PectaSol Modified Citrus Pectin Powder Super-Nutrient to Support Cellular & Immune Health, Joint Support - 454 Grams - Formulated by Dr. Isaac Eliaz of ecoNugenics

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PectaSol Modified Citrus Pectin Powder Super-Nutrient to Support Cellular & Immune Health, Joint Support - 454 Grams - Formulated by Dr. Isaac Eliaz of ecoNugenics

PectaSol Modified Citrus Pectin Powder Super-Nutrient to Support Cellular & Immune Health, Joint Support - 454 Grams - Formulated by Dr. Isaac Eliaz of ecoNugenics

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Unmodified citrus pectin does not have the same short, systemically available polysaccharide chains as MCP … and thus remains in the gastrointestinal (GI) tract. And other “modified” pectins may simply indicate that the pectin has been altered in some way, but doesn’t contain the shorter polysaccharide chains and molecular structure required for efficacy. In 2018, for example, clinical results from an ongoing multicentre trial on this form of MCP in biochemically relapsed prostate cancer were presented at the American Society for Clinical Oncology Genitourinary Conference. Reported in the Journal of Clinical Oncology, the study — “Effects of Pectasol-C Modified Citrus Pectin Treatment on PSA Dynamics in Non-Metastatic Biochemically Relapsed Prostate Cancer Patients” — demonstrated the ability of the only researched form of MCP to significantly slow PSA doubling time and halt disease progression in the majority of subjects. 1 What is galectin-3 (Gal-3)? Chemoresistance is a heavy burden in the treatment of cancer, especially since a large number of patients already display metastatic disease at the time of diagnosis. The vast majority of anti-cancer drugs currently used act by inducing apoptosis via the intrinsic pathway. Numerous mechanisms underlie cancer chemoresistance ( Rebucci and Michiels, 2013), but it appears that galectin-3 which is overexpressed in numerous tumor types, suppresses cell apoptosis and hence, decreases sensitivity of cancer cells to chemotherapeutic drugs ( Glinsky and Raz, 2009). Since MCP has been shown to target galectin-3, several works were dedicated to delineate MCP-induced possible re-sensitization of cancer cells to different cytotoxic molecules. Johnson et al. (2007) showed that galectin-3 targeting via MCP or via a more specific inhibitor, lactosyl- L-leucine (LL), decreased malignant endothelial cell proliferation by themselves and sensitized these cells to the cytotoxic effect of doxorubicin. These two compounds also increases metastatic-derived MDA-MB-435 cells sensitivity to taxol both in vitro and in vivo ( Glinsky et al., 2009). GCS-100, a commercially form of pH-MCP, enhanced bortezomide and dexamethasone-induced apoptosis in multiple myeloma cells and decreased viability. The effect was accompanied by a marked decrease in galectin-3 protein level ( Chauhan et al., 2005). GCS-100 also induced calpain activation in prostate cancer cells that led to their sensitization to cisplatin treatment ( Wang et al., 2010). Combination of modified pectin with different anti-cancer agents may thus represent an efficient new strategy to overcome resistance in cancer patients. Use of Pectin as a Vehicle for Drug Delivery in Cancer

Anti-cancer activities of pH- or heat-modified pectin Frontiers | Anti-cancer activities of pH- or heat-modified pectin

These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease. Cancer cell proliferation, migration and colony formation, induced pancreatic cancer cells apoptosis, suppressed autophagy


After treatment with MCP, the cells were cultured in serum-free RPMI-1640 medium for 24 h. The supernatant of the culture medium was collected, centrifuged at 1000 × g for 5 min, and stored at −20 °C. The levels of TGF-β and VEGFA in culture supernatants were assessed separately using ELISA kits (Proteintect, China) according to the manufacturer’s instructions. Flow cytometry Meanwhile, animal studies have shown that MCP can reduce galectin-3 levels in rats [ 15]. Could the same be true for humans? And could MCP therefore help to lower galectin-3 levels and improve thinking? Possibly. But of course, further study is needed here. Side Effects of Modified Citrus Pectin Z.Y. Zhao, et al., “The Role of Modified Citrus Pectin as an Effective Chelator of Lead in Children Hospitalized with Toxic Lead Levels,” Altern. Ther. Health Med. 14(4), 34–38 (2008).

PectaSol-C (Modified Citrus Pectin) Lime Infusion, 551g

Taking this combination for up to 51 weeks led to a 12.1% reduction of unhealthy LDL compared to just 1.3% for placebo. Total cholesterol was also 8.5% lower compared to 0.8%, and the LDL compared to HDL ratio was 9.4% lower compared to 1.5% higher for those in the placebo group [ 5].luc orthotopic tumor mouse model: 4T1-luc cells (5 × 10 5/100 μL/each mouse) were injected into the mammary fat pad under #3 mammary gland of each mouse. When the tumor volume reached about 100 mm 3, MCP (low-dose: 350 mg/kg every day; high-dose: 700 mg/kg every day) was given orally at once a day, clodronate liposomes (100 μL/10 g) was administered intravenously every 3 days. Each treatment was performed for consecutive 28 days. The field of Gal-3 continues to expand to previously undocumented conditions, as shown recently with findings in sepsis, mental illness, brain injury and others. Concurrently, we can expect the therapeutic significance of the correct form of MCP — the only commercially available natural Gal-3 inhibitor — to likewise increase, making it perhaps the most important ingredient available to support and maintain long-term health and wellness.

PectaSol-C (Modified Citrus Pectin) 150g – ecoNugenics

With over 75 published studies, PectaSol-C® Professional is the original and only proven form of modified citrus pectin, derived from citrus pith and modified to precise molecular weight and structure. This specialized modification process ensures bioavailability via absorption into the circulation, and gives PectaSol-C professional its’ broad-spectrum bioactivity resulting in systemic benefits for healthy cell, tissue, and organ function.* luc metastasis tumor mouse model: 1 × 10 5 4T1-luc cells (1 × 10 5/100 μL/each mouse) were intravenously injected to each mouse by tail vein. MCP (low-dose: 350 mg/kg every day; high-dose: 700 mg/kg every day) was given orally at oCell transfection was determined according to Micropoly-transfecter Cell Reagent (#MT115, Micropoly, Nantong, China) protocol. The sequence of galectin-3-siRNA was 5'-CAC GCT TCA ATG AGA ACA ACA-3'. The sequence of scrambled control was 5'-TTC TCC GAA CGT GCT GTC TTT-3'. Preparation of conditioned medium (CM)

Modified Citrus Pectin BenefitsConners Clinic | Alternative

Cell proliferation, ↓ caspase-3 activity, ↑ substrate-dependent adhesion in the presence of rhGal-3 Galectin-3 seems to be a target of MCP. Galectin-3 protein can be found intra- and extracellularly and contains a lectin domain. It has pleiotropic functions, amongst which, it mediates cell-cell as well as cell-extracellular matrix adhesion, through binding to glycoconjugates. Indeed, this lectin-domain has a high affinity for ß-galactoside residues. Galectin-3 expression is dysregulated in transformed cells, being highly expressed in numerous different types of cancer cells ( Newlaczyl and Yu, 2011). MCP has been shown to decrease liver metastasis in a mouse colon cancer model, in a dose-dependent manner. This effect may be linked to the higher expression of galactin-3 in the liver metastases ( Liu et al., 2008). The relationship between MCP structure and its inhibitory activity on galectin-3 was investigated in several studies. One such example is the work by Sathisha et al. (2007) who compared the activation of pectins from different dietary plants. Pectins rich in galactose and arabinose and in arabinogalactan significantly inhibited galectin-3-dependent hemagglutination of MDA-MB-231 cells to erythrocytes ( Sathisha et al., 2007). Pectin nearly mainly composed of RG-I isolated from okra, a tropical plant, arrested cell cycle of B16F10 cells in G2/M phase and induced apoptosis probably through interaction with galectin-3 ( Vayssade et al., 2010). Gao et al. (2012) suggested that MCP ability to inhibit galectin-3 resides in its RG-I regions and more particularly from galactan, of which the nature of last residue is the most important. Gunning et al. (2013) confirmed that neutral galactan side chains did selectively bind to recombinant galectin-3. These active fragments can be obtained by enzymatic treatment of isolated RG-I regions from potato pectin ( Gunning et al., 2009).


Circulating Gal-3 is often substantially elevated in patients with cancer, particularly metastatic cancer. Because of its primary roles in cancer formation and progression, Gal-3 has been termed “the guardian of the tumour microenvironment.” 6 Suppressed the viability in MDA-MB-231, MCF-7 and T47D human Breast cancer cells, ↓ mRNA expression of galectin-3 Both the green banana and the pectin significantly improved intestinal permeability and also reduced diarrhea [ 13]. Increasing Sepsis Survival Nearly 1.7 million new cases of breast cancer arise annually worldwide, accounting for 25.2% of all cancer cases (WHO). Approximately 15% of breast cancer patients die following diagnosis, second only to lung cancer [ 10, 11]. Complex, molecular breast cancer occurs when gene mutations cause abnormal cell growth and proliferation [ 12]. In vitro and in vivo studies have shown that pectin-derived chemicals slow cell development and promote apoptosis [ 13]. The synergistic and additive effects of MCP have been studied in human breast cancer cells. Polybotanical compounds BreastDefend (BD) or ProstaCaid (PC) used in combination with MCP reduced the invasive potential of highly metastatic human breast cancer MDA-MB-231 cells. MCP may also prevent the development of human breast cancer in mice by reducing angiogenesis, a crucial mechanism for tumor growth. The α-galactosidase binding protein Gal-3 is one potential mediator of MCP’s inhibition of breast and prostate cancer cell adhesion, migration, and invasion [ 7]. MCP inhibits urokinase-type plasminogen activator (uPA) synthesis in breast and prostate cancer cells, and the uPA receptor (uPAR) regulates cell adhesion, migration, and invasion [ 14]. In addition to activating macrophages, CP decreased activator protein 1 (AP-1) and NF-κB signaling but increased LPS/Toll-like receptor 4 (TLR-4) signaling [ 15]. In another study, CP and apple pectin (AP) inhibited MDA-MB-231, MCF-7, and T47D breast cancer cells, finding that CP and AP inhibited cancer cells in the S and G1 or G2/M phases of the cell cycle. Similarly, the expression of Gal-3, a lectin implicated in cell adhesion, cell cycle, and death, was reduced by CP and AP. In addition, oxidative and strand-break DNA damage was observed in MDA-MB-231 cells, slowing proliferation [ 16]. The most well-established pathogenic role of Gal-3 is in the development and migration of cancer. Gal-3 is over-expressed on the surface of cancer cells, acting as the primary adhesion molecule that allows cancers to proliferate, metastasize and evade the immune system.

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