IP(6) - Inositol Hexaphosphate - phytic acid - is found in bran, seeds, legumes & nuts to varying degrees. In supplement form, it probably comes from rice bran.
IP(6) is a store of phosphorus in plants. Ruminants produce the enzyme phytase, which releases the phosphorus. Elsewhere, I write about the importance of limiting phosphorus intake, which inhibits conversion of hormonally active vitamin D. We do not want to liberate the phosphorus of IP(6), but gut bacteria may produce some phytase - perhaps more so in vegetarians.
Phytic acid is classed as an antinutrient. This is because it binds to minerals. When used as a supplement, IP(6) should not be taken with food, as it will bind to minerals in the meal & they will not be absorbed.
 PCa Cell & Mice Studies (oldest first).
[2a] Shamsuddin is the man behind "IP-6 Gold". He patented a ratio of (Inositol Hexaphosphate):(Inositol) = 22:80. [2a1] Competing supplements have to avoid combining the two in anything like that ratio.
Source Natural sells IP-6 powder (400 g) with a dose of 1.5 tsp = 3.7g [2a2], & they also sell Inositol powder (16 oz) with a dose of 0.25 tsp = 845 mg [2a3]. It's cute that one is packaged in grams & the other in ounces, & doses are given in g & mg, but I think the intent is clear. If they had used an IP-6 dose of 1.25 tsp, rather than 1.5 tsp, the ratio would be almost identical to Shamsuddin's.
(Look in Amazon for cheaper options.)
At those weights, the powder lasts forever. I measure, mix in water, & swallow while my 5 a.m. coffee is brewing. It has no taste to speak of. Wait at least an hour before eating.
<Shamsuddin "Inositol Hexaphosphate"> gets 35 hits on PubMed, for those interested in his non-PCa IP(6) papers. The studies span ten years & stopped ten years ago.
[2a4] (1995 - U.S. - Shamsuddin)
"Inositol hexaphosphate inhibits growth and induces differentiation of PC-3 human prostate cancer cells."
[2b] Agarwal (Colorado) has done most of the research on IP(6) & PCa. Twelve PubMed papers (2000-2013). Some are too technical to comment on here, but links are provided for [2b1] through [2b12], below signature. Some extracts follow.
[2b4] "Our results suggest that IP6 could be a potent dietary agent in controlling the growth of advanced PCA cells and inducing their apoptotic death, in part, by its inhibitory effect on constitutively active NF-kappa B signaling pathway."
[2b5] (Mouse study) "IP6 suppresses hormone-refractory PCA growth accompanied by inhibition of tumor cell proliferation and angiogenesis and increased apoptosis. IP6-caused increase in IGFBP-3 and decrease in VEGF might have a role in PCA growth control."
IGFBP-3 is the major binding protein for IGF-I (insulin-like growth factor I) & is down-regulated by PCa. It reduces free IGF-I (a good thing). VEGF is the growth factor for new blood vessels, so a decrease is a good thing too.
[2b7] A full-text review paper.
[2b12] "Constitutive activation of ... (PI3K)-Akt pathway transmits growth-regulatory signals that play a central role in promoting survival, proliferation, and angiogenesis in human prostate cancer cells. Here, we assessed the efficacy of inositol hexaphosphate (IP6) against invasive human prostate cancer PC-3 and C4-2B cells and regulation of PI3K-Akt pathway. IP6 treatment of cells suppressed proliferation, induced apoptosis along with caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and inhibited constitutive activation of Akt and its upstream regulators PI3K ... "
"These findings suggest that, by targeting the PI3K-ILK1-Akt pathway, IP6 suppresses cell survival, proliferation, and angiogenesis but induces death in prostate cancer cells, which might have translational potential in preventing and controlling the growth of advanced and aggressive prostate cancer for which conventional chemotherapy is not effective."
[2c] Other PCa studies.
[2c1] "Inositol hexaphosphate represses telomerase activity and translocates TERT from the nucleus in mouse and human prostate cancer cells via the deactivation of Akt and PKCalpha."
"Since the activation of telomerase is crucial for cells to gain immortality and proliferation ability, we examined the role of IP6 in the regulation of telomerase activity in prostate cancer cells. Here, we show that IP6 represses telomerase activity in mouse and human prostate cancer cells dose-dependently."
The telomere is a primitive counter. It shortens with each cell division. This limits the number of times a cell can divide (Hayflick limit). PCa restores telomerase, which prevents the shortening of the telomere. IP(6) inhibits telomerase.
[2c2] (2014 - China) Seems to verify upregulation of IGFBP-3.