late stage group, there was a 0.3% increase in BMD in the ipriflavone group and a 2.3% decrease in the placebo group at 6 months of treatment, and similar changes were seen at 18 months (1.4% increase and 3.9% decrease. Ipriflavone suppressed bone loss compared with placebo, however, did not prevent acute bone loss in the early stage following ovariectomy. The effect of ipriflavone alone on bone loss in the early stage is not sufficient to reduce the risk of osteoporosis in later life.
Eur J Pharm Sci. 2009. Pharmacokinetics of ipriflavone and its two metabolites, M1 and M5, after the intravenous and oral administration of ipriflavone to rat model of diabetes mellitus induced by streptozotocin. Lee DY, Chung HJ, Choi YH, Lee U, Kim SH, Lee I. College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Shinlim-Dong, Kwanak-Gu, Seoul, South Korea.