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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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| SREBP1 is a key transcription factor that regulates genes involved in fatty acid and triglyceride synthesis. It primarily governs lipid metabolism by controlling the expression of enzymes required for de novo lipogenesis, such as fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACC), among others. Two main isoforms—SREBP1a and SREBP1c—with SREBP1c being more involved in the regulation of lipogenesis in metabolic tissues. Many cancers display elevated levels of SREBP1 activity. Increased expression or activation of SREBP1 supports the metabolic reprogramming that is characteristic of cancer cells, enabling them to meet the enhanced lipid requirements for membrane synthesis and energy storage during rapid cell proliferation. Elevated SREBP1 activity is often linked to more aggressive cancer phenotypes. High SREBP1 levels can drive rapid proliferation, metastasis, and resistance to certain therapies, thereby correlating with poorer clinical outcomes in several cancers. SREBF1 - Sterol Regulatory Element-Binding Transcription Factor 1 / SREBP-1 Abbreviation: SREBF1, SREBP-1, SREBP1 Type: Lipogenic transcription factor / basic helix-loop-helix leucine zipper transcription factor Function: SREBF1 encodes SREBP-1, a master regulator of fatty-acid synthesis, lipid homeostasis, and metabolic gene expression. SREBP-1 is synthesized as an inactive endoplasmic-reticulum membrane precursor and, following SCAP-dependent processing and proteolytic cleavage, its active N-terminal transcription factor enters the nucleus. SREBP-1 regulates genes involved in de novo lipogenesis including FASN, ACACA/ACC, SCD1, and ACLY. The SREBF1 gene produces the SREBP-1a and SREBP-1c isoforms. Cancer: ↑ Frequently increased or activated in cancer. Elevated SREBP-1 promotes de novo fatty-acid synthesis and metabolic reprogramming required for rapid tumor-cell proliferation. SREBP-1 can also promote survival, epithelial-mesenchymal transition, invasion, metastasis, tumor-microenvironment adaptation, ferroptosis resistance, and resistance to chemotherapy and radiotherapy. Genetic or pharmacological inhibition of SREBP-1 suppresses tumor growth in multiple preclinical cancer models. |
| 7636- | Ins, | Myo-Inositol: Pharmacokinetics, Biological Functions, and Therapeutic Potential in Liver Protection: Insights from Preclinical Models |
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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