Mebendazole (MBZ) has been in use as an anti-helminthic since 1971, but within the last few years, MBZ has been added to the growing list of meds that are part of a movement to repurpose already known ‘safe’ molecules for novel or unexpected purposes. Mebendazole is known to interfere and inhibit the assembly of the spindles (see video), thus preventing the ability of the cells to divide, potently inhibiting hedgehog signaling (SMO, PTCH, GLi) , blocking glucose uptake, so this can have useful effects for reducing tumor growth. Over time, the cell eventually dies of old age or apotosis or programmed cell death (PCD).
MBZ is highly selective and somehow targets only tumor cells (as well as a host of intestinal parasites). It has been found useful with or without chemotherapy for adrenal, colon, brain, melanoma, HNSCC, bile duct, gastric, breast, lung , renal, ovarian, leukemia, acute myeloid leukemia (AML) , pancreatic, and fibrosarcoma tumors. [source]
MEBENGRAV™ is a broad-based nutraceutical formula containing 200mg of MBZ & herbal extracts; Graviola, Reishi, Cordyceps & Black Pepper which have been shown individually to provide antitumor support. MBZ works by the depolymerisation of tubulin in tumor cells inhibiting mitotic spindle formation, and therefore inducing mitotic arrest and apoptosis, it has very low levels of toxicity but you should be aware of tumor ‘lysis’ raising liver enzymes.
MEBENGRAV™ may be used as an adjuvant to standard care, as a primary antineoplastic as part of a metabolic fuel-blocking approach along with GLUTAHIB , FASNHIB, AUTOPHIB, or to activate caspases for the kill phase of the same strategy illucidated in the book by Jane McLelland (below).
So as well as choosing supplements which help target various oncogenes and tumor suppressors, the other aspects driving the Tumor is metabolic syndrome, this is how the Tumor gets it’s fuel, when you cutoff fuel availability to the cells, you weaken them, then after some months you can go in for the kill and be more effective than attacking strong growing Tumor cells.
These 3 main metabolic fuel pathways exploited by Tumors are the subject of Jane McLelland’s superb book: ‘How to Starve Cancer’ , where Jane shares her strategy for using Re-purposed drugs such as Metformin, Doxycyline, Dipyridamole, Niclosamide, Aspirin and a statin to target and inhibit these pathways which drive the TCA cycle within each Tumor cell with the aim of to weakening it over time. MBZ also interferes with VEGFR kinase by competing with ATP which is the energy used within the TCA Cycle of every cell.
MEBENGRAV™ is a broad-based nutraceutical formula containing 200mg of Mebendazole & herbal extracts; Graviola, Reishi, Cordyceps & Black Pepper which have been shown individually to provide antitumor support. MBZ works by the depolymerisation of tubulin in tumor cells inhibiting mitotic spindle formation, and therefore inducing mitotic arrest and apoptosis, very useful in the kill-phase, it has very low levels of toxicity but you should be aware of tumor ‘lysis’ raising liver enzymes.
Mechanism of Action
: The anti-parasitic action of MBZ is due to its action as a microtubule-disrupting agent acting to prevent the polymerisation of tubulin in the gut of
helminths, causing the parasites to die . Tubulin is vital to cell division and is therefore a Tumor target for several widely used chemotherapy drugs, including paclitaxel, colchicine, and vincristine. MBZ, as with the other benzimidazoles, binds to the colchicine-binding domain of tubulin .The inhibition of tubulin polymerisation by MBZ has been confirmed in vitro in a glioblastoma model and in a melanoma model . The latter work suggested that the apoptotic response to microtubule disruption is mediated by Bcl-2 phosphorylation. Subsequent work on melanoma confirmed this result, and also showed that MBZ decreased the levels of X-linked inhibitor of apoptosis (XIAP), but to date this
has not been confirmed in non-melanoma cell lines.
MBZ appears to be effective through p53-dependent and independent pathways. For example, in lung Tumor cell lines, it was found that MBZ treatment caused post-translational p53 stabilisation and the downstream expression of p21 and MDM2. In p53-null lung Tumor cells exposure to MBZ caused cytochrome c accumulation, activation of caspase-9 and caspase-8, and cleavage of PARP and procaspase-3. This independence of p53 status is also evident in the analysis of melanoma cells, where wild-type and mutant p53 cell
lines were sensitive to MBZ . [source]
To better understand these concepts, we urge you to get a copy of her book. Jane McLelland: ‘How to Starve Cancer’
Caspase Activation via P53, Bax and BCL-2
Cysteine proteases, called CASPASES (Cysteine Aspartate Specific ProteASEs) can be subdivided into three functional groups: initiator caspases (caspase 2, 8, 9 and 10), executioner caspases (caspase 3, 6 and 7), and inflammatory caspases (caspase 1, 4, 5, 11 and 12). Initiator caspases initiate the apoptosis signal while the executioner caspases carry out the mass proteolysis that leads to apoptosis. Inflammatory caspases do not function in apoptosis.
Apoptosis can be induced either from the cell surface, triggering of death receptors (e.g: FAS; TNF-R1; TNF related apoptosis, TRAIL/DR4 and TRAIL/DR5), or by the stimulation of intracellular receptor proteins, such as apoptotic protease activating factor (Apaf-1), which is activated by its ligand cytochrome-c once it is released from damaged mitochondria.
MBZ appears to be effective through p53-dependent and independent pathways. For example, in lung cancer cell lines, it was found that MBZ treatment caused post-translational p53 stabilization and the downstream expression of p21 and MDM2 . In p53-null lung cancer cells exposure to MBZ caused cytochrome c accumulation, activation of caspase-9 and caspase-8, and cleavage of PARP and procaspase-3. This independence of p53 status is also evident in the analysis of melanoma cells, where wild-type and mutant p53 cell lines were sensitive to MBZ .
It can be taken daily for a short period of 3-5 days followed by a detox using charcoal, LD Aspirin, Liposomal R-ALA and Epsom baths to to reduce effects of tumor breakdown. It should be taken with a little fat such as ghee, butter, avocado, Vit E or coconut oil, 2 x caps with water in the morning after food and 2 x Caps in the evening after food or as directed by your health professional. May be suitable as an adjuvant. May best be supported with FASNHIB™ Fatty Acid & GLUTAHIB™ metabolic fuel supply inhibiting formula, EGAMMA™, AUTOPHIB™, CURCUBOS™, CURCUMEL™, ZERO Sugar/Fat Diet, METFORMIN, LD/ASPIRIN and/or STATIN, DIPYRIDAMOLE & MILDRONATE. Avoid White Rice, Sesame Oils & Flax-oils which can lessen the effect of statins.
Quality Assurance Declaration
Werone.co endeavors to use the most potent source materials within our formulas. Our herbal extracts are sourced and tested by the only Government-certified large scale producer of crude herb (powder-free) TCM concentrates in Asia who manufacture to GMP / ISO 9001/2000 pharmaceutical grade and also operate an ISO17025/TAF-certified laboratory where they subject all plant extracts to strict quality inspections free from heavy metals, pesticides or microbes before release to the clinics all over the world. The formulas and tinctures are assembled without fillers in small batches by a BHMA member herbal dispensary.
Nutraceutical DisclaimerThese statements have not been evaluated by the Food and Drug Administration or MHRA and the items are not intended to diagnose, treat, cure, or prevent any disease nor are they associated, endorsed, affiliated or sponsored by Anthony William, Medical Medium® Joe Tippens or Jim Gordon.
Repurposing Drugs in Oncology (ReDO)—mebendazole as an anti-tumor agent
Mebendazole Elicits a Potent Antitumor Effect on Human Tumor Cell Lines Both in Vitro and in Vivo
Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors.
Anti-Neoplastic Cytotoxicity of Gemcitabine-(C4-amide)-[anti-EGFR] in Dual-combination with Epirubicin-(C3-amide)-[anti-HER2/neu] against Chemotherapeutic-Resistant Mammary Adenocarcinoma (SKBr-3) and the Complementary Effect of Mebendazole. https://www.ncbi.nlm.nih.gov/pubmed/25844392
The anthelmintic drug mebendazole induces mitotic arrest and apoptosis by depolymerizing tubulin in non-small cell lung Tumor cells.
The anthelmintic drug mebendazole inhibits growth, migration and invasion in gastric Tumor cell model.
Repositioning of the anthelmintic drug mebendazole for the treatment for colon Tumor cells.