| Features: | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Vitamin like substance. Found in cereals, nuts and legumes. Inositol hexaphosphate (IP6) is a dietary component that constitutes approximately 1 to 5% of the weight of most cereals, nuts, oil seeds, legumes, and grains [1, 2]. In particular, approximately 9.5 to 14.5% of the weight of rice bran is composed of IP6. IP6 (inositol hexaphosphate) — also called myo-inositol hexakisphosphate, InsP6, phytic acid, or phytate, is a naturally occurring highly phosphorylated inositol carbohydrate abundant in cereal grains, legumes, nuts, seeds, and rice bran and also present at lower concentrations in mammalian cells. It is formally classified as a dietary phytochemical / polyphosphorylated inositol and is marketed as a dietary supplement rather than an approved anticancer drug. Standard abbreviations include IP6 and InsP6. Its unusually high negative charge gives it strong multivalent-cation binding properties, particularly toward iron, zinc, calcium, and magnesium. Experimental anticancer effects are broad but predominantly preclinical, and the extracellular millimolar concentrations commonly used in cancer-cell experiments are far above measured circulating human concentrations. Primary mechanisms (ranked):
Bioavailability / PK relevance: Oral IP6 is measurably absorbed in humans but systemic exposure is very low. Human studies report basal plasma concentrations around 0.07 mg/L during an IP6-poor diet and approximately 0.26 mg/L during a normal IP6-containing diet, with a plasma maximum occurring roughly 4 hours after an oral dose. IP6 is highly charged, undergoes gastrointestinal interactions with minerals, and can be dephosphorylated to lower inositol phosphates after uptake. Oral exposure therefore does not reproduce the extracellular millimolar concentrations commonly used in cell culture. In-vitro vs systemic exposure relevance: This is a major translational limitation. Many anticancer experiments use approximately 0.5–5 mM IP6, equivalent to roughly 330–3300 mg/L, whereas measured human plasma IP6 is typically well below 1 mg/L. Thus common in-vitro concentrations exceed measured circulating exposure by roughly three to four orders of magnitude. At millimolar concentrations IP6 also strongly chelates cations and can alter culture-medium chemistry, so some reported effects require cautious interpretation. Tissue uptake, local gastrointestinal exposure, and formation of lower inositol phosphates may nevertheless produce biological effects not predicted solely from plasma IP6 concentration. Clinical evidence status: Small human / adjunct use; not established anticancer therapy. The strongest cancer evidence remains cell-culture and animal work. Small randomized or prospective breast-cancer studies of IP6 with myo-inositol and/or topical IP6 during chemotherapy have reported better quality-of-life measures and attenuation of some treatment-associated hematologic or local symptoms, but these trials were small and were not adequate demonstrations of improved tumor response, progression-free survival, or overall survival. IP6 has no established regulatory approval for cancer treatment. A separate long-term oral IP6 study in superficial siderosis is registered but remains listed as not yet recruiting and does not establish efficacy. The principal practical safety constraint is mineral chelation: high phytate exposure can reduce iron and zinc absorption, particularly when nutritional status is marginal. Caution is also appropriate with significant iron deficiency and with anticoagulant therapy because antiplatelet effects have been reported. IP6 Cancer-Relevant Mechanisms
|
| Source: |
| Type: |
| Destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis. Mitochondria are organelles within eukaryotic cells that produce adenosine triphosphate (ATP), the main energy molecule used by the cell. For this reason, the mitochondrion is sometimes referred to as “the powerhouse of the cell”. Mitochondria produce ATP through process of cellular respiration—specifically, aerobic respiration, which requires oxygen. The citric acid cycle, or Krebs cycle, takes place in the mitochondria. The mitochondrial membrane potential is widely used in assessing mitochondrial function as it relates to the mitochondrial capacity of ATP generation by oxidative phosphorylation. The mitochondrial membrane potential is a reliable indicator of mitochondrial health. In cancer cells, ΔΨm is often decreased, which can lead to changes in cellular metabolism, increased glycolysis, increased reactive oxygen species (ROS) production, and altered cell death pathways. The membrane of malignant mitochondria is hyperpolarized (−220 mV) in comparison to their healthy counterparts (−160 mV), which facilitates the penetration of positively charged molecules to the cancer cells mitochondria. The MMP is a critical indicator of mitochondrial function, directly reflecting the organelle's capacity to generate ATP through oxidative phosphorylation. |
| 7724- | IP6, | Inositol hexakisphosphate blocks tumor cell growth by activating apoptotic machinery as well as by inhibiting the Akt/NFkappaB-mediated cell survival pathway |
| - | in-vitro, | Cerv, | HeLa |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:103 Target#:197 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid