Why Ivermectin + MCP = Cancer Remission

AI Ranks Galectin-3 Cancers & Reveals the CSC-Galectin-3 Connection

Blocking Galectin-3 Blocks Cancer Growth

While I normally wait until the weekend to update my Substack, today’s AI discovery is too important to delay.

Readers need to know now. Especially anyone with Pancreatic Cancer, Lung Cancer, Thyroid, Liver, and many others I will soon review.

Why?

Because Galectin-3 is a powerful driver of metastases. And because at least ten different cancers are high in Galectin-3 Activity. Thus, if one suffers from one of these types, adding a Galectin-3 Inhibitor just might save your life.

Modified Citrus Pectin is in our recently released protocols for a reason. And it is not just because it blocks Galectin-3. It also can fight cancer’s immune evasion.

Galectin-3 Driven Cancers Ranked:

Here are the Top Two Galectin-3 Driven Cancers:

#1. Thyroid Cancer. Galectin-3 is overexpressed. Galectin-3 levels are in crucial marker in Papillary Thyroid Cancer diagnosis and treatment.

#2. Pancreatic Cancer. Galectin-3 activity is “very high” and plays a critical role in Kras-mutation driven Pancreatic Cancers.

Galectin-3 interacts with Ras, especially K-Ras proteins which stimulate some of the most aggressive cancers such as Pancreatic and Lung.

K-Ras, as we shall soon learn, is also overactive in Colon Cancer, and blocking K-Ras activity can improve outcomes in these cancers.

Lung, Gastric, and Liver Cancers are all high in Galectin-3 activity:

As we reviewed in previous articles, Galectin-3 Inhibitors such as Modified Citrus Pectin, can significantly improve Galectin-3 driven cancers.

However, Modified Citrus Pectin has been mostly studied clinically against Prostate Cancer where it has proven quite effective against Biochemical Relapse.

Dr. Marik recognized the widespread Galectin-3 activity across many other cancers, and given MCP’s safety profile - it is derived from orange peels - we included it in our recently announced protocols.

We are feverishly working on improving these and we are currently revising these to target specific cancer types.

When Dr. Marik and I reviewed our provisional cancer-specific protocols this weekend, we noticed that Pancreatic Cancer seemed incredibly resistant to many repurposed drugs.

So, when I discovered today that Pancreatic Cancer is the second highest in Galectin-3 activity, I immediately evaluated whether blocking Galectin-3 would reduce metastatic potential, and the answer was “yes.”

Here is AI’s analysis on precisely which cancers would respond best if Galectin-3 blockers - like MCP - were added. And now we see Pancreatic Cancer is #1.

So now we see that in the worst cancers, Galectin-3 is a common denominator.

Why?

The Stunning CSC Link to Galectin-3

Galectin-3 nourishes and accelerates the growth of Cancer Stem Cells.

• The more Galectin-3, the bigger and rounder the Cancer Stem Cell and the more powerful its resistance against any form of treatment.

• And Galectin-3 stimulates Key CSC Growth Pathways including WNT and Notch. In addition, Galectin-3 helps makes cancer stem cells bullet-proof against chemotherapy.

Galectin-3 in CSC Drug Resistance and Survival

A hallmark characteristic of cancer stem cells is their inherent resistance to chemotherapeutic agents, which contributes significantly to cancer recurrence and treatment failure.

• Research has demonstrated that galectin-3 plays a central role in conferring this drug resistance to CSCs.

• In ovarian cancer, overexpression of galectin-3 significantly inhibited cisplatin and paclitaxel-induced cell death in A2780 and OVCAR3 cells.

• Conversely, depletion of galectin-3 enhanced paclitaxel-induced apoptosis in SKOV3 cells, while overexpression of galectin-3 reduced such apoptosis in A2780 cells.

• These findings suggest that galectin-3 protects cancer stem cells from chemotherapy-induced cell death, allowing them to survive treatment and potentially contribute to disease recurrence.

• Similarly, in gastrointestinal cancers, galectin-3-positive CSCs demonstrated resistance to chemotherapeutic agents and death-receptor-mediated apoptosis compared to galectin-3-negative populations.

• When galectin-3 was silenced, this resistance was significantly reduced, further establishing the causal relationship between galectin-3 and drug resistance.

The mechanisms behind galectin-3-mediated drug resistance appear to be multifaceted. In metastatic colon cancer cells, cell surface galectin-3 was found to be responsible for resistance to Tumor Necrosis Factor Related Apoptosis Inducing Ligand (TRAIL) by blocking the trafficking of death receptors prior to apoptosis.

In bladder carcinoma cells, galectin-3 knockdown stimulated TRAIL-induced apoptosis by downregulating the Akt/PI3K pathway.

These diverse mechanisms suggest that galectin-3 employs multiple strategies to protect cancer stem cells from various death stimuli.

If you want to eradicate CSCs, you should target Galectin-3. Since Galectin-3 is easily measured at Lab Corp with a simple blood test, it is easy to measure progress in killing CSCs.

Galectin-3 Promotes Metastasis

Metastasis remains the primary cause of cancer-related mortality, and cancer stem cells are thought to be critical drivers of this process.

• Galectin-3 has been shown to promote invasion and metastatic potential in cancer stem cells through multiple mechanisms.

• In ovarian cancer, silencing of galectin-3 significantly reduced the migration and invasion of cancer cells, while overexpression of galectin-3 enhanced these capacities.

• Similar effects have been observed in lung cancer stem cells, where galectin-3 overexpression increased invasion and colony formation abilities.

• The mechanisms by which galectin-3 promotes metastasis include effects on cell adhesion, epithelial-mesenchymal transition (EMT), and extracellular matrix degradation.

• Galectin-3 contributes to tumor cell's ability to invade and degrade basement membrane by increasing the activity of matrix metalloproteinases (MMPs)5.

• Silencing galectin-3 has been shown to reduce the secretion of MMP-2 and decrease the invasive ability of melanoma cells.

Furthermore, galectin-3 has been implicated in promoting EMT, a process by which epithelial cells lose their cell-cell adhesion and polarity to gain migratory and invasive properties. For those of you not familiar with EMT, I use a butterfly analogy in my book.

Galectin-3 interacts with and mediates the expression of many proteins that contribute to EMT during tumor cell migration and invasion.

Galectin-3 Blockers Suppress Metastases

The expanding understanding of galectin-3's role in cancer stem cell growth and maintenance has significant implications for cancer treatment. Since CSCs are often responsible for therapy resistance, tumor recurrence, and metastasis, targeting galectin-3 could potentially address these challenging aspects of cancer therapy.

• In ovarian cancer, increased expression of galectin-3 was detected in advanced stages (stages 3 and 4) compared to earlier stages (stages 1 and 2), suggesting that galectin-3 supports stemness in more aggressive disease.

• This observation highlights the potential value of galectin-3 as a prognostic marker and therapeutic target, particularly in advanced disease where treatment options are limited.

Galectin-3 Inhibitors Reduce Metastases in a Dose Dependent Manner

Several studies provide evidence supporting the hypothesis that cancers with higher galectin-3 expression may respond better to galectin-3 inhibitors.

In a mouse model of colon cancer liver metastasis, where galectin-3 was significantly overexpressed, MCP demonstrated dose-dependent inhibition of metastatic spread.

The percentage of liver metastasis in groups receiving increasing concentrations of MCP (0%, 1.0%, 2.5%, and 5.0%) was 100%, 80%, 73.3%, and 60%, respectively.

The more MCP, the fewer metastases. This suggests that for cancers with elevated galectin-3 expression, MCP can effectively reduce metastatic potential.

What is the Leading Galectin-3 Inhibitor?

Modified citrus pectin (MCP) stands as the most common and widespread galectin-3 inhibitor currently used against cancer.

This natural compound, derived from the peel and pulp of citrus fruits, has gained significant attention for its potential anti-cancer properties and favorable safety profile.

The Science Behind Galectin-3 Inhibition

Galectin-3 is a protein that plays a crucial role in cancer pathogenesis and progression.

• It functions as a molecular glue in the body, bringing together molecules with specific sugars, and is significantly overexpressed in various types of cancer.

This overexpression is often associated with poor clinical outcomes for patients.

• Galectin-3 promotes cancer through multiple mechanisms, including increasing invasiveness, facilitating metastasis, promoting tumor growth, and inhibiting the patient's immune system, thereby preventing immune cells from killing tumor cells.

MCP Safety Profile and Tolerability

• One of the most significant advantages of MCP as a galectin-3 inhibitor is its excellent safety profile. The U.S. Food and Drug Administration has categorized MCP as "Generally Recognized as Safe".

• In clinical trials, patients treated with MCP for extended periods showed minimal side effects. In the prostate cancer study, none of the patients experienced grade 3 or 4 toxicities during 18 months of therapy.

• The most common side effect reported was grade 1 toxicity consisting of transient and reversible bloating that did not require treatment discontinuation.

Alternative Galectin-3 Inhibitors: Belapectin

While MCP is the most widely used galectin-3 inhibitor, belapectin (GR-MD-02) represents another important compound in this class that is currently undergoing clinical development.

• Belapectin is a complex carbohydrate drug that targets galectin-3 and is being evaluated in combination with immunotherapy for cancer treatment.

• The combination of belapectin and pembrolizumab (an anti-PD-1 checkpoint inhibitor) has shown early potential for disease control with acceptable tolerability in patients with metastatic melanoma and head and neck cancer.

• This combination approach aims to enhance tumor responses by simultaneously blocking the immunosuppressive effects of galectin-3 and the PD-1/PD-L1 pathway.

Cancers Where Galectin-3 Inhibitors are Most Beneficial & Synergy with Ivermectin

Before we go into the specific cancers, it is important to ask the question of how much of a role Galectin-3 plays in blocking our immune system’s activity and what repurposed drugs might help this.

• And the answer is Ivermectin once again.

When combined with pembrolizumab, Ivermectin made “cold” tumors “hot” to the extent they became flooded with T cells. This created complete responses in nearly half the treatment mice tested.

Furthermore, AI ranked Ivermectin #1 in Natural Immune Checkpoint Blocker activity:

But if we combine Modified Citrus Pectin with Ivermectin?

This would be the equivalent of combining belapectin and pembrolizumab as shown below:

But I digress.

• Allow me to share with you the Cancers most likely to benefit from Galetin-3 blocking which are those cancers highest in Galectin-3 activity.

And in the section below, I will also provide a list of cancers most likely to respond to immune agent T-cell boosting of the type Ivermectin can provide as a natural checkpoint inhibitor.

• What I am getting at is that the combination of MCP + Ivermectin can be a game changer when the cancer is high in Galectin-3 activity and also in immune evasion. This applies to many of the most aggressive and unfortunately common cancers.