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| Inositol is a form of sugar your body needs to grow. myo-inositol is a sugar alcohol and a glucose isomer found in many food including grains and fruits. Inositol — Inositol is a naturally occurring six-carbon cyclitol (sugar alcohol-like carbohydrate), with myo-inositol being the predominant biologically active stereoisomer in humans and the form most commonly used as an oral supplement. It is formally classified as a nutrient/metabolic signaling molecule rather than an established anticancer drug; common abbreviations include MI, myo-Ins, and Ins. Myo-inositol is obtained from foods and is also synthesized endogenously from glucose-6-phosphate through ISYNA1-dependent metabolism. It is a precursor for phosphatidylinositol and phosphoinositide second-messenger systems. Myo-inositol should be distinguished from inositol hexaphosphate (IP6/phytic acid), which has substantially more preclinical anticancer literature and is listed separately in this database. Primary mechanisms (ranked):
Bioavailability / PK relevance: Myo-inositol is orally absorbed through sodium-dependent inositol transport systems, with human serum concentrations peaking approximately 1.5–3 hours after oral administration. A 100 mg/kg oral dose produced an estimated peak serum concentration of about 100 µM in a small human kinetic study. Bioavailability varies with formulation and can be reduced by competing D-chiro-inositol and some sugars/transporter substrates. Renal elimination is important. High-dose oncology studies have used approximately 18 g/day; gastrointestinal intolerance becomes dose-limiting at higher doses. In-vitro vs systemic exposure relevance: Exposure is concentration-driven. A recent DU-145 prostate-cancer study reported an approximate myo-inositol IC50 of 0.06 mg/mL after 72 hours, equivalent to about 330 µM; this is several-fold above the approximately 100 µM peak serum concentration observed after a 100 mg/kg oral human dose, although substantially higher oral doses have been used clinically. Some mechanistic experiments use still higher concentrations, so direct systemic translation of in-vitro cytotoxicity should be interpreted cautiously. Chemopreventive and signaling effects may occur below directly cytotoxic concentrations. Clinical evidence status: RCT-level chemoprevention evidence but no demonstrated anticancer efficacy. A randomized double-blind phase IIb trial used myo-inositol 9 g twice daily for six months in smokers with bronchial dysplasia. It did not significantly improve the primary dysplasia-response endpoint versus placebo, although BAL IL-6 decreased and responders showed reduced airway PI3K-activation signatures. Earlier phase I work established approximately 18 g/day as a tolerated dose and suggested lesion-regression activity. Myo-inositol is therefore best classified as an experimental chemopreventive/metabolic adjunct rather than an established cancer treatment. Inositol Cancer-Relevant Mechanisms
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| Source: HalifaxProj(inhibit) |
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| Cyclooxygenase-2 (COX-2) is an enzyme that plays a critical role in the conversion of arachidonic acid to prostaglandins, which are lipid compounds involved in various physiological processes, including inflammation, pain, and fever. COX-2 is an inducible enzyme, meaning its expression is typically low in normal tissues but can be upregulated in response to inflammatory stimuli, growth factors, and certain oncogenic signals. -Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis. -COX-2 is an inducible enzyme that is upregulated in response to pro-inflammatory signals, including cytokines (e.g., IL-1β, TNF-α) and growth factors. COX-2 is often overexpressed in various tumors, including colorectal, breast, lung, and prostate cancers. The prostaglandins produced by COX-2, particularly prostaglandin E2 (PGE2), have several effects that can facilitate cancer progression: Cell Proliferation: PGE2 can promote the proliferation of cancer cells by activating signaling pathways such as the PI3K/Akt and MAPK pathways. Nonselective NSAIDs, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. Epidemiological studies have suggested that regular use of NSAIDs may reduce the risk of certain cancers, particularly colorectal cancer. Drugs specifically targeting COX-2, such as celecoxib, have been developed. COX-2 and xanthine oxidase are ROS-producing pro-oxidant enzymes that contribute to inflammation. Elevated COX‑2 levels, often found in inflammatory conditions or certain types of cancers, can contribute to increased production of ROS. |
| 7631- | Ins, | IP6, | Broad Spectrum Anticancer Activity of Myo-Inositol and Inositol Hexakisphosphate |
| - | Review, | Var, | NA |
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
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