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.
Ipriflavone Research review
Ipriflavone modulates IGF-I but is unable to restore
bone in rats.
Phytother Res. 2005. Deyhim F, Smith BJ, 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, Smith JR. 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 (IC50) 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 December. 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, Lee MG. College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Shinlim-Dong, Kwanak-Gu, Seoul, South Korea.